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The lifeflight legacy: 40 years in 40 photos, july 29, 2024, study sheds new light on autism, but there’s more work to be done.

A target of their investigations is serotonin, a signaling molecule that is well known for its critical roles in regulating mood and which also plays an important role in the development of the brain and nervous system.

A rise in a mother’s blood levels of serotonin — a neurotransmitter that regulates mood, memory and gastrointestinal function — is associated with some, but not all forms of autism in children. (illustration by Diana Duren with Adobe Stock)

Researchers from Columbia and Vanderbilt universities, the University of Illinois Chicago and colleagues across the country are making steady progress in their decades-long quest to understand autism spectrum disorder (ASD), a brain development condition that affects social interaction, communication and behavior.

In a recent study, the researchers measured blood levels of serotonin in women whose children were diagnosed with ASD. Some of the children carried rare genetic variations that strongly contribute to the risk of autism, while others did not.

In their paper, published July 4 in the Journal of Clinical Investigation , the researchers reported that higher serotonin levels were primarily found in women whose children who did not carry the rare variants.

This finding suggests that elevated maternal serotonin levels are associated with autism in a subset of children who have multiple common genetic or environmental factors which likely contribute to risk. Elevated levels are not found as frequently when a single, rare genetic variant explains most of the risk.

The link between autism-associated genetic variations and maternal serotonin levels was first described more than 60 years ago.

But it is a complicated picture that is not fully understood, noted James Sutcliffe , PhD, a pioneer in autism genetics at Vanderbilt University.

The study probed genetic samples from the University of Illinois Chicago (UIC) Autism Center of Excellence and from the UIC and Vanderbilt sites of the Simons Simplex Collection , a repository of samples from 2,600 families of children with ASD maintained by the Simons Foundation Autism Research Initiative.

The study did not have a control group — it did not compare maternal serotonin levels to those from women whose children do not have autism. Another limitation was that serotonin blood levels in the women were measured after their children had been diagnosed with ASD.

Taking measurements throughout pregnancy would provide a more complete picture of how maternal serotonin levels may relate to autism risk, said Jeremy Veenstra-VanderWeele , MD, the Ruane Professor of Psychiatry and director of the Division of Child & Adolescent Psychiatry at Columbia University Irving Medical Center in New York City.

Veenstra-VanderWeele is corresponding author of the paper. Before coming to Columbia in 2014, he directed the Division of Child and Adolescent Psychiatry at Vanderbilt University Medical Center and was medical director of the Treatment and Research Institute for Autism Spectrum Disorders ( TRIAD ) at the Vanderbilt Kennedy Center.

Sutcliffe, who co-authored the paper, is associate professor of Molecular Physiology & Biophysics and of Psychiatry & Behavioral Sciences at Vanderbilt.

Other co-authors are Edwin Cook , MD, also a pioneer in autism genetics who directs the Center for Neurodevelopmental Disorders and the Division of Child and Adolescent Psychiatry at UI Health, and colleagues from New York University and Yale University School of Medicine.

While the true nature of the relationship between serotonin levels and ASD remains elusive, clinical trials are underway at Vanderbilt and elsewhere to evaluate drugs that, by impacting the serotonin system, may relieve irritability or improve social functioning in children with autism.

Genetic studies also have led to the identification of other, possibly related health conditions in children with ASD, including previously undiagnosed cardiac abnormalities and severe epilepsy that occurs during sleep, Sutcliffe said.

The investigators hope that further research may lead to targeted interventions based upon ASD-associated genetic variation or biomarkers. That, Veenstra-Vanderweele said, would be “transformative” for children who are severely affected by autism.

January 9, 2014

Brain-gut connection in autism.

An association between rigid-compulsive behaviors and gastrointestinal symptoms in autism spectrum disorder may point to a common biological pathway that impacts both the brain and the gut.

By Leigh MacMillan

January 28, 2016

Autism study links sensory difficulties, serotonin system.

Vanderbilt researchers have established a link between the neurotransmitter serotonin and certain behaviors of some children with autism spectrum disorder (ASD), a link that may lead to new treatments for ASD.

By VUMC News and Communications

August 12, 2024

Researchers seeking children ages 10-16 with autism, intellectual disability for theater intervention study.

The intervention is free for participants and would include evaluations before and after the program.

Suramin for Autism Update: 2023 and Beyond

Brought to you by the BRAIN Foundation In partnership with PaxMedica

About the event

An exclusive interview with Howard Weisman, CEO of PaxMedica, on the latest developments and plans for FDA approval for suramin, a potential breakthrough treatment for autism.

Hosted by the BRAIN Foundation on June 17, 2023, this online interview provided an update on the development of suramin as an evidence-based therapeutic for autism, clinical trial results, go-forward plans to seek FDA approval, international availability, and the possibility of expanded access for compassionate use for autism.

Watch the recording of the event

About suramin

Suramin is a 100 year old drug that has been traditionally used to treat African sleeping sickness and river blindness. In addition to its antiparasitic action, it is also a non-selective inhibitor of purinergic signaling, or in other words, an antipurinergic drug.

The Naviaux Lab at University of California, San Diego led by Robert K. Naviaux, MD, PhD, discovered that the unique properties of suramin made it the first in a new class of drugs that could be used to test the cell danger response (CDR) hypothesis for the origin and treatment of Autism Spectrum Disorder (ASD). Suramin successfully improved all the core symptoms of ASD and the metabolic and GI abnormalities in both animal models and a small human clinical trial.

About suramin clinical trials

This human clinical trial, published in 2017, was a small, randomized Phase 1 study of low-dose suramin in 10 children with ASD. The results demonstrated that a single intravenous dose of suramin improved core symptoms of autism in the five children who received the drug, compared to placebo. The improvements were noted in the domains of language, social interaction, and repetitive behaviors.

This study was followed by PaxMedica’s Phase 2 trial of Pax-101 (IV suramin) for ASD, the results of which were presented to AACAP in October 2021. This study was a dose-ranging, randomized, double-blind, placebo-controlled, multi-dose trial evaluating the safety and efficacy of suramin in 52 children with autism (with moderate to profound support needs) across 6 sites in South Africa.

About PaxMedica

PaxMedica is a clinical-stage biopharmaceutical company developing innovative treatments for unmet needs in neurodevelopmental disorders, including ASD. Read more about PaxMedica here .

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Fragile x held him back. an experimental drug is helping him break free.

Jon Hamilton

There’s evidence fragile X symptoms can be reduced with an experimental drug

Jason Mazzola walks to work at The Residence at Natick South, an LCB Senior Living community in Natick, MA. August 22, 2024. Jodi Hilton for NPR hide caption

For 22 years, Jason Mazzola’s life was defined by Fragile X, a genetic condition that often causes autism and intellectual disability.

Jason, who is 24 now, needed constant supervision. He had disabling anxiety, and struggled to answer even simple questions.

All that began to change when he started taking an experimental drug called zatolmilast in May of 2023.

“It helps me focus a lot, helps me get more confident, more educated,” Jason says.

His mother, Lizzie Mazzola, credits zatolmilast with transforming her son.

“I have a different child in my house,” she says. “He gets himself to work, he walks downtown, gets his haircut, gets lunch. He wouldn't have done any of that before.”

Other parents of children with Fragile X are also reporting big changes with zatolmilast.

Those anecdotes are supported by data.

A 2021 study of 30 adult male participants with Fragile X found that taking zatolmilast for 12 weeks improved performance on a range of memory and language measures.

Now, two larger studies are underway that will determine whether zatolmilast becomes the first drug approved by the Food and Drug Administration to treat Fragile X.

Brain, interrupted

Mazzola realized early on that Jason was falling behind.

August 22, 2024, Natick, MA. Photos of the twins Jason and Jessie as children. Both were born with Fragile X syndrome.

August 22, 2024, Natick, MA. Photos of the twins Jason and Jessica as children. Both were born with Fragile X syndrome. Jodi Hilton for NPR/Jodi Hilton for NPR hide caption

“He could hardly talk by three,” she says. “At four he started to put some words together, but really wasn’t talking in sentences.”

Genetic tests revealed the cause: Fragile X.

The inherited condition affects the X chromosome, making one segment appear fragile or broken. This anomaly blocks production of a protein that’s important to brain development.

The result can be autism, ADHD, anxiety, sensory sensitivity, and a range of intellectual disabilities.

For Jason, many of these symptoms were severe. Like many people with Fragile X, his IQ was in the 40s, and he was often paralyzed by anxiety.

Jason’s twin sister, Jessica, also has Fragile X, but the symptoms are absent or much milder.

That’s often true of females with the condition. They typically benefit from having two X chromosomes, one of which is unaffected.

So while Jessica went on to college, Jason was still barely able to converse, even with his parents.

“He’s always wanted to be social. He’s a friendly person,” Mazzola says. “But because his communication skills were so impaired, he struggled to put his thoughts into words.”

August 22, 2024, Natick, MA. Jason Mazzola at home with his twin sister Jessie and dog Marley.

August 22, 2024, Natick, MA. Jason Mazzola at home with his twin sister Jessica and dog Marley. Jodi Hilton for NPR/Jodi Hilton for NPR hide caption

Repurposing an Alzheimer’s drug

By the time Jason was a teenager, scientists had begun studying the link between Fragile X and an enzyme that plays a role in memory and cognitive impairment.

Much of the funding for this research came from the FRAXA Research Foundation , a group founded by the parents of a child with Fragile X.

FRAXA-funded researchers knew there were drugs that could tweak the enzyme in a way that might help a Fragile X brain work better. But the drugs all had side effects that made them unsuitable for people.

Then one day FRAXA got a call from Tetra Therapeutics , a small drug company in Michigan.

“They had this drug in clinical trials for Alzheimer’s disease,” recalls Dr. Michael Tranfaglia, FRAXA’s co-founder and medical director. “They wanted to explore the possibility of using their drug in Fragile X.”

That made sense because the drug targeted the same enzyme FRAXA had been studying and it didn’t seem to cause the side effects that had ruled out similar drugs.

The next stop for Tetra was Dr. Elizabeth Berry-Kravis , a professor at RUSH University Medical Center in Chicago. Berry-Kravis had been studying the way Fragile X affects brain development for nearly three decades, and was receiving funding from FRAXA.

So she got a visit from a Tetra executive.

“ Mark Gurney , who was the head of the company at the time, came to my office and said, ‘Hey, you’ve got this mechanism that you’ve been waiting for a drug for for 28 years, and we’ve got a drug,’ ” Berry-Kravis recalls.

The drug was zatolmilast.

August 22, 2024, Natick, MA. Jason Mazzola works as a dishwasher at The Residence at Natick South. Jodi Hilton for NPR/Jodi Hilton for NPR hide caption

Jason unbound

A flurry of research showed that zatolmilast worked in fruit flies and mice with Fragile X. The 2021 study of 30 male adults extended the promising results to people.

“We saw an improvement in their memory and their vocabulary and their ability to read,” Berry-Kravis says.

The next step was to have Berry-Kravis oversee a pair of larger studies – one in males from 9 to 17, the other in males from 18 to 45. The studies got underway in 2022, with funding from the Japanese drug company Shionogi, which had acquired Tetra.

Mazzola decided to enroll her son, Jason, who was now in his 20s. She was optimistic about zatolmilast, despite having witnessed the failure of other promising drugs for Fragile X

“It just seemed different,” she says. “It was affecting their cognition and IQ scores.”

At first, Mazzola and her husband didn’t know if their son was getting zatolmilast or a placebo.

Within a few weeks, though, Jason did something remarkable: He walked into his father’s home office and started a conversation.

“My husband said, ‘He has to be on the drug. He’s never done that,’ ” Mazzola says.

Jason is still taking the drug, and still improving, Mazzola says. He has a job washing dishes at a local assisted living facility. He helps his mom coach high school field hockey and lacrosse.

Jason himself offers perhaps the most compelling evidence that the drug is working.

August 22, 2024, Natick, MA. Jason Mazzola getting his haircut by Jose Nieves at Title City. Jodi Hilton for NPR/Jodi Hilton for NPR hide caption

At his home in a Boston suburb, the young man who was once paralyzed by simple questions agrees to an interview.

When I ask Jason to tell me something about himself, he’s got an answer:

“I play a lot of sports like hockey, basketball and golf,” he says. “Golf is really fun because I play with my dad.”

“You good off the tee with the driver?” I ask.

“Yeah, the driver,” he says, “and the six iron and the seven and the putter.”

A scientific verdict on the drug will come when the study is completed, probably in 2025.

medical research
medications
experimental drugs

Treatment for autism symptoms earns ASU researchers patent

Microbiota Transplant Therapy offering hope to those with autism spectrum disorder

ASU Professor Rosa Krajmalnik-Brown and Assistant Professor Daewook Kang wearing white lab coats in a lab setting.

ASU Professor Rosa Krajmalnik-Brown and Assistant Professor Daewook Kang (now with the University of Toledo) in an ASU file photo from 2017. Krajmalnik-Brown, Kang and Professor James Adams are three of six co-inventors who were awarded a patent for their treatment for autism and related symptoms.

Editor’s note: This story is featured in the 2022 year in review .

A new treatment for autism, created by Arizona State University researchers and their colleagues, has been granted a patent by the U.S. Patent Office. The therapy, called Microbiota Transplant Therapy (MTT), is aimed at improving chronic gastrointestinal symptoms often associated with the disorder.

Receiving the approval of the patent for this promising treatment is also an important step toward developing a Food and Drug Administration approved medication for treating the core symptoms of autism. An initial study of Microbiota Transplant Therapy suggests that it may be effective in treating both core autism symptoms and chronic gastrointestinal symptoms.

Rosa Krajmalnik-Brown , ASU professor and director of the Biodesign Center for Health Through Microbiomes, and a pioneer in research on the gut microbiome and autism, is a co-inventor of the treatment.

“Our mission at the ASU Biodesign Center for Health Through Microbiomes is to improve human health by developing new methods to modify the microbiome. This is at the core of our center, and it’s exciting that we have a patent to achieve this,” said Krajmalnik-Brown, a professor with the School of Sustainable Engineering and the Built Environment.

Autism now affects one in 44 children in the United States, often presenting major challenges in language, social interactions and behavior. Many people with autism have significant health problems, including 30–50% with chronic gastrointestinal symptoms such as constipation, diarrhea and abdominal pain. These symptoms are difficult to treat and can persist for many years or even decades. Chronic pain caused by gastrointestinal distress can worsen other symptoms associated with autism, including irritability, attention deficits, behavioral issues and sleep disturbances.

“We are excited about this patent approval. Our open-label pilot study and two-year follow-up study found major improvements in gastrointestinal and autism symptoms. Now, we are conducting randomized clinical trials to fully evaluate the efficacy of treatment with MTT,” said co-inventor James Adams . Adams is a professor with the School for Engineering of Matter, Transport and Energy, one of the seven Ira A. Fulton Schools of Engineering at ASU.

James Adams

In 2017, the ASU researchers and their collaborators developed MTT to improve gastrointestinal symptoms. MTT involves pre-treatment with a special antibiotic to eliminate harmful bacteria, a bowel cleanse to remove remaining bacteria, and purified intestinal microbiota from healthy, carefully screened human donors.

The treatment, similar to the fecal transplant commonly used to treat intestinal infections such as C. Difficile, involves 10 weeks of intense daily therapy. The approach is based on pioneering research by Dr. Thomas Borody with the Centre for Digestive Diseases in Australia, who first used this method to successfully treat his patients with autism, and Professors Alex Khoruts and Michael Sadowsky at the University of Minnesota, who developed the methods for producing purified microbiota.

In their 2017 study, Adams, Krajmalnik-Brown and their research team found that MTT reduced gastrointestinal symptoms by approximately 80%, and initially reduced autism symptoms by about 25%. But, as an open-label study, they observed some placebo-effect. A follow-up study of all 18 participants two years after the treatment was completed found that most continued to see a considerable improvement in gastrointestinal symptoms. Additionally, an expert autism evaluator reported a nearly 50% reduction in core autism symptoms.

Measurements of the participants’ microbiota at Krajmalnik-Brown’s lab by Assistant Professor Daewook Kang (now with the University of Toledo) showed that although the children, aged 7 to 16 at the time of the study, initially had a low diversity of gut bacteria, the diversity and presence of beneficial microbes had increased and improved in the two years following the treatment. Based on these promising results, the FDA granted “fast track” status for MTT in 2019, which means a rapid review and more assistance from the FDA.

Recent research suggests our gut microbiomes affect brain communication and neurological health. Worldwide, interest is growing in the idea that changes in normal gut microbiota may be responsible for triggering various conditions. At ASU, a research team is exploring using the microbiome to treat autism symptoms. Image by Shireen Dooling

Approval of the patent is also important because pharmaceutical companies can invest in conducting Phase 2 and Phase 3 clinical trials, which are required for FDA approval and release of the treatment to the public. The patent has been licensed to Finch Therapeutics, which is planning clinical trials in mid-2022.

Meanwhile, the ASU team is continuing its own Phase 2 clinical trials for adults with autism (the final participants have started treatment) and children with autism (half of the participants have started treatment). These studies will be important for ultimately winning FDA approval.

Information on the patent, as well as a full list of collaborators, can be found on the U.S. Patent Office website (U.S. Patent number 11202808).

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An Update on Psychopharmacological Treatment of Autism Spectrum Disorder

Affiliations.

1 Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California Davis, 2825 50th Street, Sacramento, CA, 95817, USA.
2 Khoo Teck Puat-National University Children's Medical Institute, National University Health System, 5 Lower Kent Ridge Road, Singapore, 119074, Singapore.
3 Department of Pediatrics, Yong Loo Lin School of Medicine, National University of Singapore, 1E Kent Ridge Road, Singapore, 119228, Singapore.
4 Association for Children With Autism, Chisinau, Moldova.
5 Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California Davis, 2825 50th Street, Sacramento, CA, 95817, USA. [email protected].
6 Department of Pediatrics, University of California Davis School of Medicine, 4610 X St, Sacramento, CA, 95817, USA. [email protected].
7 Department of Pediatrics, University of California Davis School of Medicine, 4610 X St, Sacramento, CA, 95817, USA.
PMID: 35029811
PMCID: PMC9130393
DOI: 10.1007/s13311-022-01183-1

While behavioral interventions remain the mainstay of treatment of autism spectrum disorder (ASD), several potential targeted treatments addressing the underlying neurophysiology of ASD have emerged in the last few years. These are promising for the potential to, in future, become part of the mainstay treatment in addressing the core symptoms of ASD. Although it is likely that the development of future targeted treatments will be influenced by the underlying heterogeneity in etiology, associated genetic mechanisms influencing ASD are likely to be the first targets of treatments and even gene therapy in the future for ASD. In this article, we provide a review of current psychopharmacological treatment in ASD including those used to address common comorbidities of the condition and upcoming new targeted approaches in autism management. Medications including metformin, arbaclofen, cannabidiol, oxytocin, bumetanide, lovastatin, trofinetide, and dietary supplements including sulforophane and N-acetylcysteine are discussed. Commonly used medications to address the comorbidities associated with ASD including atypical antipsychotics, serotoninergic agents, alpha-2 agonists, and stimulant medications are also reviewed. Targeted treatments in Fragile X syndrome (FXS), the most common genetic disorder leading to ASD, provide a model for new treatments that may be helpful for other forms of ASD.

Keywords: Autism; Autism spectrum disorder; Medications; Pharmacology.

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The authors declare no competing interests.

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What we know about autism—and how to treat it—could change after new UCSF study

by Jason Fagone, San Francisco Chronicle

By fusing the power of artificial intelligence with new molecular techniques that also seem ripped from science fiction, researchers at UCSF have mapped the microscopic world of autism spectrum disorder in unprecedented detail, pointing toward possible therapies for a subset of patients who have specific genetic mutations, according to a new study.

"This opens up kind of a Goldilocks of potential treatment targets," said one of the study's authors, Matthew State, a UCSF child psychiatrist and geneticist. "It's an opportunity for shots on goal that we just have not had before, because of the complexity of autism."

The results are novel for a few reasons, researchers said. It's the first time that the cellular workings of a neuropsychiatric disorder like ASD have been explored this deeply, opening a door for similar investigations of other neuropsychiatric disorders such as attention deficit hyperactivity disorder and schizophrenia.

The study also combined a basket of new technologies in an original way. Those technologies include stem cells, CRISPR-based genetic tools and AlphaFold 2, the Google AI that predicts the behavior of proteins.

In addition, researchers leveraged a system originally developed at UCSF to study viruses, including the pandemic-causing coronavirus. That platform is able to create comprehensive maps of the interactions between proteins, the biological machines produced by genes that carry out work in the cell.

"We've been at the bleeding edge of putting all this together," said another study leader, Nevan Krogan, director of the Quantitative Biosciences Institute within UCSF's School of Pharmacy, which coordinated the research along with the Department of Psychiatry and Behavioral Sciences.

The paper was posted Monday on bioRxiv.org , a preprint server, and will be submitted to a peer-reviewed journal. UCSF's Jeremy Willsey and Tomasz Nowakowski co-led the work, and Rezo Therapeutics, a biotech company founded by QBI and Krogan, also contributed.

Over the last decade, scientists including State have discovered over 100 mutated genes that are connected to autism. But translating that knowledge into therapies has been difficult, State said. The brain is intricate, and just knowing the right genes isn't enough.

The UCSF-led team took a new approach, focusing on the proteins manufactured by those genes and mapping how they interact with each other.

Researchers found 1,000 proteins and more than 1,800 interactions. About 90% of the interactions "are things we've never seen before," State said.

The team then looked for clues about how the mutations lead to the disorder by using specific mutations from a subset of ASD patients. The scientists exploited AlphaFold's predictive abilities and various molecular techniques to pinpoint the most meaningful interactions, studying how those proteins function in human cells and in "brain organoids" grown from stem cells .

These findings could one day lead to new drugs for patients, State and Krogan said.

"We're shining a brand-new light on autism," Krogan said.

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Open access
Published: 10 June 2024

New advances in the diagnosis and treatment of autism spectrum disorders

Lei Qin 1 ,
Haijiao Wang 2 ,
Wenjing Ning 1 ,
Mengmeng Cui 1 &
Qian Wang 3

European Journal of Medical Research volume 29 , Article number: 322 ( 2024 ) Cite this article

3666 Accesses

1 Citations

Metrics details

Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders that affect individuals' social interactions, communication skills, and behavioral patterns, with significant individual differences and complex etiology. This article reviews the definition and characteristics of ASD, epidemiological profile, early research and diagnostic history, etiological studies, advances in diagnostic methods, therapeutic approaches and intervention strategies, social and educational integration, and future research directions. The highly heritable nature of ASD, the role of environmental factors, genetic–environmental interactions, and the need for individualized, integrated, and technology-driven treatment strategies are emphasized. Also discussed is the interaction of social policy with ASD research and the outlook for future research and treatment, including the promise of precision medicine and emerging biotechnology applications. The paper points out that despite the remarkable progress that has been made, there are still many challenges to the comprehensive understanding and effective treatment of ASD, and interdisciplinary and cross-cultural research and global collaboration are needed to further deepen the understanding of ASD and improve the quality of life of patients.

Autism spectrum disorders (ASD) are a broad group of neurodevelopmental disorders that affect an individual's social interactions, communication skills, and behavioral patterns [ 1 , 2 ]. The characteristics of ASD vary significantly between individuals, from mild social impairments to severe communication and behavioral problems, a diversity that reflects the use of the term “spectrum” [ 3 ]. Although the exact causes of ASD are not fully understood, research suggests that both genetic and environmental factors play a key role in its development [ 4 ].

Characteristics of ASD

Difficulties in social interaction.

Individuals with ASD often exhibit significant difficulties in social interactions. These difficulties may include difficulty understanding the feelings and intentions of others, maintaining eye contact and facial expressions, and adapting to social norms and expectations. Individuals with ASD may experience challenges in establishing and maintaining friendships, they may not understand the two-way nature of social interactions, or they may feel uncomfortable sharing interests and activities [ 5 ].

Communication disorders

Communication deficits are another core feature of ASD. This may manifest itself in delays in language development, including delays in uttering first words or simple sentences. Some individuals with ASD may not use language to communicate at all. Even among individuals with ASD who have normal language skills, they may have difficulty using language in conversations to communicate thoughts, feelings, or needs. In addition, nonverbal communication, such as the understanding and use of body language and facial expressions, may also be affected [ 6 ].

Repetitive behaviors and interests

Individuals with ASD often display restricted, repetitive patterns of behavior and interests. These may include a strong fixation on specific topics or activities, repetitive body movements (e.g., rocking, clapping), and an overreliance on daily routines. These repetitive behaviors are sometimes seen as a way of self-soothing or as an attempt to control an environment that otherwise feels unpredictable and overwhelming to them [ 7 ].

Sensory sensitivity

Many individuals with ASD have abnormalities in sensory processing and may have very strong or delayed responses to sound, light, touch, taste or odor. For example, some individuals with ASD may find background noises in their everyday environment unusually harsh, or they may not notice pain or other bodily sensations [ 8 ].

Epidemiologic profile of ASD

According to the World Health Organization (WHO), the average prevalence of ASD among children globally is approximately 1% [ 9 ]. However, this figure varies significantly between regions and countries. For example, the Centers for Disease Control and Prevention (CDC) reports that the prevalence of ASD among 8-year-olds in the U.S. is 1 to 54. ASD is significantly more prevalent in males than females, at a ratio of approximately 4:1 [ 10 ]. This gender difference may reflect differences in genetic susceptibility and/or gender bias in the diagnostic process. Early diagnosis is key to improving developmental outcomes for children with ASD. Despite this, many children are not diagnosed by age 3. The CDC reports that most children are first evaluated for ASD by age 4, but diagnosis may occur later. Research suggests that ASD is highly heritable, but multiple genetic variants are associated with disease risk and environmental factors also play a role [ 11 ]. For example, there is an increased risk of ASD in preterm and low birth weight infants. Socioeconomic factors influence ASD diagnosis and treatment access. Families of lower socioeconomic status may face greater challenges, including barriers to accessing early intervention services, etc. ASD is a global public health problem, and its incidence, time to diagnosis, and treatment access are influenced by multiple factors [ 12 ]. Ongoing epidemiologic research and the advancement of a deeper understanding of ASD are critical to the development of effective prevention, diagnosis, and interventions.

Historical background

Early history of research and diagnosis of asd.

The concept of ASD was first clearly defined in the 1940s, when a group of children exhibiting extreme self-isolation and lack of responsiveness to the environment was first described by American psychiatrist Leo Kanner [ 13 ]. Almost simultaneously, Austrian child psychologist Hans Asperger described a similar but higher level of functioning in a condition that came to be known as Asperger’s syndrome [ 14 ]. These two independent studies laid the foundation for the modern understanding of ASD. For the first few decades, ASD was considered extremely rare and was often confused with schizophrenia. Due to a lack of in-depth understanding of ASD, early diagnostic criteria were unclear and treatment was largely limited to behavioral interventions and psychotherapy. Over time, researchers began to pay more attention to the genetic and neurobiological underpinnings of ASD, thus contributing to a more comprehensive understanding of this complex condition. Since the 1990s, the diagnosis of ASD has risen significantly, as diagnostic criteria have continued to be refined and public awareness has increased. This period has also witnessed an increased awareness of the importance of early diagnosis and intervention for ASD, which has led to significant improvements in the prognosis and quality of life for many children and adults with ASD [ 15 ].

Evolution of research paradigms

The research paradigm for ASD has undergone a remarkable evolution since the mid-twentieth century, a process that reflects a deepening of the understanding of ASD as well as advances in scientific research methods [ 16 ]. In the early stages, ASD research focused on behavioral observations and psychoanalysis, when ASD was often mistaken for an emotional disorder due to an indifferent mother. During this period, understanding of ASD was relatively limited and treatments focused primarily on psychotherapy and behavior modification. Into the second half of the twentieth century, with advances in genetics and neuroscience, researchers began to explore the biological basis of ASD. This marked a shift from a psychosocial to a biomedical model, and the focus of research gradually shifted to genetic factors and abnormalities in brain structure and function. Through a large number of family and twin studies, scientists found that ASD has a high genetic predisposition, while neuroimaging studies revealed the specificity of brain development in ASD patients. In the twenty-first century, with the application of bioinformatics and high-throughput gene sequencing technology, the study of ASD has entered a new stage [ 17 ]. Researchers have not only been able to identify specific genetic variants associated with ASD, but have also begun to explore the interaction between environmental factors and genetic susceptibility. In addition, the adoption of interdisciplinary research approaches, such as combining neuroscience, genetics, psychology, and computational modeling, has provided new perspectives for understanding the complexity of ASD.

Recently, the concepts of precision medicine and personalized treatment strategies have been introduced to the study of ASD, aiming to develop customized intervention programs based on each patient’s genetic background and symptom profile. With advances in technology and improved methods of data analysis, future research on ASD is expected to reveal more knowledge about its pathomechanisms and provide more effective support and treatment for patients with ASD.

Etiologic studies

Genetic factors, monogenic genetic cases.

The etiology of ASD is multifactorial, involving a complex interaction of genetic and environmental factors. Although most cases of ASD are thought to be the result of polygenic interactions, there are some cases that are directly associated with variations in a single gene, and these are referred to as monogenic genetic cases. Monogenic genetic cases provide an important window into understanding the genetic basis of ASD, although they represent a relatively small proportion of all ASD cases [ 18 ]. A number of specific genetic syndromes, such as fragile X syndrome, tuberous sclerosis, 15q11-q13 duplication syndrome, and Rett syndrome, have been found to be associated with a higher risk of ASD. These conditions, often caused by mutations or abnormalities in a single gene, can lead to significant differences in brain development and function, thereby increasing the probability of an ASD phenotype. Fragile X syndrome is one of the most common forms of inherited intellectual disability and the single-gene disorder known to be most strongly associated with ASD. It is caused by a repeat expansion on the FMR1 gene [ 19 ]. Tuberous sclerosis (TSC) is an inherited disorder that affects multiple systems and is caused by mutations in the TSC1 or TSC2 genes, and the prevalence of ASD is higher in patients with TSC. 15q11-q13 duplication syndrome (Dupuy 15q syndrome) involves a region of chromosome 15, the duplication of which is associated with an increased risk of ASD [ 20 ]. Rett syndrome, which predominantly affects females, is caused by mutations in the MECP2 gene, and patients often exhibit some of the features of ASD, such as impaired social interactions [ 21 ]. The association of these classical candidate genes with ASD is summarized in Table 1 .

The discovery of these monogenic genetic cases is not only crucial for understanding the genetic mechanisms of ASD, but also potentially valuable for the development of interventional and therapeutic strategies targeting specific genetic variants. However, even in these cases, the expression of the genetic variants showed a degree of heterogeneity, suggesting that the diversity of phenotypic features and clinical manifestations, even in monogenic genetic cases, may be influenced by other genetic and environmental factors. Therefore, an in-depth study of these conditions will not only improve our understanding of the genetic basis of ASD, but also provide clues for the development of more personalized therapeutic strategies.

Multigene interactions

The development of ASD is widely recognized as a result of the interaction of genetic and environmental factors, with polygenic interactions occupying a central position in the genetic background of the disease. Unlike monogenic cases, polygenic interactions involve variants or polymorphisms in multiple genes that together increase the risk of ASD. These genetic variants may contribute a smaller effect in each individual, but when acting together they can significantly increase the probability of ASD development [ 30 ]. Current research suggests that no single gene can explain all cases of ASD. Instead, hundreds of genetic loci have been identified that are associated with an increased risk of ASD. These genes are often involved in key processes such as brain development, neuronal signaling, and intercellular communication, suggesting that ASD involves extensive regulation of brain function and structure. The complexity of multigene interactions means that genetic studies of ASD require large-scale genomic data and sophisticated statistical methods to reveal those genomic variants that increase risk.

Meta-analyses of large-sample genome-wide association studies (GWAS) have identified several consistently replicated ASD risk gene loci, such as those in the chromosomal regions 3p21, 5p14, 7q35, and 20p12. These loci contain genes like CNTN4, CNTNAP2, and NRXN1, which play crucial roles in neurodevelopment and synaptic function, particularly in processes such as synaptic adhesion and neurotransmission. These findings provide a more robust understanding of the genetic architecture of ASD and highlight the importance of integrating genetic findings with functional studies to advance our understanding of the disorder. They also have implications for future research, such as the development of personalized diagnostic and therapeutic strategies based on an individual's genetic profile. Through genome-wide association studies (GWAS) and other genomic approaches, scientists are gradually unraveling the genetic landscape of this complex disease. Understanding the impact of multiple gene interactions on ASD not only helps us understand its genetic basis, but also opens up the possibility of developing personalized treatment and intervention strategies [ 31 ].

Environmental factors

Maternal exposure.

Exposure during pregnancy refers to a mother’s exposure to specific environmental factors or substances during fetal development, which may increase the child's risk of developing ASD in the future. These exposures include certain prescription medications (e.g., anti-seizure medications and opioids), environmental pollutants (e.g., heavy metals and air pollutants), infections (e.g., rubella and influenza viruses), and poor nutrition or deficiencies in specific nutrients (e.g., folic acid). These factors may increase the risk of ASD by affecting fetal brain development and the maturation process of the nervous system. Understanding the effects of exposure during pregnancy can help to take preventive measures to reduce the incidence of ASDs [ 32 ].

Effects of early developmental stages

The early developmental stages of ASD are influenced by a variety of factors that include genetic predisposition, environmental exposures, and early life experiences. During a child's early development, the brain experiences rapid growth and the formation of neural networks. Any disruption during this critical period may interfere with the proper development of brain structure and function, thereby increasing the risk of ASD. For example, very early lack of social interaction, delayed language development or abnormal sensory processing may be early signs of ASD. These developmental abnormalities reflect difficulties in the brain’s nervous system in processing information, making connections and adapting to environmental changes. Early identification and intervention are essential to promote optimal development in children with ASD [ 33 ].

Genetic–environmental interactions

The genetic–environmental interactions are summarized in Fig. 1 . ASD develops as a result of the interaction between genetic and environmental factors, and this interaction reflects the complexity of the combination of genetic background and external environmental factors that influence ASD risk. Specifically, certain genetic susceptibilities may be activated in response to environmental triggers, leading to the development of ASD. For example, genetic variants may make individuals more sensitive to certain environmental exposures (e.g., substance use during pregnancy, environmental pollutants, or maternal nutritional status), which together may increase the risk of ASD by acting on key brain developmental stages [ 34 ]. This complex genetic–environmental interaction underscores the need to understand multifactorial etiological models of ASD and the importance of developing personalized intervention strategies.

Advances in diagnostic methods

Traditional diagnostic methods.

Traditional diagnostic methods for ASD rely heavily on detailed assessments of behavior and developmental history. These assessments are usually conducted by specialized health care providers such as pediatricians, neuropsychologists, or psychiatrists. The diagnostic process encompasses direct observation of the child as well as in-depth interviews with parents or caregivers to gather information about the child's social interactions, communication skills, and behavioral patterns [ 35 ]. Diagnostic tools include, but are not limited to, the Childhood Autism Rating Scale (CARS), the Autism Diagnostic Observation Scale (ADOS), and the Autism Diagnostic Interview-Revised (ADI-R). These tools are designed to identify core symptoms of ASD, such as social communication deficits and repetitive behaviors or interests. In addition, the doctor may perform a series of developmental or cognitive assessments to rule out other conditions that may explain the child’s behavior, such as language disorders or other neurodevelopmental disorders [ 36 ]. While these traditional diagnostic methods are highly effective in recognizing ASD, they rely on subjective assessments and the experience of the professional, and therefore may have some degree of variability. In recent years, with a deeper understanding of ASDs, new diagnostic techniques and methods are being developed and adopted to improve diagnostic accuracy and efficiency.

Latest diagnostic techniques and tools

Genetic testing.

Genetic testing for ASD is a method of identifying risks associated with ASD by analyzing genetic variants in an individual's DNA. This testing looks for specific genetic variants that have been linked by scientific research to the development of ASD. Although the genetic background of ASD is extremely complex, involving multiple genes and the interaction of genes with environmental factors, variants in specific genes have been identified as having a significant impact on ASD risk [ 37 ]. For example, variants in the SHANK3 gene are associated with Phelan–McDermid syndrome, and patients with this syndrome often exhibit ASD features. Variants in the FMR1 gene are responsible for fragile X syndrome, which is the most common single-gene cause of ASD known to be associated with ASD. Mutations in the MECP2 gene have been associated with Rett syndrome, and patients with Rett syndrome often exhibit ASD condition. In addition, variants in the NRXN1 and NLGN3/4 genes have been found to increase the risk of ASD [ 38 ]. Genetic testing can help provide more precise diagnostic information, and in those cases of ASD where the cause is unknown, it may even reveal the underlying genetic cause. This will not only help to understand the genetic mechanisms of ASD, but also provide more targeted intervention and support strategies for patients and families.

Neuroimaging

Neuroimaging techniques in the study of ASD provide a non-invasive way to explore changes in brain structure and function, helping scientists better understand the biological basis of ASD. These techniques include functional magnetic resonance imaging (fMRI), structural magnetic resonance imaging (sMRI), diffusion tensor imaging (DTI), and positron emission tomography (PET). Through these neuroimaging techniques, researchers are able to observe structural and functional differences in specific regions and networks of the brain in individuals with ASD [ 39 ]. For example, fMRI can reveal patterns of brain activity when performing specific tasks, helping to understand the impairments in social, language, and cognitive functioning in individuals with ASD. dTI focuses on the microstructure of the brain’s white matter, revealing the connections of bundles of nerve fibers, which can help to study neural connectivity issues in ASD. PET scans, on the other hand, are able to assess the activity of specific chemicals in the brain, providing clues to study the neurochemical basis of ASD [ 40 ]. With these advanced neuroimaging techniques, researchers will not only be able to delve deeper into the neurodevelopmental abnormalities of ASD, but also identify possible novel therapeutic targets that can provide a scientific basis for developing more effective interventions. However, while these techniques provide valuable perspectives in understanding ASD, a complete understanding of the complexity of the brain remains a challenge for future research.

Early screening methods

Recently, the field of early screening for ASD has witnessed the application of a number of innovative techniques designed to improve the accuracy and convenience of screening. One notable new approach is the use of artificial intelligence (AI) and machine learning techniques to analyze children's behavioral videos and biomarkers. By training algorithms to recognize specific behavioral patterns and physiological signals associated with ASD, these technologies can help physicians and researchers identify potential ASD symptoms earlier [ 41 ]. Another area of innovation is eye-tracking technology, which assesses children’s social and cognitive development by analyzing their eye movement patterns when viewing pictures or videos. Studies have shown that the eye movement patterns of children with ASD while viewing social scenes differ from those of typically developing children, providing a non-invasive window for early screening [ 42 ]. The application of these state-of-the-art technologies not only improves the efficiency and accessibility of early screening, but also provides new perspectives for understanding the complexity and individual differences in ASD [ 43 ]. Although these approaches are still in the research and development stage, they demonstrate the great potential of utilizing technological advances to improve the process of ASD screening and diagnosis. With further validation and refinement of these techniques, it is expected that they will make a significant contribution to the early identification and intervention of ASD in the future.

Treatment approaches and intervention strategies

Behavioral and educational interventions, applied behavior analysis (aba).

Applied behavior analysis (ABA) is an intervention approach based on the principles of behavioral psychology that is widely used in the treatment of children with autism spectrum disorders (ASD). ABA works to understand and improve specific behaviors, particularly to enhance social, communication, academic skills, and daily living skills, while reducing maladaptive behaviors. It helps individuals learn new skills and behaviors by systematically applying reinforcement strategies that encourage and reward desired behaviors [ 44 ]. ABA therapy is highly individualized and customized to each child’s specific needs and abilities. Treatment planning begins with a detailed behavioral assessment to identify target behaviors and intervention strategies. Learned behaviors are then reinforced and cemented through one-on-one teaching sessions using positive reinforcement. ABA also emphasizes the importance of data, which is collected and analyzed on an ongoing basis by the therapist to monitor progress and adjust the treatment plan as necessary [ 45 ]. Research has shown that ABA is an effective way to improve social interactions, communication skills, and learning in children with ASD. Through early and consistent intervention, ABA can significantly improve the independence and overall quality of life of children with ASD. Although ABA treatment requires a commitment of time and resources, the long-term benefits it brings to children with ASD and their families are immeasurable.

Social skills training

Social skills training (SST) for children with autism spectrum disorders (ASD) is an intervention designed to improve their ability to interact socially in everyday life. This training focuses on teaching children with ASD the ability to understand social cues, establish effective communication skills, and develop friendships. Through SST, children learn how to recognize and interpret other people's facial expressions, body language, and social etiquette, which are essential for building positive relationships [ 46 ]. Social skills training typically includes a series of structured instructional activities such as role-playing, social stories, interactive group exercises, and peer modeling. These activities are designed to provide practice in real-world social situations in a supportive and interactive manner, helping children with ASD learn and practice new skills in a safe environment [ 47 ]. In addition, SST can include teaching emotion management and conflict resolution skills to help children with ASD better understand and express their emotions and cope with challenges in social interactions. Through regular and consistent practice, children with ASD can improve their self-confidence, increase their social engagement, and ultimately improve their social competence and quality of life. SST has been shown to be significantly effective in enhancing social adjustment and interpersonal interactions in children with ASD [ 48 ].

Medical treatment

While there is no cure for ASD, certain medications can be used to manage specific symptoms associated with ASD, such as behavioral problems, attention deficits, anxiety, and mood swings that are common in individuals with autism. Medication is often used as part of a comprehensive intervention program designed to improve the quality of life and daily functioning of the patient [ 49 ]. Medications commonly used for ASD symptom management include antipsychotics, antidepressants, stimulants, and anxiolytics. For example, two antipsychotics, risperidone and aripiprazole, have been approved by the FDA for the treatment of stereotypic and aggressive behavior in children and adolescents with ASD. In addition, selective serotonin reuptake inhibitors (SSRIs) may be helpful in managing anxiety and depressive symptoms in individuals with ASD.

Importantly, medication needs to be closely monitored by a physician to ensure the effectiveness and safety of the medications, as they may have side effects. We have summarized the research evidence on the efficacy and safety of commonly used medications in ASD, including antipsychotics for treating irritability and aggression, antidepressants for co-occurring anxiety and depression, and other medications such as stimulants and melatonin. While these medications can be helpful in managing specific symptoms, they also carry potential side effects and risks, such as weight gain, metabolic disturbances, and behavioral activation. Therefore, a thorough diagnostic evaluation, individualized treatment planning, close monitoring, and regular follow-up are essential when considering pharmacotherapy for individuals with ASD. The decision to medicate should be based on an individualized assessment that takes into account the patient’s specific needs, the severity of symptoms, and possible side effects. At the same time, pharmacological treatments are often used in combination with non-pharmacological treatments such as behavioral interventions and educational support to achieve optimal therapeutic outcomes [ 50 ].

Biofeedback and neuromodulation

Biofeedback and neuromodulation are innovative approaches that have been explored in recent years in the treatment of ASD, aiming to reduce ASD symptoms by improving brain function. Biofeedback techniques enable individuals to learn how to control physiological processes that are not normally under conscious control, such as heart rate, muscle tension, and brainwave activity. Through real-time feedback, patients can learn how to regulate their physiology, resulting in improved concentration, reduced anxiety, and improved emotional regulation. Neuromodulation, specifically transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS), affects neural activity in the brain through external stimulation. tMS utilizes a magnetic field to affect neuronal activity in specific areas of the brain, while tDCS modulates neuronal excitability by applying a weak electrical current. These methods have been studied for improving social communication skills and reducing stereotypical behaviors in people with ASD [ 51 ].

Biofeedback helps individuals develop self-regulation skills by providing real-time feedback on physiological states, while neuromodulation techniques like TMS and tDCS modulate cortical excitability and neural plasticity in aberrant circuits implicated in ASD. Current research suggests potential benefits of these techniques in improving emotional regulation, social functioning, and cognitive performance, but mixed results highlight the need for larger, well-controlled trials to validate efficacy, safety, and optimal protocols. Despite challenges, these techniques show promise as adjunctive therapies in the comprehensive management of ASD, warranting further research to guide their translation into clinical practice. Although biofeedback and neuromodulation show potential in the treatment of ASD, research on these techniques is currently in its infancy. More clinical trials and studies are needed to evaluate their effectiveness, safety, and long-term effects and to determine which patients may benefit from these interventions. Nevertheless, as non-pharmacologic treatments, they offer promising complementary options to the comprehensive treatment of ASD.

Emerging intervention approaches

Technology-assisted interventions.

Technology-assisted interventions have become an important development in the field of ASD treatment in recent years, providing new ways for children with ASD to learn and communicate. These interventions utilize computers, tablets, smartphone apps, and virtual reality technology to design a range of interactive learning tools and games designed to improve social skills, communication, and cognitive functioning in children with ASD [ 52 ]. A key advantage of technology-assisted interventions is their ability to provide highly personalized learning experiences. Software and applications can be adapted to a child's specific needs and interests, ensuring that learning content is both engaging and appropriate to the individual's developmental level. In addition, the feedback provided by technology is often immediate and consistent, helping children with ASD to better understand and process information. The use of virtual reality technology, by simulating social situations, provides a safe and controlled environment for children with ASD to practice social interaction and problem-solving skills, which is often difficult to achieve in traditional educational and therapeutic settings [ 53 ]. Although technology-assisted interventions have demonstrated great potential, research on their long-term effects and optimal implementation is still ongoing. To maximize the benefits of these tools, it is often recommended that technology-assisted interventions be used in conjunction with other therapeutic approaches to provide a comprehensive intervention program.

Diet and nutrition interventions

Dietary and nutritional interventions have received increasing attention in the treatment of ASD, based on the observed potential link between nutritional imbalances and ASD symptoms. This intervention approach aims to improve the behavioral performance and overall health of children with ASD by optimizing their diet. Specific strategies include restricting certain foods that may exacerbate symptoms, such as gluten and lactose, as well as increasing intake of foods rich in essential nutrients to support brain development and function [ 54 ]. Several studies support the potential benefits of specific dietary interventions, such as implementing a gluten-free lactose-free (GFCF) diet, which may help improve behavioral and digestive symptoms in some children with ASD. In addition, supplementation with omega-3 fatty acids, vitamins, and minerals (e.g., magnesium and zinc) have been proposed as potentially beneficial strategies to support neurologic health and alleviate ASD-related symptoms [ 55 ]. However, the effectiveness of dietary and nutritional interventions may vary by individual and more scientific research is needed to gain a deeper understanding of their long-term effects on children with ASD. Before implementing any dietary intervention, it is recommended to consult with a physician or nutritional expert to ensure that the individual needs of the child are met and to avoid malnutrition. In combination, dietary and nutritional interventions can be used as part of a comprehensive treatment plan for ASD, complementing traditional behavioral and educational interventions.

Social and educational integration

Educational integration of children with asd.

Educational integration of children with ASD is an inclusive educational practice that seeks to integrate children with ASD into the mainstream educational system to learn and grow with their typically developing peers. This integration model emphasizes individualized learning plans and adaptive teaching strategies to meet the unique needs of children with ASD while promoting their social inclusion and emotional development. Through educational integration, children with ASD are provided with opportunities to interact with other children, which is essential for them to learn social skills, enhance their communication abilities, and improve their ability to adapt to society. To support the successful integration of children with ASD, schools often provide special education services such as speech and language therapy, occupational therapy, and behavioral interventions, which take place in classroom settings to ensure their academic and social progress. Educational inclusion is not only beneficial for children with ASD, but it also helps to foster a sense of inclusion and diversity among their peers. By learning and playing together, all children learn to respect and understand differences, laying the foundation for a more inclusive society. However, effective integrated education requires close collaboration among teachers, parents and professionals, as well as the availability of appropriate resources and support systems [ 56 ].

Social integration and employment of adults with ASD

The social integration and employment of adults with ASD is a current focus of attention in ASD research and social services. For many adults with ASD, social integration challenges include establishing stable relationships, participating in community activities, and finding and keeping a job. Although adults with ASD may have unique skills and interests in specific areas, social communication deficits and fixed patterns of behavior may make it difficult for them in traditional work settings. In recent years, more and more organizations and businesses have begun to recognize the value of diversity and inclusion and are working to create work environments that are better suited for adults with ASD. This includes providing flexible work arrangements, clear communication guidelines, and individualized support measures such as workplace co-worker support and professional career counseling. In addition, social service programs and non-profit organizations offer training and job readiness programs specifically designed for adults with ASD to help them develop necessary vocational skills and social competencies. Through these efforts, adults with ASD will not only be able to find jobs that meet their interests and abilities, but also find a place for themselves in society, enhancing their independence and life satisfaction. However, the realization of this goal requires sustained social awareness-raising and the construction of an ASD-friendly environment [ 57 ].

Future research directions

Application of precision medicine in asd treatment.

The application of precision medicine in the treatment of ASD represents a paradigm of a personalized treatment strategy that aims to tailor the treatment plan to each patient's genetic information, biomarkers, history of environmental exposure, and lifestyle factors. The philosophy behind this approach is that, although ASD is classified as a spectrum, each patient's etiology, symptoms, and their severity are different, and therefore treatment should be highly individualized [ 58 , 59 ]. By fully sequencing a patient's genome, scientists and physicians can identify specific genetic variants that may affect ASD symptoms, allowing them to develop targeted treatments. For example, if a particular ASD patient's symptoms are linked to an abnormality in a specific metabolic pathway, that pathway could be modulated through dietary adjustments, nutritional supplements, or specific medications with a view to improving symptoms. In addition, precision medicine involves the consideration of environmental factors and personal behavior to ensure that treatment options are not only scientifically effective, but also appropriate to the patient's lifestyle. Although precision medicine is still in its early stages in the field of ASD, it offers great potential for delivering more personalized and effective treatment regimens, which are expected to significantly improve the quality of life of people with ASD [ 60 ].

Prospects for emerging biotechnologies

Emerging biotechnologies in the field of ASD, such as gene editing, stem cell therapies, and biomarker development, are opening up new possibilities for treating and understanding ASD. Gene editing technologies, particularly the CRISPR-Cas9 system, provide researchers with the means to precisely modify genetic variants associated with ASD, promising to reveal how specific genetic variants affect brain development and function, thereby providing clues for the development of targeted therapies [ 61 ]. Stem cell therapies utilize a patient's own induced pluripotent stem cells (iPSCs) to study the pathomechanisms of ASD by mimicking the neurodevelopmental process in vitro, as well as exploring potential cellular alternative treatments. In addition, the discovery of biomarkers facilitates early diagnosis and monitoring of disease progression, making personalized treatment possible [ 62 ]. In addition, induced pluripotent stem cell (iPSC)-derived brain organoids from ASD patients have emerged as a powerful tool for studying the neurodevelopmental abnormalities associated with ASD. These 3D, self-organizing models recapitulate key features of human brain development in vitro, allowing researchers to investigate the cellular and molecular mechanisms underlying ASD pathogenesis. By comparing brain organoids derived from ASD patients with those from healthy controls, researchers can identify alterations in neuronal differentiation, migration, and connectivity that may contribute to the development of ASD. Moreover, patient-derived brain organoids provide a personalized platform for drug screening and testing, enabling the identification of targeted therapies that can be tailored to an individual's genetic background. This approach has the potential to revolutionize the development of precision medicine strategies for ASD, by providing a more accurate and relevant model system for investigating disease mechanisms and testing novel therapeutic interventions. As the field continues to advance, iPSC-derived brain organoids are expected to play an increasingly important role in unraveling the complex etiology of ASD and guiding the development of personalized treatment strategies [ 63 ]. The development of these technologies has not only improved our understanding of the complex etiology of ASD, but also provided more precise and effective treatment options for ASD patients. Although most of these emerging biotechnologies are still in the research phase, they bring hope and anticipation for the future of ASD treatment and management. As research progresses and technology matures, it is expected that these innovative approaches will bring substantial benefits to individuals with ASD and their families.

Interaction between social policy and ASD research

The interaction between social policy and ASD research is key to achieving better social inclusion and quality of life for individuals with ASD and their families. Effective social policies can provide the necessary financial support and legal framework for ASD research, promoting a deeper understanding of ASD and the development of new treatments. For example, policies can promote collaboration in interdisciplinary research, encourage the use of innovative technologies and methods, and support long-term follow-up studies. In addition, social policies play a crucial role in ensuring that ASD research results are translated into practical applications and that education, employment, and social services are provided to individuals with ASD. Through the development of inclusive education policies, employment assistance programs, and the provision of integrated social services, policies can help individuals with ASD realize their potential and better integrate into society. At the same time, advances in ASD research also provide a scientific basis for the development of more targeted and effective social policies, helping policymakers understand the needs of individuals with ASD and develop more precise support measures. Thus, there is a close interplay between social policy and ASD research, which together have contributed to the advancement of the understanding of ASD and coping strategies.

Limitations of the current research

Although significant progress has been made in ASD research, a number of key limitations remain. First, the etiology of ASD is extremely complex, involving genetic and environmental factors and their interactions, making it extremely challenging to identify specific etiologies and develop targeted treatment strategies. Second, the heterogeneity of ASD is reflected in the extreme variability of symptoms among patients, which makes it difficult to develop uniform diagnostic criteria and treatment approaches. In addition, most studies have focused on children, and adult patients with ASD have been relatively understudied, which limits the understanding of the full lifespan of ASD. In terms of research methodology, most current ASD research relies on small, short-term studies, which may affect the broad applicability of results and the assessment of long-term effectiveness. In addition, although advances in technology have provided new tools for ASD diagnosis and intervention, the popularization and application of these technologies still face economic and resource constraints. Finally, ASD research is unequal across the globe, with far more research conducted in resource-rich countries and regions than in resource-limited areas. This imbalance limits a comprehensive understanding of ASD in different cultural and social contexts. Therefore, to overcome these limitations, more interdisciplinary, cross-cultural, and long-term research, as well as global collaborations, are needed to deepen the understanding of ASD and improve the quality of life of individuals with ASD.

Perspectives on future research

The outlook for future prevention and treatment of ASD points in a more individualized, integrated, and technology-driven direction. With a deeper understanding of the genetic and environmental factors of ASD, it is expected that more targeted interventions and therapeutic strategies will be developed that will be based on an individual's specific genetic background and pathologic characteristics. The application of precision medicine is expected to improve treatment outcomes, reduce unwanted side effects, and optimize resource allocation. Meanwhile, technological advances, particularly artificial intelligence, machine learning, and virtual reality, are expected to revolutionize the way ASDs are diagnosed, monitored, and treated. These technologies are capable of delivering customized learning and treatment programs that enhance the acceptability and effectiveness of interventions. In addition, interdisciplinary research will be strengthened, and social policies and public health strategies will focus more on early screening and intervention, as well as increasing public awareness and understanding of ASD. Most importantly, the future of ASD prevention and treatment will place greater emphasis on the needs of patients and families, promote social integration and employment of patients, and improve their quality of life. As society's awareness of diversity and inclusion increases, individuals with ASD will receive more support and respect and enjoy fuller opportunities for social participation.

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Department of Rehabilitation, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, China

Lei Qin, Wenjing Ning & Mengmeng Cui

Department of Intensive Care Medicine, Feicheng People’s Hospital, Taian, Shandong, China

Haijiao Wang

Department of Central Laboratory, The Affiliated Taian City Central Hospital of Qingdao University, Taian, China

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LQ, HW and WN wrote the draft of the manuscript. MC and QW revised this manuscript. All the listed authors have made a substantial, direct, and intellectual contribution to the work, and approved its publication.

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Qin, L., Wang, H., Ning, W. et al. New advances in the diagnosis and treatment of autism spectrum disorders. Eur J Med Res 29 , 322 (2024). https://doi.org/10.1186/s40001-024-01916-2

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Accepted : 01 June 2024

Published : 10 June 2024

DOI : https://doi.org/10.1186/s40001-024-01916-2

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Autism spectrum disorder (ASD)
Diagnostic methods
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Precision medicine
Emerging biotechnology

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A Drug That Cures Autism? Neuroscience Study Yields Promising Results

The behavioral disorders observed in autism are associated with a multitude of genetic alterations. Scientists have now found another molecular cause for this condition. The transcription factor MYT1L normally protects the molecular identity of nerve cells. If it is genetically switched off in human nerve cells or in mice, the functional changes and symptoms typical of autism occur. A drug that blocks sodium channels in the cell membrane can reverse the consequences of MYT1L failure and alleviate the functional and behavioral abnormalities in mice.

Disorders from the autism spectrum (ASD, autism spectrum disorders) are not only manifested by impairments in social interaction, communication, interest formation, and by stereotypical behavior patterns. This is often accompanied by other abnormalities such as epilepsy or hyperactivity.

Scientists are intensively searching for the molecular abnormalities that contribute to this complex developmental disorder. A multitude of genetic factors that influence the molecular programs of the nerve cells have already been linked to the development of autism.

Moritz Mall from the Hector Institute for Translational Brain Research (HITBR) has long been researching the role of the protein MYT1L in various neuronal diseases. The protein is a so-called transcription factor that decides which genes are active in the cell and which are not. Almost all nerve cells in the body produce MYT1L throughout their entire life span.

Human Brain Cells Programmed From Stem Cells

Mall had already shown a few years ago that MYT1L protects the identity of nerve cells by suppressing other developmental pathways that program a cell toward muscle or connective tissue, for example. Mutations in MYT1L have been found in several neurological diseases, such as schizophrenia and epilepsy, but also in brain malformations. In their current work, which is funded by the European Research Council ERC, Mall and his team examined the exact role of the “guardian of neuronal identity” in the development of an ASD. To do this, they genetically switched off MYT1L — both in mice and in human nerve cells that had been derived from reprogrammed stem cells in the laboratory.

The loss of MYT1L led to electrophysiological hyperactivation in mouse and human neurons and thus impaired nerve function. Mice lacking MYT1L suffered from brain abnormalities, such as a thinner cerebral cortex. The animals also showed several ASS-typical behavioral changes such as social deficits or hyperactivity.

What was particularly striking about the MYT1L-deficient neurons was that they produced an excess of sodium channels that are normally mainly restricted to the heart muscle cells. These pore-shaped proteins allow sodium ions to pass through the cell membrane and are thus crucial for electrical conductivity and thus also for the functioning of the cells. If a nerve cell produces too many of these channel proteins, electrophysiological hyperactivation can be the result.

In clinical medicine, drugs that block sodium channels have been used for a long time. These include the agent lamotrigine, which is supposed to prevent epileptic seizures. When MYT1L-deficient nerve cells were treated with lamotrigine, their electrophysiological activity returned to normal. In mice, the drug was even able to curb ASD-associated behaviors such as hyperactivity.

“Apparently, drug treatment in adulthood can alleviate brain cell dysfunction and thus counteract the behavioral abnormalities typical of autism — even after the absence of MYT1L has already impaired brain development during the developmental phase of the organism,” explains Moritz Mall. However, the results are still limited to studies in mice; clinical studies in patients with disorders from the ASD spectrum have not yet been conducted. The first clinical studies are in the early planning phase.

Reference: “ MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention” by Bettina Weigel, Jana F. Tegethoff, Sarah D. Grieder, Bryce Lim, Bhuvaneswari Nagarajan, Yu-Chao Liu, Jule Truberg, Dimitris Papageorgiou, Juan M. Adrian-Segarra, Laura K. Schmidt, Janina Kaspar, Eric Poisel, Elisa Heinzelmann, Manu Saraswat, Marleen Christ, Christian Arnold, Ignacio L. Ibarra, Joaquin Campos, Jeroen Krijgsveld, Hannah Monyer, Judith B. Zaugg, Claudio Acuna and Moritz Mall, 14 February 2023, Molecular Psychiatry . DOI: 10.1038/s41380-023-01959-7

The Hector Institute for Translational Brain Research (HITBR) is a joint institution established by the Central Institute of Mental Health (ZI), the German Cancer Research Center (DKFZ) and the Hector Foundation II. The aim of HITBR is to identify new molecular and functional targets for the therapy of severe psychiatric diseases and brain tumors.

Groundbreaking study reveals autism’s genetic triggers and therapeutic hope, breakthrough treatment for autism spectrum disorder within reach: scientists discover key clue, does autism begin in the womb research breakthrough may lead to new treatment strategies, common autistic personality test unreliable, psychologists say, new way to treat hypersensitivity to noise and other neurological disorders, new drug combo shows promise for treatment of depression and addiction, genomic analysis reveals roots of neuropsychiatric diseases, yale study links increased impulsivity and hostility with recreational marijuana use, diuretic drug could help treat autism, 76 comments.

I was on Lamictal for most of my teens leading into it has done nothing but cause more side effects such as severe rage, shaking hands, etc. Lamictal is not a cure and its not even new to ASD.

This article is certainly overstating (eg “a cure for autism?”) the significance of this paper. These are undoubtedly interesting findings, but a long way off from anything like a “cure”. Lamictal is a tricky drug even in epilepsy. And it seems highly unlikely that it would “cure” a disorder that has been present since fetal development. Alleviate some portion of symptoms, in some portion of patients? Perhaps. But even there, this is a long ways off from being ready for prime-time.

I think it’s interesting, and unfortunate, that there is so much anger (directed, weirdly, at other members of the autism and science community) being expressed in these comments. “Autism” is a very large basket, and there are a wide variety of experiences of those who have it or love someone with it. Some folks don’t view it as a problem for them at all – good on them. Others find it very distressing and disabling – totally understandable. It hits everyone differently, and the “high-functioning/mild” vs “low-functioning/severe” split doesn’t even do justice to the variety of symptoms and experiences it causes. Can we all just take a breath and be supportive of each other? If there are medicines that help with symptoms then great – those who are bothered by their symptoms can take the medicine, but no one has to take anything.

But again, the above article is a mere suggestion of something that *might* someday be helpful for *some* people. I’m glad that scientists are making some progress in understanding the biology of this very complex disease (which, for what it’s worth, I imagine will turn out to be more a collection of various neuronal, genetic and molecular processes that produce phenotypically similar symptoms, rather than one unifying cause). Hugs all around, especially to those here who are suffering.

Jesus Christ we’ve been saying for ages that we DON’T WANT A “CURE!” Is it that challenging to be a decent and respectful human being?

What’s wrong with you?

People like you wanting to cure us like some disease!

Then don’t take it!

Cure = Genocide They have already done it to fetuses with Down Syndrome so we know they will eliminate all autistic people without our consent. It will not be upto the individual at hand whether they are cured or not. I have consumed Lamotrigine for 30+ years, the maximum dosage, and I have not been cured of autism. Another problem is who’s entitled to the “cure” will be dependent on wealth, if you can’t spare $10,000 sorry, you’re not entitled to be cured.

Don’t you recognise the simple truth that they don’t even know what autism is as researchers have not intended to identify it, just prevent it? Don’t you realise all the “symptoms” are not specific to autism as there’s many nonautistic people who experience the same?

If they knew what autism is they would be able to do a brain scan and say whether the person is or isn’t autistic. If they know what autism is why can’t it be diagnosed directly?

Cure > Less diversity > Human extinction

Can we cure all the normal people instead please and make them autistic. This article is as ignorant as it is nauseating

YOU don’t want this. Don’t presume to speak for all autistic people. Unlike you, i have been BEGGING for a cure for years. Can selfish @ssholes like you stop saying “we” as though you speak for the community writ large? It’s it that challenging to be a decent and respectful human being?

I think no I’m 98% sure my 3 yr old has some kind of autism. I don’t know where to go or what to do. It makes me so sad for her. I’m lost. I love her so much. Any suggestions or any help available. We live in des moines, ia.

You lier don’t you dare to speak instead of me! I want a cure, this disorder ruined my life!

Fellow Autistic human here . . . just a wondering, was it Autism that ruined your life or was it ableism and a persistent lack of empathy from neurotypical people?

Yeah you should be ashamed even publishing this article. We don’t need fixing. What next, pills to make people straight or to make people of color, white.

I need a cure. Stop pretending to be royal using “we” instead of “me”. Just speak for yourself and let me be.

None of these actually “cure” autism nor could they ever cure it. Autism is a brain difference. These cures strictly make your “behavior” more socially acceptable. And you’d have to take the cure forever.

Personally, I’m going to pass on the cure. Being socially acceptable is overrated.

Also, whilst reading this article and another like it, I’m not getting a real idea of what “behaviors” they are even talking about that would “cure” anything. There’s lacking of anything of substance here.

Autism isn’t a disease that needs to be cured. Its a different operating system, different doesn’t mean broken. Neuro-diversity is actually a good thing for the human species.

My son has severe autism. He can’t speak. He’s very hyper. He has self stimulatory behaviors, self injury and aggression. I understand the angst of many individuals with high functioning autism. all of my favorite people have Asperger’s, and contribute amazing things to this world. but when one insults the commitment of researchers, and the consequential identification of causes of autism, and treatments for autism, that is likewise very offensive. I am always seeking therapies that will better my sons quality of life and the quality of life from our family. Thank you doctors and scientists.💕🙏

My autism is a disorder that I want to be cured from. I am broken, my life is broken and that is the truth. It improved over the years but it prevented me from having enjoyable life. Speak for yourself!

as an autistic adult, this is just confirming the idea that autistic people need to be ‘fixed’. we dont need to be fixed, the way people view us needs to be fixed. just treat us with some respect please.

As autistic adult myself, can you treat me with respect please and stop pretending that you can speak in my behalf. If you don’t want to be fixed, than don’t. I want to have options open! Besides, you insulted all medicine taking population.

The things those of you who desire a cure claim have wrecked your life are not specific to autism, there’s nonautistic people who have the same experiences. If you could cure autism and took the cure you would actually still be autistic.

Scientists don’t even know what autism is which is why it has always been a moving target, this article is not even about a cure to autism. Secondly, who’s entitled to a cure is dependent on your wealth, if you can’t spare $10,000 sorry, no cure for you. Just like today’s interventions bankrupt parents, a cure will bankrupt parents.

Here come the self-appointed spokespeople for the autism community. If you don’t want to be cured, don’t take the cure. There are people who are suffering who could benefit. It is not your place to decide what treatment options are available for other people.

Have any autistic person told you personally that they are suffering due to their autism. If an autistic or a disabled person in general haven’t told you they suffering then don’t assume they are. A lot of autistic people like me don’t want a cure because we aren’t suffering because of our autism, if we are suffering from anything it’s society not accommodating and be accepting of us.

Hello, autistic person here to tell you that i am suffering due to my autism. I suffer daily, I detest my life, and the ugly, awful person that my autism has made me. I have tried multiple times to end my own life because of my autism. I want to thank people like Darius for defending people like me whose voices are drowned out by the overwhelming selfishness of people who believe that because they do not want something it means nobody should have it.

So you want to change your brain, how it functions, how you’ve learned, and part of who you are because its hard? There is nothing wrong with Autism. Autism is literally how certain brains function. I understand that it sucks & hurts. But changing your brain & it’s function isn’t going to do much. You will still have your tendencies that you’ve always had. Since habits aren’t easy to break. All you’ll be doing is hurting yourself & the people around you. You simply have to change how you react, how you handle your emotions too. Medication &/or Therapy can help with that. A Cure for Autism won’t. And a Cure would hurt more people than it’ll help. Please take that into consideration.

It’s more selfish for you to want your own way to bring humanity to extinction. You’ve indoctrinated yourself with Francis Galton’s doctrine, people who suffer only do so because of how you choose to view life. Reality is observer dependent, the reality you see is the reality you choose to see.

All the other autistic ppl here saying “we” don’t want to be fixed, I want to be fixed,and no, it’s not because the neurotypicals told me it’s not okay, i’ve actually only encountered positivity and acceptance from those that know i am, i just know that my life would’ve been much better if i didn’t have it, i think it’s valid to have these types of researches, because those that do want to make a change for themselves, i do however think that they shouldn’t be given to children, in case there maybe be adults that want to force them into taking these drugs, it should be something that they should do out of their own choice whenever they are old enough to choose, but as this comment section shows, there are ppl who find their autism as a burden, and they want a way to change it,for their sake, there should be a way to solve this issue.

These drugs make me confused.It doesn’t help my Asperger’s only my epilepsy.And we see here,a mouse is not a human.Dont work for Asperger.

I’m autistic, this article read as a little insensitive. I don’t want a cure to act “normal” I want to not be stigmatized and given opportunities for accommodation in day to day life. I have been on things like Lamotrigine and all it’s maybe helped with one symptom only to turn around and make everything else worse.

For all of you who are saying you do not want a cure and stop trying to cure autism are you going to take care of the children when their parents die and the children are unable to talk if you are so smart and knowledgeable why don’t you understand that this is a spectrum disorder and many autistic people do not have the ability to read right and communicate and make a fuss like you do so stop saying you don’t want a cure and stop saying that nobody needs a cure you are not the parents just be grateful that you could talk and communicate and you don’t have to worry where you’ll end up as an adult It’s because of people like use that slow down the process and made it a trendy thing for autism that we cannot even find proper solutions because you and others have made it a trend and defensive to try to help somebody with autism you should be ashamed of yourself Don’t speak for everyone there are hundreds of thousands perhaps millions of people that have low functioning autism that would love to have a cure so go fly a kite please with your politically correct information

😡 ! Autism is NOT a disease or a disorder!!

The following extract should have no place in a so-called science journal :

“Disorders from the autism spectrum (ASD, autism spectrum disorders) are not only manifested by impairments in social interaction, communication, interest formation, and by stereotypical behavior patterns. This is often accompanied by other abnormalities such as epilepsy or hyperactivity.”

You know what cures autism, not injecting toxins into kids!! It’s free too, and no side effects!!! Stop medicating our kids!!!

I’m not fully sure what you mean by injecting tonics but if you mean vaccines. Then I hope you’re not implying that vaccine causes autism because it doesn’t. There is no proof that vaccines causes autism The scientist who the experiment that is the reason everyone still that vaccine is the cause, he got his license taken away because he lied about his results! You can look in to it if you don’t believe me.

Not just lied about results, he did illegal procedures on the children in the study.

Yes. I am an autistic person and i suffer greatly due to my autism. I lack the capacity to feel genuine happiness for other people and it makes me feel disgusting. I have no friends, am unable to save a job, i am incapable of forming relationships. I can barely care for my self and I am desperate to be able to have these things. I am so lonely it causes me physical pain that i have tried to stop by taking own life. Stop trying to take away any last shred of hope i have for a life. Please. I am begging you. Stop this crusade. You are actively harming people like me.

What you describe here sounds like antisocial personality disorder, not autism. Not saying you’re not autistic but inability to feel empathy isn’t an autistic trait, it’s an aspd trait. Look into dbt, that can help aspd, lamotrigine certainly doesn’t affect autistic traits beyond making people feel doped up and detatched from the world.

Let me know the dose that cures it, because it clearly isn’t 200mg every day for 10 years. Seriously; I would honestly love a cure. Those who say that “autism isn’t a disorder and there doesn’t need to be a cure” don’t speak for all of us. And yes, I was professionally diagnosed at age 11; I’m not some TikTok tweenager with a WebMD degree.

Also, by textbook definition, ASD is absolutely a disorder. GTFO with your fake activism; you’d kick me to the curb before you’d actually help me IRL.

Thank you. Thank you a thousand times. Seeing these selfish replies best so overwhelming i almost give up hope. Thank you for existing, and using you voice to let people know that some of us DO want this

Don’t rely on Lamotrigine, I’ve been consuming the maximum dosage 300 twice a day for 30+ years and it hasn’t effected my autism, not even the symptoms.

I would have been diagnosed as Autistic in today’s world, just by the hand-shaking alone from what I’ve read. I was also very anti-social towards adults. I got diagnosed as “shy” all the time. But did anyone ever treat me with respect and ASK me WHY I was shy? I wasn’t “living in my own world”. I simply felt like adults treated me like I was stupid. I sometimes didn’t get along with other children my age because my IQ is around 140 and I wasn’t into eating boogers and paste. I was writing short stories by 3rd grade that were 12-20 pages long and reading books in the 400-600 page range in 2nd grade. Yes, I loved to flap my hands. I head to break myself of the habit because people think you are “special” (trying not to use the musical word meaning slow, but that’s what they used then when in fact, I was quite the opposite).

I know many “autistics” that are Valedictorians and I think the problem is “society’s expectations” of what they consider “normal” that is the real problem. By normal, they mean AVERAGE and I’m sorry, but I make no apologies for being smarter than 98% of the planet. Shyness is fear of people LABELING you, which is exactly what all these “doctors” do when they apply a stigmatizing label like “Autistic” to you. Maybe they should just work on improving communication instead of labeling people freaks because they don’t enjoy bull-bleeping about the weather or pretending they’re interested in something they’re not.

They seem scared of us. They’re terrified of Elon Musk. They defame him, they defame us. They would love nothing more than your 140 IQ and my 128 to be 98 like them.

absolutely disgusting, you should be ashamed of yourselves for publishing this.

My son who has autism (pdd/nos) as well as epilepsy was onced placed on lamictal (as an alternative to keppra) and it was one of our worst experiences ever. The side effects were awful, and included making our son terrified of literally everything, especially while outside, whereas before he loved being outside. He eventually went back to his normal self once he was transitioned off lamictal, but it was literally hell in the meantime. And no, he doesn’t need to be cured, he just needs to have his seizures controlled.

Ngl, I would take this if it were proven to reduce traits. I’m dealing with ADd on top, and between the two I will take whatever help I can get. I’m tired of feeling like a Martian.

Not going to speak for anyone else, but I’m a mess. I’m barely managing basic standards of functionality, although I’m able to muddle through just about. Anything is worth trying for an improvement.

You are not alone in wanting a cure, don’t let these people overwhelm you. Your opinion is valid. YOU are valid. Keep holding on, eventually there will be help.

If you want better functioning focus more on making your environment cater to your needs. When organisms are in suitable environments it increases and strengthens neural networks increasing functioning.

During lock down from COVID-19 autistic children excelled with their development and learning once they settled at home to remote learning. Motor skills, reading, writing, communication, mathematics all increased more than ever. The stressful school environment not catering to their needs is what hindered and prevented the autistic children developing and learning.

This staging of this is frankly disgusting. There is a “cure” for autism because there doesn’t need to be one. It’s not a disease. Equally, the drug they are talking about isn’t new, it’s been used for years to treat epilepsy & is already known to have an effect on hyperactivity… which by the way is not a marker for autism. Really disappointing to see this information presented this way. – ADHD adult with an Autisic child

So, not a cure; just a questionable treatment for certain specific conditions associated with autism in some people. Enough with the click-baity headlines and ableist writing. It only feeds the trolls.

Lamotrigine has a black box warning i.e. for “serious adverse reactions such as: Serious skin rashes, including Stevens-Johnson syndrome and toxic epidermal necrolysis.”

Wow. Talk about a straw man argument. If you can’t articulate an actual relevant thought, just stay quiet.

I don’t need to be fixed. What would be good is a society that cares and is inclusive. It’s not hard. That also applies to disabled people who are also treated appallingly.

lol wow fat acceptance has now moved into autism acceptance…what next, sepsis acceptance???

The new politically correct term for pedophile is “Minor Attracted Person”, so guess what’s up next for acceptance?

@asD – It’s not about Autism acceptance. It’s that they increasingly place everyone who does not “behave” the way they “think they should” into this increasingly meaningless label. There might be some real cases where people have some kind of mental or functional disability, but when I read hand flapping is a sure sign of Autism, I cringe because while I have no idea why “flapping” my hands when I got excited made me feel even better, it certainly has nothing to do with intelligence or communication abilities in my case.

Assumptions that “odd” behaviors make someone deserving of some “label” that seems to fit “everything we can’t explain” is ridiculous. The Fibromyalgia label does that increasingly to abnormal degrees. There is something there for real, but labeling every ache and pain that can’t be explained by say hitting your hand on something isn’t a disease. It’s a symptom of something else. I had unexplained pains around my neck and they blamed a slightly bulging disc in my neck. It turns out I had frozen shoulder syndrome from pulling a tendon and it tightening up when it healed and nerves going nuts in the immediate vicinity around my shoulder and neck. That didn’t stop six doctors from suggesting it was fibromyalgia out of complete ignorance to the real cause (the specialist found it in 20 seconds and the weird neck sensations went away after just one week of physical therapy.

I find lazy doctors don’t want to look too hard. They make more money moving the conveyor belt along yet they talk to me like I’m stupid when I often seem to know more about various diseases than they do despite my degrees being in EE/EET and a minor in English. As an industrial machinery electronic technician, my job has a lot of down time when things are running OK to read on everything under the sun whereas I doubt many of them really keep up with the latest medical findings, but when you read an article like this, you have to wonder if the people blowing smoke keep blowing it on down the line.

It’s like Dark Matter and Dark Energy. They’re just totally unproven theories, but people keep building upon them like they’re a rock instead of shifting sand and the house inevitably will fall down as the latest observations from the Webb telescope make it obvious they don’t exist and the BBT probably didn’t happen (observations of galaxies do not match predictions and the whole red shift idea of Doppler-like measurements may be in question as the alternate theory of “light dimming” may in fact be true as space isn’t “empty” like we once thought in the early 20th Century), but the “many” will probably take decades to realize this since it’s career wasting/ending.

They say Science isn’t a religion, but the pig-headed stubbornness against change of long-held theories (beliefs) sure resembles it to me.

Not necessarily true. My son is high functioning autistic, was on Lamictal & it did NOTHING for him. Surely there are people who may or truly do see improvement but I would not go as far as claiming it to be a “cure” for autism.

There are different levels of autism some are high functioning and some are 34 year olds unable to speak forever in diapers who attack those around the and run into traffic so if you think autism doesn’t need a cure you are wrong for those with more severe autism they are unable to be independent or express themselves or their needs feeding bathing dressing is something they will need help with forever they don’t understand not to play with their own s*** or eat their own s*** or run into traffic so yes a cure would be fabulous

I am autistic. Let me echo that there CAN’T be a ‘cure’ because Autism isn’t a disease. It’s a neurotype. ALSO The study does not even claim to alleviate Autism writ large. Just certain symptoms. A brain that is fully formed CANNOT be changed by a drug like lamotrigine. That is just not scientifically possible. A lot of aspects of autism are only disruptive/weird because society is neurotypical and not built for people with Autism. Autistic people DO suffer when having to deal with this society but any autistic person who claims to want a ‘cure’ has likely been exposed to ridicule from a young age for their autism – perhaps even from parents. Autism Speaks claimed to be looking for a ‘cure’ and was essentially seeking to eliminate Autism altogether. This convinced a LOT of parents that autism was bad and their child was broken. Add to that virulent antivaxxers who believe that vaccines cause autism and you have kids and now adults who have been told they are broken, unfit for society, and they have to be fixed and wer’re just waiting for the science to catch up. Which is WRONG! My heart breaks for these kids (and adults). Autism != broken!!!! Now, would a drug that might lessen the sense of being overwhelmed, or over stimulated or some other purported ‘bad’ aspect of social behavior be welcome when dealing with neurotypical society? Of course. I personally take an anti-depressant and I take adderall in order to focus at work (I have ADHD as well). They help me to function in an NT world. But that’s a personal choice. At any rate, this article’s title is terrible and show a huge lack of understanding by the author. I allow that this might be for the clickbait but it doesn’t change the fact. Do better.

Also I was on lamotrigine and it didn’t do anything for ‘autism’. Your mileage may vary.

As others have said autism isn’t something that needs to be cured. These editors are stupid

I agree with the above commenters and am on the spectrum, too, and won’t beat the dead horse but Aspies tend to be nerds and the authors of this had to be, at least, somewhat aware of the backlash they were going to get. Talking about curing autism to a STEM audience is going to go over about as well as conversion therapy at a gay nightclub. Like, anyone with the most peripheral cognizance of the Aspie communiy would have been able to anticipate the uproar of livid anger.

This article is ridiculous. There is no “cure” for autism. If you take a Claritin and it helps you to alleviate excessive sneezing did you “cure” your allergies? Also, I was prescribed Lamotrigine at one time and took it for well over a year. It did absolutely nothing to curb any of my symptoms. Lastly, autism is a neurological disorder causing positive differences as well as negative ones. It is not a disease! Too many people look at bad behaviour and blame it on autism, then look at all the good behaviours and think those behaviours are in spite of, not due to the individuals neuro diversity. It’s really getting sickening seeing all these posts about curing autism. Its an integral part of who I am. Everything I experience is through an autistic filter. Essentially, you are saying that who we are is so wrong we don’t deserve to be alive.

What the actual f*ck? Autism ISNT A DISEASE. Stop trying to ‘find a cure’ it is a NEUROTYPE. I seriously don’t know what’s wrong with you, but you’re gonna cause so much harm and pain to autistic people and children around the world. We should be working on changing a world to accommodate for all neurodiverse people, not trying to change the fact that we have neurodiversity in the first place. Extremely disappointed and frankly disgusted with someone of you researchers and scientists.

There are a lot of low support needs in the comments here speaking for the rest of us, like always. Level 1 and low support needs are always speaking for the rest of us. Some of us who are level 2 and 3 and who have higher support requirements would like a cute. If your autism is not causing you hardship don’t drag the rest of us down with you and say we don’t want help. Some of us want and need help.

From reading the comments and from my personal experience as a women with autism I feel like I’ve never been accepted as being “special” I have grown up masking and hating that part of myself and have only just started the long road of working through my trauma and acceptedong me for who I am. Things like these articles make it a lot harder for me to do that. Instead I wish that people who post and explore how to help, specifically adults, adapt and thrive as an adult. I understand that some people desperately need this, but don’t call me selfish for wanting to feel accepted by society, I know how it feels to hate yourself to the point where you have suicidal thoughts, everyone is different but I do have some understanding from the last six months. So saying I don’t support this isn’t saying I don’t support finding help for those people, but don’t call it a cute like there is a disease in me instead of my brain just physically being wired differently. Just look at me like in a person, not something that needs to be studied and looked at without every actually talking and asking the people they are looking at.

The only way to ‘cure’ (if you can even call it that ugh) is to invent a time machine to go back and rewire our brain before we are born. Autism is not a fricking disease nor can it it be ‘cured’. This article is pure ignorance and discrimination. It is a SPECTRUM. Some of us suffer and some of us don’t. Some of us can function and some of us can’t. Retract this hateful %h*t. Seriously, stuff like this genuinely makes me want to unalive my self in minecraft.

You are royal, referring of yourself as “we”? I want the cure! I need it! You don’t know what are you talking about!

I can’t stand being autistic, always on the sideline of society, never participating. If you’re okay with your autism, that’s fine, but don’t force your views on me, I do want a f***ing cure!

Neurotype! I understand that high functioning autistics don’t want to be labelled with a disorder. But my son has low functioning autism. He is 11 and can’t talk, can’t communicate and can’t do even the basic self care. I worry about him everyday. Where will he end up when I’m not around? Who will look after him? He has no independence and relies on me 100%. It’s very scary and yes I would love a cure! You people need to understand that it’s a spectrum!!!

I have a problem with the assumptions I am required to imbibe without question, by proxy. The first one being the most obvious….what do mice & humans have to do with each other? Because we are both mammals? THAT’S the hill your gonna die on? And you want me to trust my health on such flimsy evidence? Not only, but my allegiance is demanded & monitored so that snowflakes don’t feel triggered or offended Who decides what a spectrum consists of? Those who fall within its parameters are dismissed in favor of experts whose bank accounts grow exponentially. But I am pilloried for saying how it is?

I think that one of the things that is missing from the discourse happening in the comments is a distinction between individualism and communal approaches and the difference in responsibility between Autistics talking about their own experiences and Allistics, particularly in science and journalism, framing things in a very specific and narrow way.

For instance, many individual autistics may talk about or desire a “cure” because they are disabled by structural issues that continue to marginalize Autistics, particularly high-support-needs Autistics and this causes them extreme distress and pain. This is entirely valid and true to their experience of the world. In contrast, the pursuit of a “cure” for Autism without also addressing the many social and structural issues that are in fact the predominant disabling factors treads alarmingly close to eugenecist narratives. Collectively, this is extremely harmful.

Both of these things can be true at once. We can create space for the myriad Autistic experiences while also expressing concern and even condemning the trajectory of a pathological model. I, as an Autistic person, can even disagree with other Autistics on this issue. I personally do not feel that I need to be cured, but i am low-support needs by comparison to others. I prefer a social model of disability that chooses instead to focus on structural issues that marginalize and disable my community as a whole, particularly high-support-needs, BIPOC, and LGBTQIA+ Autistics.

The applicability to Autism in this research is overstated, and I highly doubt that any specific gene target that will lead to meaningful genetic therapies will be found soon, but I do see how studying the blockage of sodium channels could potentially be useful in neuropsychology more broadly. The issue here, for me, is that this focus on Autistic traits (some listed of which would not indicate autism according to DSM criteria–hyperactivity being one) seem irrelevant, centered on stigma, and makes correlation in mice that is very far from indicating an impact in humans–for instance, how does one quantify “Autistic traits” in mice without also looking at the rampant stigma, misinformation, misapplication of assumption, and bias in the study of Autistic traits in human beings (nost of which also have tiny sample sizes). It is difficult to look at this, and the mouse model of Autism broadly, and not believe that the primary interest is not to help Autistics but to eliminate us.

As an advocate who has Asperger’s who understands both sides I feel I can give my two cents. I will address both sides here.

Neurodivergents:

Although “we” in the neurodiversity movement understand that you all want a cure, when we say “we” we aren’t referring to those who want a cure. We are referring to the neurodiversity movement. “We” view autism as a gift and are against a cure and prevention because we believe the good things about autism outweighs the bad things. Literal thinking, being unable to lie due to being brutally honest, being super smart, pure of heart, mind of a child, ect; are gifts and autistic people can see and figure out things neurotypicals can’t. We have intelligence beyond measure. Why would anyone want to prevent that or get rid of it? That’s how WE see things. That being said, I personally feel sorry for those of you who are against being autistic and it breaks my heart you were brainwashed into believing autism was bad because of the circumstances you went through. Value yourselves for who you are. You are perfect the way you are. That being said, you also have a right to be normal if you want but you DO NOT have a right to bully the neurodiversity movement for believing differently. We are NOT disrespecting you just because we identify differently. Respect goes both ways. Respect all sides.

Now I address the neurodiversity movement:

I’m on your side. I too believe autism is a gift for the reasons stated above. I too am against a cure and prevention. Try to understand how those who are neurodivergent are feeling. They obviously has things happen that made them feel the way they do. I used to be neurodivergent myself and I too used to support ABA, a cure and prevention until my psychologist addressed the good qualities of autism. I am now a full member of the neurodiversity movement and proud of it. The fact people get offended when you speak out and react in anger means you’re on the right side. People don’t get offended unless they know you are right. That’s basic psychology. Notice only the neurodivergents are reacting with anger and “we” are NOT. That should tell you something. Regardless be kind to them and neurodivergents I mean no offense with all this but you all really need to learn to respect other peoples opinions.

Please keep all comments kind and respectful. If I see any negativity I will be reporting it as harassment. Thank you.

I realize these comments were made months ago but I do have to say – the ones on here saying that they are autistic and it can’t be cured and it’s a neurotype & it isn’t something to be fixed – all of these comments are very frustrating for me – no one is trying to “fix” you or “cure” you. I am neurodivergent and I have a daughter who is as well and she struggles, every day, to do all the things the majority of us take for granted. So yeah – I am hopeful that at some point there will be medication to help her struggle less, just like there is medication that helps me struggle less. No one is trying to erase who I am or who she is – I am still the same person, but now I can actually function in the world, able to have relationships, children, a career. I can only hope there is something similar for my daughter at some point.

Autism literally is who we are, there’s no so-called normal person behind autism. Autism influences everything about us, cure autism and we will not be who we are, we will be an entirely different person meaning the person we are you wish didn’t exist. In other words, you believe the world would be better without us like Francis Galton, Adolf Hitler, and the Nazis.

It’s unbelievable how many of you want to bring humanity to extinction.

They’re disguising their eugenics. They’re already aborting more black people than white, they already disallow disabled people to be born, more females are aborted than males, all advertisements of designer babies are images of white males. There’s advertisements of anti aging which has nothing to do with sicknesses or diseases, if it was only about sicknesses and diseases they wouldn’t of ever thought of touching the human germline. This is racism, sexism, ableism, eugenics and capitalism.

They do not have the right to mess with a person’s genes just because they perceive something about them as a “problem”. Autism is not a problem, they claim they value all humans equally, since they want to rub us out of existence they clearly do not see us as equal, they are full of discriminatory thoughts like Hitler doing eugenics. The problem is clearly they’re view of autism and other primarily genetic conditions. I love being autistic, I wouldn’t give it up for the world.

Molecular biologist Miroslav Radman writes, “Mutagenesis has traditionally been viewed as an unavoidable consequence of imperfections in the process of DNA replication and repair. But if diversity is essential to survival, and if mutagenesis is required to generate such diversity, perhaps mutagenesis has been positively selected for throughout evolution.”

This will bring us to extinction. Especially since there’s contradictory evidence.

Evelyn Fox Keller explains: “We now know that mechanisms for enduring genetic stability are a product of evolution. Yet a surprising number of mutations in which at least some of these mechanisms are disabled have been found in bacteria living under natural conditions. Why do these mutants persist? Is it possible that they provide some selective advantage to the population as a whole? Might the persistence of some mutator genes in a population enhance the adaptability of that population? Apparently so. New mathematical models of bacterial populations in variable environments confirm that, under such conditions, selection favors the fixation of some mutator alleles and furthermore, that their presence accelerates the pace of evolution.”

The mutants behind autism and other conditions like Down Syndrome offer some great advantages to the human race, diminishing the genes is a great risk because without those mechanisms there is no asurety of genetic stability pushing us in the direction of extinction.

Psychologist Howard Gardner warns: “With the coming of age of genetics, the danger magnifies. Beyond doubt we will discover genes that are important for reading alphabetical scripts; and there is already evidence that a small set of genes may be related to reading problems. As with the brain evidence, such information can be helpful for early intervention; but it could easily be used for stigmatising purposes. Indeed, it might become relevant for marriage prospects, holding a job, securing insurance, or even eugenic purposes. And no doubt, especially in our interventionist society, individuals with a genetic predisposition for reading problems will look into different kinds of genetic engineering or therapy. It is possible that such interventions will work and have no negative side effects, but it is perhaps more likely that they will have unanticipated effects. And we might even want to consider which valued human abilities – eg. spatial or pattern recognition skills – might be placed at risk were we to target our interventions specifically at reading disorders.”

They really want to destroy all alternative perceptions and ways of thinking. They’re ignoring how many abilities they are going to destroy and how impoverished they are going to make our world because of their cultural myopia. Each time they have tried playing God they have only caused harm. Who caused the climate change? Scientists playing God trying to control nature, did the Gods anticipate the climate change?

They are not only messing with humans, this whole earth is interconnected, they are messing with the entire ecosystem, with all life. How many species have been brought to extinction because of humans manipulating nature, there’s endangered species today thanks to humans manipulating nature.

If we fail to understand and take care of the natural world, it can cause a breakdown of these systems and come back to haunt us in ways we know little about. A critical example is a developing model of infectious disease that shows that most epidemics — AIDS, Ebola, West Nile, SARS, Lyme disease and hundreds more that have occurred over the last several decades — don’t just happen. They are a result of things people do to nature. The diseases they claim they want to cure were caused by doing this, so why are they doing it again? Was the world ready for COVID-19 to strike? I doubt it. World War II was caused by eugenics, why are they following Adolf Hitler’s steps?

Mutations are not random or accidental, malaria is endemic in Africa and Africans have developed mutations that protect them from malaria through adaptation, the sickle cell mutation is a defence mechanism against malaria. Europeans don’t have these mutations, if a European goes to Africa they are more likely to get a disease. It was mutations that enabled the Europeans to survive the 14th century bubonic plague. Editing one gene may cure a disease but at the same time make them more susceptible to other diseases. Eliminate the sickle cell mutation from the gene pool and you’ve destroyed the only defence mechanism against malaria. Such foolishness.

This is wicked and pure evil to think we don’t deserve to be born just because we are different. CRISPR-Cas9 is a direct violation of human rights, especially human autonomy. They need to sort their discriminatory thoughts out and not touch us without our consent!

“The Human Genome Project is founded upon a fallacy. There is no such thing as “the human genome.” Neither in space nor in time can such a definite object be defined. At hundreds of different loci, scattered throughout the twenty-three chromosomes, there are genes that differ person to person. No body can say blood group A is “normal” and O, B, and AB are “abnormal.” So when the Human Genome Project publishes the sequence of the typical human being, what will it publish for the ABO gene on chromosome 9? The project’s declared aim is to publish the average or “consensus” sequence of 200 different people. But this would miss the point in the case of the ABO gene, because it is a crucial part of its function that it should not be the same in everybody. Variation is an inherent and integral part of the human – or indeed any – genome.”

The BBC Reported: This complete, single human genome will be a monumental technical achievement. Only 70 years have passed since the double-helix structure of DNA was first revealed, thanks in part to a grainy black and white image taken by Rosalind Franklin, transforming our understanding of how genetic information is stored. Today we have the capability to read the entire genetic ‘textbook’ that makes a person unique. But the geneticists involved say it is also a beginning, not an end. They now want to sequence the genomes of people from around the world, to build up a true picture of our species’ genetic diversity. They want to understand what the previously unsequenced sections of DNA are doing. And they want to roll out end-to-end genome sequencing in clinics, to help doctors diagnose and treat us when we get sick. In short, the human genome will never be complete. We will never be done reading it.

This is a framing issue. This drug does not “cure” autism because autism is a neurotype. What it likely does do is helps alleviate neurological and/or nerve issues that are a comorbidity for many of the folks who also have intellectual disability. These folks will still be autistic but this medication may help them regulate.

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Doreen Samelson, Ed.D., MSCP, and Lisa Ruble Ph.D.

Rethinking the Gold Standard for Autism Treatment

Research shows some autistic children may get more treatment hours than needed..

Posted September 19, 2024 | Reviewed by Margaret Foley

What Is Autism?
Find counselling to help with autism
New research shows that high-hour autism treatments may not improve developmental outcomes.
Families may consider starting with fewer treatment hours, adjusting based on the child’s needs.
Caregiver-mediated interventions offer flexible options without requiring high-hour clinical treatment.

By Doreen Samelson, Ed.D., MSCP and Lindsey Sneed, Ph.D., BCBA-D

If a little bit is good for you, more must be even better. Patients frequently take this approach to health treatments, sometimes to their detriment.

In our specialty, care services for autistic children, some healthcare providers hold a similar view. Many professionals believe the “gold standard” for intervention is high-hour treatment—up to 40 hours a week—including for children under 5 years old. A recent meta-analysis in JAMA Pediatrics challenges this assumption head-on, with findings that could significantly alter how we approach crucial early interventions for autistic children.

The Study in Context

The JAMA Pediatrics study looked at the relationship between the amount of intervention provided (hours per day, duration, and cumulative intensity) and the outcomes for young autistic children. Researchers analyzed data from 144 studies involving more than 9,000 children, making it one of the most comprehensive analyses of its kind.

Contrary to what many have long believed, the study found no significant association between the amount of intervention and improved developmental outcomes. As the authors write, “health professionals recommending interventions should be advised that there is little robust evidence supporting the provision of intensive intervention.”

The authors of the meta-analysis looked at studies of any nonpharmacological intervention for autistic children, but their findings will likely have the greatest impact on interventions based in applied behavior analysis (ABA). The most common intervention utilized with autistic children, ABA uses the principles of operant conditioning (changing behavior through reinforcement or consequences) in real-world settings. The practice became widespread after the publication of a paper by clinical psychologist O. Ivar Lovaas in 1987. That and other publications helped establish the long-held view that high-hour intervention is the best approach for autistic children and their families.

The JAMA Pediatrics research directly challenges this view.

What This Means in Practice

The implications of this meta-analysis are profound. Instead of defaulting to high-hour interventions, this research suggests families and practitioners should utilize this approach sparingly. A better approach may be to start with lower hours and titrate up, if needed. Other personalized treatment options that practitioners and caregivers may consider (that do not require high intervention hours) include speech therapy, psychotherapy (for issues such as anxiety and depression ), and caregiver -mediated interventions (including those based on ABA principles).

The authors included studies of caregiver-mediated interventions in their research—but found they were unable to include many of these studies because they often did not report daily data on the intensity of treatment (as needed for the meta-analysis). The researchers also noted the potential complexity of comparing clinician-mediated interventions with caregiver-mediated interventions. They write that caregiver-mediated interventions “even when they are delivered with relatively high intensity, may be less likely to interrupt child participation in everyday family activities and instead simply alter the nature of their participation. Our methods did not allow us to differentially examine the impact of clinician-delivered vs. caregiver-delivered intervention hours, but future investigations should more closely examine this question.”

Broader Impact: Access and Cost

Another consideration is the potential impact on access to care. As autism diagnoses continue to rise —1 in 36 children is now identified as having autism—the demand for intensive interventions places a significant burden on both families and healthcare systems. High-hour treatments are an expensive and resource-intensive approach in a field that is already struggling to keep up.

Anecdotally, we often encounter families who have waited many months or even years to begin treatment. Research suggests the problem is getting worse . In 2016-2017, the proportion of autistic children receiving treatment by age 4 was 60 percent. In 2020-2021, the most recent available data, that figure fell to 48 percent.

By allowing providers to work with more families, lower-hour interventions could help expand access, mitigate workforce shortages, and reduce wait times.

Risks of High-Hour Treatment

High-hour autism interventions may also impose significant burdens on the people they are supposed to benefit. The study authors write, “very intensive interventions could perceivably cause harm by depriving children of time to engage in other activities, such as rest, recreation, and time with family and community members.”

Additionally, for siblings, parents, and other caregivers, having a provider in the home for extended periods can be disruptive. Frequent travel to providers’ offices may also impose a burden.

How Many Hours?

The JAMA Pediatrics study does not offer families or providers guidance on the ideal number of hours. The authors write, “It is likely that there is a minimum amount needed for intervention to have any benefit at all and, potentially, an optimal amount of intervention that is dependent on the child. Unfortunately, current evidence does not offer clear values or ranges for those amounts.”

For families currently receiving high-hour interventions, the suggestion that their child’s hours of treatment should be cut may be cause for concern. The same is likely true for the professionals who provide that care. We hope the findings of this research will reassure both groups that there appears to be little risk that children’s outcomes will be negatively affected by lower-hour treatments.

We encourage providers and families to try alternatives to high-hour interventions—keeping a careful eye on the well-being of the child and the family as a whole—while staying ready to recalibrate if needed.

Lindsey Sneed, Ph.D., BCBA-D, is vice president of clinical excellence at the nonprofit Catalight, which provides access to innovative, individualized care and clinical research. She is also an adjunct faculty member at the University of San Francisco. She conducts applied research evaluating the efficacy of different models of care for children with developmental disabilities and contributes to the development of new care models.

To find a clinician, visit the Psychology Today Therapy Directory .

Doreen Samelson, EdD, MSCP, taught at the University of Oregon and he chief clinical officer at the nonprofit Catalight. Lisa Ruble, Ph.D. , is the Earl F. Smith Distinguished Professor in Special Education and Autism at Ball State University in Indiana.

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Research Studies

Currently Recruiting or Active Research Studies

Please download the document below for our current recruiting studies organized by age range.

Study Title

Study description, spark (simons powering autism research) study.

Available in English and Spanish.

If you or your child has a professional diagnosis of autism, Stanford University invites you to learn more about SPARK, a new online research study sponsored by the Simons Foundation Autism Research Initiative. The mission of SPARK is clear: speed up research and advance understanding of autism by creating the nation’s largest autism study. Joining SPARK is simple – register online and provide a DNA sample via a saliva collection kit in the comfort of your own home. Together, we can help spark a better future for all individuals and families affected by autism.

SPARK está trabajando para fomentar la investigación y mejorar nuestra comprensión del autismo. Stanford y más de 30 de las principales escuelas de medicina y centros de investigación del autismo del país forman parte de este esfuerzo.

Participar en SPARK es gratis y se puede hacer completamente desde casa.
Muchas de las encuestas de SPARK aportan informes personalizados.
Los participantes serán notificados en caso de haber otras oportunidades de investigación.
Los individuos con autismo podrán recibir códigos de regalo de Amazon por un valor de hasta 50 dólares (uno por familia) después de la recepción de sus muestras de saliva.

Para inscribirse en SPARK: https://sparkforautism.org/Stanford/ES

La inscripción suele llevar unos 20 minutos y puede empezar y parar si lo necesita. Una vez que se registre y complete unos cuestionarios en línea, le enviaremos un kit para recolectar saliva a su domicilio. Para obtener más información, envíe un correo electrónico a [email protected]

Language Treatment Trial for Children with Autism

Researchers at Stanford University are currently recruiting children with autism spectrum disorder to identify MRI-based markers of response to treatment with Pivotal Response Treatment (PRT) targeting language abilities. Children with autism spectrum disorder between the ages of 2 and 4 years 11 months are invited to participate. This study involves up to a 5 month time commitment. The participant must be willing to complete cognitive and behavioral assessments (such as IQ and language testing) and be able to either sleep (young children) or lie still in the scanner during an MRI. After a successful MRI, the participant will be randomized into the PRT trial or DTG (Delayed Treatment Group). PRT will consist of 16 weekly, 60-90 minute sessions of parent training in PRT over a 16 week time period. DTG will consist of your child’s treatments as usual in the community and measurements and questionnaires will need to be filled out on three study visits over the course of the 16 weeks. After completion of the DTG, the participant will be offered PRT parent training sessions similar to the PRT group. There is no cost to participate in the study. If you would like to participate or if you have any questions please call (650) 736-1235 or email: [email protected] to discuss the study in more detail.

2 and 4 years,11 months

Targeting the Neurobiology of Restricted and Repetitive Behaviors in Children with Autism Using N-acetylcysteine Randomized Control Trial

We are recruiting children autism to participate in a study examining the treatment effects of an over-the-counter dietary supplement on the brain.

Eligibility: Children with autism spectrum disorder who -

· are aged between 3 and 12 years old

· exhibit restricted and repetitive behaviors

· will drink N-acetyl cysteine dissolved in water

· will undergo brain scanning (asleep or awake) with magnetic resonance imaging (MRI)

· will undergo brain scanning with electroencephalography (EEG)

The study will take place over 3 to 6 visits (some remotely over Zoom) and the approximate time required is about 10 to 12 hours. Individuals that are able to complete both of the MRI/EEG sessions will be compensated $50.

You can find more information about our NAC studies at https://redcap.link/NACforAutism .

If you have any questions please call 650-736-1235 or email: [email protected] .

3 to 12 years

Autism Center of Excellence Sleep Study

Dear Parents,

We are excited to tell you about a new research study for children. We are looking to partner with parents who have children that are between the ages of 4 and 17 years old, with and without an Autism Spectrum Disorder (ASD) diagnosis.

What is involved?

In-person cognitive and behavioral assessments
Day-time Electroencephalogram (EEG)
In-home, 2 night sleep monitoring session
Collection of saliva to measure cortisol and melatonin levels
Wearing a watch device that tracks sleep and daily activity

What will I receive if I participate?

Research sleep report and behavioral testing summary upon request
$50 for each in-person visit to Stanford and $100 for the 2 night in-home sleep assessment

Treatment extension study:

If your child has ASD, sleep difficulties, and ages 8-17, they may also qualify for sleep medication trials

Interested in participating or want to learn more? Click Here!

If you would like to reach out to our team directly with any questions, please contact our team below!

Email: [email protected]

650-498-7215

4 to 17 years

Pregnenolone Randomized Controlled Trial

Neurosteroid Pregnenolone Treatment for Irritability in Adolescents with Autism

Medication treatments for core symptoms of autism spectrum disorder (ASD) continue to be unmet medical needs. The only medications approved by the U.S. Food and Drug Administration (FDA) for the treatment of individuals with ASD are effective in treating irritability and associated aggressive behaviors, but these medications can also cause severe long-term side effects such as diabetes and involuntary motor movements. Therefore, effective medications with more tolerable side effect profiles are highly desirable. This profile is consistent with pregnenolone (PREG). PREG belongs to a new class of hormones known as neurosteroids, which have been shown to be effective in treating various psychiatric conditions including bipolar depression and schizophrenia. As compared to currently FDA-approved medications, our preliminary data suggested that PREG may represent a potentially effective and well-tolerated agent for treating irritability in individuals with ASD. In addition, our experience suggests that PREG might be helpful in improving selected core symptoms such as social deficits and sensory abnormalities of ASD. This study provides the opportunity to further explore the usefulness of PREG in the treatment of irritability and some core symptoms of ASD. We are performing a 12-week randomized double-blind controlled pilot trial to examine the effectiveness of orally administered PREG in reducing irritability and associated behaviors in adolescents with ASD. In this study, we also aim to examine the usefulness of biomarkers (blood levels of neurosteroids, eyetracking and brain wave recording) in predicting treatment response and assessing biologic changes with PREG treatment.

Link to study in Stanford's Clinical Trials Directory

14 to 25 years

Trial of Center-Based vs. In-Home Pivotal Response Treatment (PRT) in Autism (PRT-HvC)

Do you have a child (2-5 years old) with autism and want an intensive center-based or in-home intervention?

Stanford University researchers are recruiting children with autism and their parents to participate in a study examining the effectiveness of a center-based vs. in-home Pivotal Response Treatment (PRT) program in targeting social communication abilities in young children with autism.

Participants must:

Be diagnosed with Autism Spectrum Disorder
Be between the ages of 2 years and 5 years 11 months
Be able to attend 3-hour research treatment sessions 4 days per week and participate in parent training

Based on behavioral screening assessments, children who are eligible will be randomly assigned to either center-based intervention, in-home intervention, or treatment as usual. Those assigned to the treatment-as-usual group will receive treatment after the 16–week period is completed.

Call 650-736-1235 or email [email protected] to learn more.

https://clinicaltrials.gov/ct2/show/NCT04899544

2 to 5 years

Improving Access to Pivotal Response Treatment (PRT) via Telehealth Parent Training

There is an urgent need for improved access to effective autism treatments. With advances in technology, distance learning models have particular promise for families who cannot access evidence-based parent training locally or may be on long wait-lists for behavioral treatments. Pivotal Response Treatment (PRT) is an established treatment for autism spectrum disorder (ASD); however, a telehealth PRT model has not yet been evaluated in a controlled trial. This study will examine the effects of training parents in PRT via secure video conferencing and investigate 1) whether parents can learn via telehealth to deliver PRT in the home setting (PRT-T) and 2) whether their children will show greater improvement in functional communication skills compared to children in a waitlist control group. Participants will include 40 children age 2 to 5 years with ASD and significant language delay. Eligible children will be randomly assigned to either PRT-T or waiting list. Weekly 60-minute parent training sessions will be delivered for 12 weeks via secure video conferencing software by a PRT-trained study therapist. Link: https://clinicaltrials.gov/ct2/show/NCT04042337

Note: Participants must live at least 200 miles away from Stanford University (i.e., this study is geared towards out-of-state families or families living at a distance)

A Center Based Randomized Controlled Trial of Pivotal Response Treatment for Preschoolers With Autism

Researchers at Stanford University are currently recruiting children with autism and their parents to participate in a study examining the effectiveness of a center-based Pivotal Response Treatment (PRT) program in targeting social communication abilities in young children with autism. We are currently recruiting children diagnosed with ASD and social communication deficits, aged 2:0 to 3:11 years. Children who are eligible based on behavioral screening assessments will be randomly assigned to either an immediate treatment (PRT) group or a delayed treatment group (DTG). If randomized into the PRT group, the 12-week treatment will consist of a combination of one weekly 60-minute individual parent training session and 12 weekly hours (approximately 3 hours per day for 4 days per week) with your child in a center-based group preschool environment at Stanford University. If randomized into the delayed treatment group, the children will wait 12 weeks to receive the PRT treatment and continue any treatment they are receiving as usual in the community. The cost of clinic-based services varies based on individual family health insurance plans.

For more information, please call (650) 736-1235 or email [email protected] to discuss the study in more detail.

2 and 3 years,11 months

Natural History Study of Individuals with Autism and Germline Heterozygous PTEN Mutations

The goal of this study is to gain a better understanding of PTEN mutation syndromes to identify early markers and ultimately effective interventions for autism spectrum disorder. Individuals 18 months or older are eligible to participate if they have been diagnosed with PTEN hamartoma tumor syndrome. The study involves five visits over a two year period. Three of the visits occur on-site at a study location. The other two visits occur as phone calls. The on-site visits include a blood draw, physical/neurological exams and behavioral testing.

Study Webpage

18 months and older

Active Studies, not Recruiting

An open-label pilot study of esomeprazole in children with autism.

Researchers at Stanford University are currently examining the effectiveness of esomeprazole in improving social communication deficits in children with Autism Spectrum Disorder (ASD). Esomeprazole is currently FDA-approved for children ages 1 and up for gastroesophageal reflux disease (GERD) and has been identified as a potential treatment for improving social communication in children with ASD. Children with ASD ages 2 through 6 years are invited to participate. The child must be willing to take esomeprazole orally for at least 8 weeks, complete diagnostic and behavioral assessments, and be free of serious medical problems. There is also an optional research blood draw. The study will require visits to Stanford University and the parent/caregiver will be required to complete questionnaires for each visit.

For more information, please go to https://is.gd/ASDstudy , call (650) 736-1235, or email [email protected] .

2 to 6 years

Vasopressin Treatment Trial for Children with Autism

The purpose of this clinical trial is to investigate the effectiveness of vasopressin nasal spray for treating symptoms associated with autism. Vasopressin is a hormone that is produced naturally within the body and has been implicated in regulating social behaviors. It has been proposed that administration of the hormone may also help improve social functioning in individuals with autism.

Link to study at clinicaltrials.gov

6 to 17 years

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Treatment Information and Resources

There are dozens of autism treatments, and choosing the right ones depends on the individual’s needs as well as challenges.

When selecting a treatment, it is important to work closely with your doctor and other healthcare professionals. It is also recommended that you inquire about the evidence supporting the effectiveness of the prescribed treatment(s). This should include positive and negative findings as well as possible side effects.

Here are some of the most common treatments for autism.

Behavioral Therapies

Applied Behavior Analysis (ABA) – ABA refers to understanding a person’s behavior in the context of their surroundings rather than in a controlled laboratory setting. The aim of this method is to improve specific behaviors and develop skills, and it is based on traditional behavior strategies such as rewarding appropriate behaviors and ignoring or discouraging inappropriate behaviors. ABA is among the most widely studied and frequently used therapies for those on the autism spectrum. There are several forms of ABA therapy including:

Pivotal-Response Treatment (PRT)
Early Start Denver Model
Functional Communication
Verbal Learning

Outpatient Therapies

Speech Therapy – Speech therapy is often recommended when a child has difficulties learning vocabulary, pronouncing words, using an appropriate tone of voice, understanding and using body language, and asking and responding to questions. Speech therapy may include alternative augmentative communication (AAC) strategies like Picture Exchange Communication System (PECS), speech output devices, and sign language.

Sensory Therapy (ST) – Your child may be over-reactive, under-reactive, or even crave certain sensory sensations. These sensations may include loud sounds, bright lights, certain tastes, light touch, and/or strong smells. Numerous sensory interventions have been developed to treat various sensory-challenges including sensory integration as well as various visual and auditory interventions.

Occupational Therapy (OT) – This therapy helps improve numerous skills and behaviors with the goal of independence. OT therapists may work on daily activities, hand-eye coordination, sleep, social interactions, and play.

Physical Therapy (PT) – The aim of PT is to improve overall motor movement. This may include posture, balance, motor coordination, and flexibility.

Evidence-based Sensorimotor Therapies

Music and Art Therapy – These therapies were designed to help individuals deal with anxiety and emotions as well as help express themselves.

Animal Therapy – This form of therapy may reduce fear and anxiety toward animals by interacting with socially-oriented animals in structured therapeutic situations. These animals often include horses , dogs, and dolphins. Those on the autism spectrum have also reported a calm feeling while interacting with these animals.

Who provides autism treatment?

Your care team will work with you to develop an effective treatment plan that may include one or more of the following professionals:

Behaviorist
Gastroenterologist
Neurologist
Nutritionist
OT/PT/ST therapists
Pediatrician
Psychiatrist
Psychologist

The best treatment for autism is the one that works

First and most important, early intervention can make a big difference. The earlier an individual receives appropriate support, the better his/her prognosis .

Your doctor can help you decide which autism treatments are appropriate for your child. Keep in mind that there is no single treatment for everyone with autism. Instead, there are a variety of therapies that may be helpful addressing symptoms depending on the individual’s needs. What works for one person may be less effective – or ineffective – for somebody else.

As your child grows and develops, some treatments might become less effective, while others become more important. You should discuss these changes with your doctor to assure the treatment plan stays current.

Gathering reports from the treatment team and completing the Autism Treatment Evaluation Checklist (ATEC) prior to meeting with your doctor will help identify issues to address and referrals that may be needed. The ATEC is a helpful tool designed to measure changes of symptoms and behaviors over time. Note: Casual observations of your child’s development are typically not an accurate way to monitor progress. The ATEC provides a free, convenient tool that can be used to track changes over time. The checklist can also be useful to help determine whether a therapy is beneficial. To track a specific approach, complete the ATEC before (baseline) and after implementing a treatment and track changes over time.

For more than 50 years, the Autism Research Institute has provided support and guidance to parents and professionals worldwide, and we will continue to do so wherever the journey takes all of us.

Healthcare Equity and Access Concerns in Autism

Melanie Glock 2024-09-06T16:08:58-05:00 May 21st, 2025 | Health , Medical Care , Research , Self Care , Webinar |

Free webinar at 1 p.m. Eastern time (US), Wednesday, March 5, 2025 Tune in for a discussion on how to achieve healthcare equity for all persons, including those with autism spectrum disorder and

Autism and Gastrointestinal Comorbidities

Melanie Glock 2024-09-06T16:11:16-05:00 March 5th, 2025 | Anxiety , Gastrointestinal , Health , Medical Care , Meltdowns , Nutrition , Research , Self Care , Self Injury , Self-Injury , Sensory , Webinar |

Free webinar at 1 p.m. Eastern time (US), Wednesday, March 5, 2025 Tune in for a review of gastrointestinal conditions commonly seen in individuals with autism spectrum disorder, along with an update on

Editorial – Fecal Microbiota Transplantation and Autism

Melanie Glock 2024-09-05T12:42:44-05:00 May 24th, 2024 | News , Uncategorized |

Over the past several years, Fecal Microbiota Transplantation (FMT) has become the subject of growing interest in the autism community due, at least in part, to the increased awareness of

Prenatal exposure to cannabis may increase likelihood of autism

Melanie Glock 2024-04-28T15:45:52-05:00 August 29th, 2023 | News |

Cannabis use during pregnancy may alter placental and fetal DNA methylation (the process of turning genes “on” and “off”) in ways that increase the likelihood of autism spectrum disorder (ASD) or other

New multi-national study adds to evidence linking alterations of the gut microbiome to autism

Melanie Glock 2024-04-28T15:46:00-05:00 August 29th, 2023 | News |

Strong new evidence linking alterations of the gut microbiome to autism spectrum disorders (ASD) comes from a new multi-national study by James Morton and colleagues. In the study, researchers in North America,

Sleep problems in infancy associated with ASD, autism traits, and social attention alterations

Melanie Glock 2024-09-10T13:40:21-05:00 July 20th, 2023 | News |

A new study from the United Kingdom indicates that sleep problems in infancy may help to predict later social skills deficits, autism traits, and autism diagnoses in children. Jannath Begum-Ali and

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Indian J Psychol Med
v.39(6); Nov-Dec 2017

Comprehensive Management of Autism: Current Evidence

Manjiri deshpande shenoy.

Indlas Child Guidance Clinic, Mumbai, Maharashtra, India

Vishal Indla

Harish reddy.

1 Malla Reddy Institute of Medical Sciences, Hyderabad, Telangana, India

Autism is a neurodevelopmental disorder characterized by impaired social interaction, verbal and nonverbal communication, and restricted repetitive behavior. The goals of treatment are to target core behaviors, improve social interactions and communication, and reduce disruptive behavior. The present paper discusses the role of applied behavioral analysis and pharmacotherapy.

INTRODUCTION

Autism is a neurodevelopmental disorder, with a multifactorial etiology, characterized by persistent deficits in social communication and social interaction and the presence of restrictive and stereotyped patterns of behavior, interests, or activities.

The prevalence of this diagnosis has increased over the past few decades, and it is unclear whether this is solely attributable to the increased awareness of milder forms of the disorder among medical providers.

The primary goals of treatment are to maximize the child's ultimate functional independence and quality of life by minimizing the core features of autism spectrum disorder (ASD), facilitating development and learning, promoting socialization, reducing maladaptive behaviors, and educating and supporting families.

In current practice, there is no curative treatment for autism, but the recommended treatment involves various therapies which include applied behavioral analysis, speech therapy, and sensory integration therapy. Medications have been used for behavioral symptoms. Techniques such as stem cell therapy and hyperbaric oxygenation are being tried.

CHANGES IN DIAGNOSTIC CRITERIA

Changes to diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders, 5 th Edition (DSM-V) included eliminating several subdiagnostic categories (i.e., Asperger syndrome, pervasive developmental disorder not otherwise specified, disintegrative disorder) and using only one term: ASD.[ 1 , 2 ]

The requirements for this diagnosis also decreased from three criteria (social reciprocity, communicative intent, and restricted and repetitive behaviors in DSM-IV-Text Revision) to two criteria (social communication/interaction and restricted and repetitive behaviors in DSM-V).[ 1 , 2 ]

The new criteria in DSM-V for ASD is as follows:[ 2 ]

Deficits in social-emotional reciprocity
Deficits in nonverbal communicative behaviors used for social interaction, and
Deficits in developing, maintaining, and understanding relationships.
Stereotyped or repetitive motor movements, use of objects, or speech
Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior
Highly restricted, fixated interests that are abnormal in intensity or focus, and
Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of the environment.
Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life)
Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning
These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay.

Intellectual disability and ASD frequently co occur. To make a comorbid diagnosis of ASD and intellectual disability, social communication should be below that expected for general development level.

Despite the advances in early diagnosis and intervention, no therapy has been yet proven to completely reverse the core symptoms of autism.

Nutritional intervention and complementary and alternative medicine approaches are highly prevalent (about 74%) among children affected with ASD.[ 3 ]

The only treatment in ameliorating the core behavioral deficits is early intensive behavioral and educational interventional therapy.[ 4 ]

A team of trained healthcare professionals such as developmental pediatrician, child psychiatrist, occupational and behavioral therapist, speech therapist, psychologist, specialist teacher, and social worker are necessary for the management of autism.

There is an improvement in the cognitive, communication, adaptive, and social functioning and reduction in inappropriate behaviors such as aggression, hyperactivity, and temper tantrums after early (initiated before 4 years of age) intensive behavioral and educational therapy in autistic children. It was postulated that early, intensive applied behavior analysis (ABA) intervention might lead to remarkable outcomes, including almost half of the children receiving this treatment gaining significant intelligence quotient (IQ) points and being mainstreamed into regular classes.[ 5 ]

Individualized one-to-one therapy is provided in a distraction-free structured environment by behavioral therapists.

APPLIED BEHAVIORAL ANALYSIS

In 1987 and 1993, Lovaas et al . published articles describing the “recovery” of almost 50% of a group of very young children with autism, treated intensively with applied behavioral analysis for several years.[ 6 ]

ABA is a treatment based on theories of learning and operant conditioning. It includes specific intervention targets, coupled with positive reinforcement (verbal praise, tokens, or edible rewards) with repetition of learning-trials a key component.[ 4 ]

A meta-analysis examining the efficacy of ABA interventions for young children with autism showed medium to large positive effects on intellectual functioning, language development, daily living skills acquisition, and social functioning, with the larger effect sizes observed on language-related outcomes.[ 7 ]

Primary goals of treatment: (Rutter, 1985)

As much as possible, facilitate and stimulate the normal development of cognition, language, and socialization
To decrease autism-bound maladaptive behaviors such as rigidity, stereotypy, and inflexibility
To reduce or even eliminate nonspecific maladaptive behaviors such as hyperactivity, irritability, and impulsivity
To alleviate stress and burden for the family.

ABA investigates people's interactions with their environment while developing intervention strategies to decrease inappropriate behavior and increase socially appropriate skills.[ 8 ]

Behavior analysis focuses on the principles that explain how learning takes place. Positive reinforcement is one such principle. When a behavior is followed by some sort of reward, the behavior is more likely to be repeated. Through decades of research, the field of behavior analysis has developed many techniques for increasing useful behaviors and reducing those that may cause harm or interfere with learning.

ABA is the use of these techniques and principles to bring about meaningful and positive change in behavior.[ 9 ]

ABA methods are used to:

Increase and maintain desirable adaptive behaviors
Reduce interfering maladaptive behaviors or narrow the conditions under which they occur
Teach new skills
Generalize behaviors to new environments or situations.

Children who receive early intensive behavioral treatment have been shown to make substantial, sustained gains in IQ, language, academic performance, and adaptive behavior as well as some measures of social behavior, and their outcomes have been significantly better than those of children in control groups.[ 10 ]

Functional behavior analysis, or functional assessment, is an important aspect of behaviorally based treatment of unwanted behaviors. Most problem behaviors serve an adaptive function of some type and are reinforced by their consequences, such as attainment of (1) adult attention, (2) a desired object, activity, or sensation, or (3) escape from an undesired situation or demand.[ 11 ]

Functional behavioral assessment involves formulating a clear description of the problem behavior (including frequency and intensity); identifying the antecedents, consequences, and other environmental factors that maintain the behavior; developing hypotheses that specify the motivating function of the behavior; and collecting direct observational data to test the hypothesis.

Effective early interventions include the following components:[ 12 ]

Provision at earliest possible age
High intensity, at least 20 h/week spent one to one with the child
Strong parental involvement, training, and support
Systematic instructions with individual goals based on ABA
Attempts to generalize acquired skills to other settings in daily life.

The techniques used in ABA are as follows:

Task analysis
Differential reinforcement.

Limitations to this form of intervention include the length of time required to see improvements, questionable generalizability of learned skills, and lack of motivation at times from the patient to work on these skills. Additional limitations to ABA interventions include the cost of these intensive therapies, which can be substantial.[ 13 ]

PSYCHOPHARMACOLOGICAL TREATMENTS FOR AUTISM

The pharmacotherapy of autism involves treatment of targeted behavioral symptoms rather than core autism features. Targets generally include hyperactivity, inattention, repetitive thoughts and behavior, self-injurious behavior, as well as aggression toward others or the environment (des Portes et al ., 2003).

Antipsychotics have traditionally been shown to improve symptoms related to aggression, social withdrawal, hyperactivity, stereotypies, self-injurious behavior, and sleep disturbances. Although typical neuroleptics, such as pimozide and haloperidol, have been reported to be more effective in treating behavioral problems, the increased risk of tardive or withdrawal dyskinesia in a substantial proportion of children with autism continues to be a major concern (Campbell et al ., 1997).

Risperidone was reported to improve self-injury, aggression, and agitation in 70% of the children and adolescents compared to the placebo response rate of 11.5%. More adverse effects, including increased appetite with associated weight gain, transient sedation, tremor, and drooling, were more common with risperidone than placebo. It is considered first line of medication for children and adolescents who display extreme irritability.[ 14 ]

Studies utilizing aripiprazole in the treatment of tantrums, aggression, and self-injury in children and adolescents with autism found aripiprazole to be efficacious and safe. Doses ranged from 5 to 15 mg/kg.[ 15 ]

Methylphenidate was found to be at least moderately efficacious at doses of 0.25–0.5 mg/kg for youth with ASD with attention deficit hyperactivity disorder. However, efficacy was lesser in this population than in those without ASD, and children with ASD developed more frequent side effects. Atomoxetine and clonidine have also found to be more effective than placebo.[ 16 , 17 ]

Selective serotonin reuptake inhibitors, second generation antipsychotics and mood stabilizers such as valproate have been used for repetitive and stereotypic behavior.[ 18 , 19 ]

Several randomized, placebo-controlled trials have examined the efficacy of naltrexone for core symptoms of autism, associated symptoms of hyperactivity and irritability, and for discrimination learning. Overall, it appears naltrexone may have some benefits in reducing hyperactivity and impulsivity in children and adolescents with ASD, but core symptoms did not appear to improve with this medication.[ 20 , 21 , 22 ]

The efficacy of melatonin for sleep disturbances in children and adolescents with ASD has been examined in multiple double-blind, placebo-controlled studies, making it one of the best-studied complementary alternative treatments used in ASD.[ 23 ]

Other modalities are sensory integration, speech therapy, and remedial education. In case of all these therapies, earlier the intervention started, better is the outcome.

Newer techniques such as stem cell therapy and hyperbaric oxygenation are being tried, but there is no conclusive evidence for the same.

Thus, treatment of autism requires a multimodal approach with a multidisciplinary team.

Financial support and sponsorship

Conflicts of interest.

There are no conflicts of interest.

Long COVID research reveals new targets for potential treatment

20 March 2023

NIHR researchers have shown for the first time that a dysfunctional immune response is linked to specific symptoms of long COVID. The findings could help in the development of treatments for those living with the disease.

Long COVID

An estimated 1.8 million people in the UK are experiencing long COVID. Debilitating symptoms can persist for months after COVID-19 infection, and include extreme tiredness and shortness of breath.

The NIHR funds research into the biological causes of long COVID. Once researchers understand more they can begin to develop effective treatments.

Migration of immune cells

Monocytes are a type of immune cell made in the bone marrow. They travel through the blood to the lungs where they surround and kill the virus. Researchers at

NIHR Manchester Biological Research Centre
NIHR Leicester Biomedical Research Centre

have discovered abnormal migration of these cells corresponds to shortness of breath.

Study design

The study was supported by the NIHR Manchester Clinical Research Facility at Wythenshawe Hospital . The researchers analysed blood samples from

71 hospitalised patients with acute COVID-19
142 patients attending clinics after discharge from COVID-19
healthy blood samples from frontline health workers

Patients filled in questionnaires which assessed their symptoms.

A link between monocyte function and different long COVID symptoms

The researchers examined the monocyte migratory signatures in patients with acute disease. Long COVID patients with shortness of breath had unique monocyte profiles compared to

Long COVID patients with ongoing fatigue
Patients who experienced no symptoms

Researchers now understand more about the immune system in patients with long COVID. The study could provide an important first step on the road to possible treatments.

Professor of Inflammatory Disease, Tracy Hussell, Programme Lead in the Next Generation Phenotyping and Diagnostics Theme at NIHR Manchester Biomedical Research Centre, said: “This study is a prime example of the ‘one Manchester’ approach that provides seamless integration between clinicians and scientists under the umbrella of our NIHR Biomedical Research Centre and the generosity of our patient population.”

The study was led by Dr Elizabeth Mann Wellcome Trust/Royal Society Sir Henry Dale Fellow at the University of Manchester’s Lydia Becker Institute and published on 16 March 2023 in the European Respiratory Journal .

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NIHR takes on management of Better Methods for Better Research Programme

New findings on the use of molnupiravir to treat COVID-19

New funding opportunities for novel brain tumour research launched

Researchers Uncover Key Actor in Spread of Breast Cancer to the Brain

Dana-Farber researchers have identified a key mechanism involving the KMT2C and KMT2D genes that drives breast cancer metastasis to the brain.
The study highlights the role of the KDM6A protein in promoting this spread, particularly in patients with triple-negative breast cancer.
This discovery opens the door to potential new treatments targeting KDM6A to prevent brain metastasis in these patients.

When breast cancer metastasizes, it often heads for the brain, where it can be exceptionally difficult to root out. The key to preventing the spread of the cancer, or thwarting it if it does reach the brain, is to understand the mechanism that turns stationary tumor cells into nomadic intruders.

Study Leaders: Kornelia Polyak and Marco Seehawer. Photo by Sam Ogden.

In a recent study, a team of Dana-Farber scientists uncovered one such mechanism, a pathway leading from two mutated genes to an overactive gene that spurs metastasis in patients with triple-negative breast cancer. The findings, published in Nature Cell Biology , suggest that a protein lying midway along this path may be an excellent target for drugs to block the cancer’s spread.

“In about half of patients with metastatic triple-negative or HER2-positive breast cancer, the cancer has spread to the brain,” says Dana-Farber’s Kornelia Polyak, MD, PhD , senior author of the study. “Compared to those whose cancer has spread to other sites, patients with brain metastases have the shortest overall survival. The need for better treatments for this group, particularly those with triple-negative cancer, is critical.”

The study grew out of a piece of circumstantial evidence. Researchers knew

that the genes KMT2C and KMT2D , which are often mutated in triple-negative breast cancer, are especially likely to be mutated in metastatic growths outside the breast. That suggests the mutations aren’t there by chance but play a role in the cancer’s spread. The nature of that role, however, was unclear.

To find out, Marco Seehawer, PhD, a postdoctoral fellow in Polyak’s lab, took samples of non-metastatic triple-negative breast cancer cells from mice and used an RNA guide to shut down the KMT2C and KMT2D genes, basically duplicating what happens when the genes are mutated. He then injected the cells into mammary tissue of a group of female mice. Another group of mice received breast cancer cells with normal KMT2C and D .

“We found that the growth of primary breast tumors – those that formed in the breast itself – was about the same in both sets of animals,” Polyak recounts. “But the mice that received cells with ‘knocked out’ [shut down] KMT2C and D had many more metastases in the liver, lungs, bones, and, especially, the brain.”

The researchers performed an array of follow-up experiments to confirm that the loss of working KMT2C and D genes contributes to brain metastasis in mouse models, mirroring what happens in human patients. They then sought to trace the steps by which this takes place.

The first clue was that KMT2C and KMT2D, the proteins made from the KMT2C and KMT2D genes, are known to exert a powerful influence on the activity of key genes. They do this by attaching methyl groups – packets of three hydrogen atoms surrounding a carbon atom – to proteins called histones, which hold DNA in place. This tends to loosen specific coils of DNA, altering the activity of genes in that region.

Advanced technology enables scientists to map the precise locations of methyl groups and other “histone markers” across the genome. By comparing the number and locations of such markers in different sets of cells, researchers can spot differences in gene activity across those sets.

Seehawer and his colleagues did just that in the new study. They began with two collections of mouse breast cancer cells: one in which KMT2C and D were normal, and one in which they were knocked out. Using an array of experimental techniques, they searched the samples for several types of histone markers.

One difference stood out. Cells with knocked-out KMT2C and D had much more of a protein called KDM6A bound to histones than cells with normal KMT2C and D did. An increase in KDM6A can have a stimulatory effect on certain genes. In the case of cells with knocked-out KMT2C and D , the gene that gets amped up is Mmp3 , researchers found.

There’s good reason for thinking that overactive Mmp3 endows breast cancer cells with the restlessness that sends them to the brain. For one, MMP-3 (the protein made from Mmp3 ) is a protease, an enzyme that breaks down proteins and can enable cancer cells to barge through surrounding tissue. For another, researchers found that tumor samples from patients with triple-negative breast cancer carrying KMT2C mutations have high levels of MMP-3.

The case against Mmp3 hyperactivity as a key factor in brain metastasis in triple-negative breast cancer was strengthened when researchers used a drug agent to block KDM6A in animal models of the disease. The effect was to lower the activity of Mmp3 and prevent brain metastasis in the animals.

“Our results point to KDM6A as a key mediator of brain metastasis in triple-negative breast cancers harboring mutations in KMT2C and D ,” Polyak says. Although MMP-3 itself is probably not a good target for therapies to prevent brain metastasis, as MMP-3 inhibitors can be quite toxic, agents that target KDM6A may be more successful. The development of such agents is a first step toward clinical trials in patients.

About the Medical Reviewer

Kornelia Polyak, MD, PhD, is a Professor of Medicine at Dana-Farber Cancer Institute, Harvard Medical School, and a co-leader of the Dana-Farber Harvard Cancer Center Cancer Cell Biology Program. Dr. Polyak is an internationally recognized leader of breast cancer research. Her laboratory is dedicated to improving the clinical management of breast cancer patients by understanding molecular and cellular determinants of breast cancer risk and tumor evolution. Dr. Polyak has devoted much effort to develop new ways to study tumors and to apply interdisciplinary approaches. Dr. Polyak has received numerous awards including the Paul Marks Prize for Cancer Research, AACR Outstanding Investigator Award for Breast Cancer Research, and the 14th Rosalind E. Franklin Award for Women in Science. She is a recipient of the NCI Outstanding Investigator award (2015 and 2022) and received a Distinguished Alumna Award from Weil-Cornell in 2020. Dr. Polyak was the American Association for the Advancement of Science Fellow in 2019, member of the Fellows of the AACR Academy in 2020, and to the National Academy of Sciences and the National Academy of Medicine in 2022. She was also a recipient of the American Cancer Society Research Professor Award in 2022 and received the 2023 AAACR Distinguished Lectureship in Breast Cancer Research award.

Investigational Treatment Dapirolizumab Pegol Shows Positive Results in Phase 3 Clinical Trial

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Investigational Treatment Dapirolizumab Pegol Shows Positive Results in Phase 3 Clinical Trial

September 24, 2024

Lupus Therapeutics, the clinical research affiliate of the Lupus Research Alliance, is proud to share positive topline results from the Phase 3 PHOENYCS GO study evaluating the investigational therapy dapirolizumab pegol in people living with moderate-to-severe systemic lupus. Results of the Phase 3 PHOENYCS GO study were reported by study sponsors UCB and Biogen.

The initial topline results showed that compared with placebo, dapirolizumab pegol in addition to standard-of-care treatment met the primary endpoint, showing greater improvement at 48 weeks in moderate-to-severe disease activity as assessed by the widely accepted measurement tool called BICLA [British Isles Lupus Assessment Group (BILAG)-based Composite Lupus Assessment (BICLA)]. This tool measures clinical disease activity based on patient medical history, clinical examination. and laboratory tests. Improvement was also seen in disease activity and flares. The safety profile of dapirolizumab pegol was consistent with that seen in previous studies.

“These results provide hope for people with lupus given the urgent need for additional treatment options to address the wide range of symptoms and complications caused by this highly heterogenous disease,” noted Stacie Bell, PhD, Executive Vice President of Lupus Therapeutics, the clinical research affiliate of the Lupus Research Alliance. “We are particularly pleased to see these results, with Lupus Therapeutics having partnered with UCB and Biogen on the PHOENYC GO trial from start-up to reporting through the Lupus Clinical Investigators Network (LuCIN).”

Based on this trial, UCB and Biogen reported plans to initiate a second Phase 3 trial of dapirolizumab pegol, PHOENYCS FLY, in 2024. Lupus Therapeutics will continue to support the UCB/Biogen development program leveraging LT clinical expertise and LuCIN. The expansive, first-of-its-kind lupus clinical research network is comprised of more than 50 top clinical research institutions throughout North America.

Source: Sept. 24 Press Release

LRA Congratulates Dr. James Chen for Prestigious Lasker Award Recognizing Breakthrough Discovery of DNA Sensing Enzyme, cGAS

Team Life Without Lupus Going the Distance for More Treatments and a Cure

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COMMENTS

Autism Breakthrough: New Treatment Significantly Improves Social Skills
A Tel Aviv University study found that hyperbaric medicine, a treatment in which patients breathe oxygen in a pressurized chamber, reduced inflammation and improved brain function in autism animal models. The researchers anticipate that the treatment may have positive implications for clinical treatment of autism caused by genetic mutations.
Study sheds new light on autism, but there's more work to be done
Researchers from Columbia and Vanderbilt universities, among others, found that higher serotonin levels in women are associated with some forms of autism in children. The study suggests that serotonin may play a role in the development of the brain and nervous system, but more work is needed to understand the complex relationship.
Suramin for Autism Update: 2023 and Beyond
Learn about the latest developments and plans for FDA approval for suramin, a potential breakthrough treatment for autism based on the cell danger response hypothesis. Watch the interview with Howard Weisman, CEO of PaxMedica, and get more information on suramin clinical trials, mechanisms of action, and international availability.
Autism cures may be closer as focus turns to early treatment
Researchers have found that some forms of autism caused by a rare genetic mutation can be reversed by supplementing missing amino acids in the brain. The study involved mice and human infants, and ...
Breakthrough Treatment for Autism Spectrum Disorder Within Reach
A research team at DGIST in South Korea identified the cell-specific molecular network of autism spectrum disorder using mass spectrometry and big data analysis. The study, published in Molecular Psychiatry, could lead to a fundamental treatment of the neuro-developmental disorder.
Therapeutic strategies for autism: targeting three levels of the
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder (NDD) that is characterized by three core symptoms: the deficits in social interaction and communication, language development, and ...
An experimental drug for Fragile X seems to be helping people ...
For 22 years, Jason Mazzola's life was defined by Fragile X, a genetic condition that often causes autism and intellectual disability. Jason, who is 24 now, needed constant supervision.
How proteins interact may hold the key to future autism treatments
The study focuses on 100 genes associated with autism spectrum disorder and how they affect protein interactions in the brain. The team uses artificial intelligence and human stem cells to identify potential targets for future treatments.
Treatment for autism symptoms earns ASU researchers patent
A new treatment for autism, created by Arizona State University researchers and their colleagues, has been granted a patent by the U.S. Patent Office. ... ASU professor and director of the Biodesign Center for Health Through Microbiomes, and a pioneer in research on the gut microbiome and autism, is a co-inventor of the treatment.
An Update on Psychopharmacological Treatment of Autism ...
While behavioral interventions remain the mainstay of treatment of autism spectrum disorder (ASD), several potential targeted treatments addressing the underlying neurophysiology of ASD have emerged in the last few years. These are promising for the potential to, in future, become part of the mainst …
What we know about autism—and how to treat it—could change after new
"This opens up kind of a Goldilocks of potential treatment targets," said one of the study's authors, Matthew State, a UCSF child psychiatrist and geneticist. ... new research suggests. 12 hours ...
New advances in the diagnosis and treatment of autism spectrum
This article reviews the definition, characteristics, epidemiology, etiology, diagnosis, and intervention of autism spectrum disorders (ASD), a group of neurodevelopmental disorders. It also discusses the challenges, opportunities, and future directions of ASD research and treatment, including the role of precision medicine and biotechnology.
The Latest Evidence on Autism Diagnoses and Treatment
Autism The Latest Evidence on Autism Diagnoses and Treatment A new report summarizes the latest research and treatment strategies. Posted January 15, 2020 | Reviewed by Gary Drevitch
A Drug That Cures Autism? Neuroscience Study Yields ...
A study by the German Cancer Research Center shows that lamotrigine, a medication for epilepsy and bipolar disorder, can restore nerve cell function and behavior in mice with autism-like features. The drug targets the transcription factor MYT1L, which is involved in nerve cell identity and sodium channel expression.
Autism spectrum disorders
Autism spectrum disorders are a group of neurodevelopmental disorders that are characterized by impaired social interaction and communication skills, and are often accompanied by other behavioural ...
Groundbreaking study connects genetic risk for autism to changes
The study used single-cell assays to identify the cell types and transcription factors affected by autism-related genes in post-mortem brain tissue. It found that the most profound changes ...
Autism News -- ScienceDaily
Find out the latest news and research on autism spectrum disorder, from genetics and brain imaging to behavior and intervention. Learn about the causes, symptoms, diagnosis, and treatment of ...
Rethinking the Gold Standard for Autism Treatment
Key points. New research shows high-hour autism treatments may not improve developmental outcomes. Families should consider starting with fewer treatment hours, adjusting based on the child's needs.
Research Studies
We are excited to tell you about a new research study for children. We are looking to partner with parents who have children that are between the ages of 4 and 17 years old, ... There is an urgent need for improved access to effective autism treatments. With advances in technology, distance learning models have particular promise for families ...
Autism Treatment Information
Learn about the most common treatments for autism, such as behavioral therapies, speech therapy, sensory therapy, and more. Find out how to choose the right treatment for your child and who can provide it, and get tips on early intervention and evidence-based approaches.
Study identifies new metric for diagnosing autism
Autism spectrum disorder has yet to be linked to a single cause, due to the wide range of its symptoms and severity. However, a recent study suggests a promising new approach to finding answers ...
Evidence-based support for autistic people across the lifespan
International standards of evidence within medicine and health care have not been applied sufficiently, despite decades of empirical research on intervention and support for autism, as demonstrated by the latest rigorously conducted reviews. 14,29,30 The efficacy research literature is composed of more single-case designs than group designs of ...
Comprehensive Management of Autism: Current Evidence
In current practice, there is no curative treatment for autism, but the recommended treatment involves various therapies which include applied behavioral analysis, speech therapy, and sensory integration therapy. Medications have been used for behavioral symptoms. Techniques such as stem cell therapy and hyperbaric oxygenation are being tried.
£8m to speed up research into new treatments for Motor Neurone Disease
NIHR is announcing its next major step in new government action to speed up research into Motor Neurone Disease (MND). This is part of a £50 million commitment to MND research over 5 years - by the Department of Health and Social Care (DHSC) and the Department for Science, Innovation and Technology (DSIT).
Long COVID research reveals new targets for potential treatment
Once researchers understand more they can begin to develop effective treatments. Migration of immune cells. Monocytes are a type of immune cell made in the bone marrow. They travel through the blood to the lungs where they surround and kill the virus. Researchers at NIHR Manchester Biological Research Centre NIHR Leicester Biomedical Research ...
Researchers Uncover Key Actor in Spread of Breast Cancer to the Brain
Dr. Polyak has devoted much effort to develop new ways to study tumors and to apply interdisciplinary approaches. Dr. Polyak has received numerous awards including the Paul Marks Prize for Cancer Research, AACR Outstanding Investigator Award for Breast Cancer Research, and the 14th Rosalind E. Franklin Award for Women in Science.
Investigational Treatment Dapirolizumab Pegol Shows Positive Results in
The initial topline results showed that compared with placebo, dapirolizumab pegol in addition to standard-of-care treatment met the primary endpoint, showing greater improvement at 48 weeks in moderate-to-severe disease activity as assessed by the widely accepted measurement tool called BICLA [British Isles Lupus Assessment Group (BILAG)-based ...