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Science Autism

mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Gene repair improves memory and seizures in adult autism

Neuroscience News | April 26, 2019

A new study challenges the presumption that people born with severe autism will benefit from medical interventions only if treated during a narrow window in infancy or early childhood.

Writing in the journal eLife, an open-access scientific journal, the Rumbaugh lab at Scripps Research in Florida reports improvement in measures of seizure and memory in adult mouse models of a genetic cause of autism, called SYNGAP1 disorder.

Children born with only one working copy of the SYNGAP1 gene don’t make enough of the critical SynGAP protein. Two broken copies is lethal. Depending on the extent of their deficit, these children can develop a range of developmental challenges as they mature. This may include intellectual disability, autism-like behaviors, disordered sensory processing, and epileptic seizures that don’t respond to medication. The disorder likely affects one to four individuals per 10,000, similar to the frequency of Fragile X syndrome, says Gavin Rumbaugh, PhD, an associate professor in the Department of Neuroscience at Scripps Research in Florida. However, patients can only be discovered through genetic tests. As a result, only a small fraction of patients with this disorder have been discovered.

To study whether treatment of SYNGAP1 disorder in adulthood could be beneficial, Rumbaugh’s team genetically restored levels of the mice’s SynGAP protein to normal. The treated adult mice showed multiple improvements. It suggests that having one broken copy of the gene not only harms the brain as it develops, but it also has effects in the adult brain, Rumbaugh says. There may be reason to treat at any stage of life once options become available, Rumbaugh adds.

“Our findings in mice suggest that neurodevelopmental disorders’ disease course can be altered in adult patients,” Rumbaugh says. “We can correct brain dysfunction related to seizure as well as memory impairments after restoring SynGAP protein levels in the adult animals.”

Significantly, the paper offers a path to measure the effectiveness of potential medications or other therapies for neurodevelopmental disorders going forward. Electrographic spikes between seizures is an indicator of epilepsy. In their paper, the scientists looked at human EEG data collected from a SYNGAP1 disorder patient registry and found that the appearance of these spikes were much more likely to occur during sleep. Similar findings were observed from mouse models of SYNGAP1 disorder, offering a useful endpoint. "Establishment of biomarkers that predict generalized improvements in brain function will be a critical step in advancing treatments for people with severe neurodevelopmental disorders," Rumbaugh says.

The need for a treatment option is clear, Rumbaugh says. Seizures typically become more frequent as children with SYNGAP1 disorders mature, and for many patients, those seizures do not respond to anti-epilepsy drugs.

“Getting to know families affected by this severe disorder has been invaluable, and drives us to develop treatments that will improve the lives of both children and adults,” Rumbaugh says. “It is encouraging that gene therapy techniques that increase pathologically low protein levels for other types of brain disorders are showing promise in the clinic now.”


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Autism diagnoses prove highly stable as early as 14 months

Neuroscience News | April 29, 2019

Diagnoses of autism spectrum disorder (ASD) by trained professionals in children as young as 14 months are remarkably stable, suggesting that accurate screening and earlier treatment is feasible, report scientists at University of California San Diego School of Medicine in a study published online April 29, 2019 in JAMA Pediatrics.

Growing evidence suggests ASD has its origins in prenatal life — most likely during the first or second trimester of pregnancy — and children begin to display symptoms of the condition by their first birthdays, such as failing to respond to their names or positively interact with others.

Early diagnosis of ASD means earlier intervention and improved therapeutic benefit. “The sooner you can address issues of ASD, the better the outcome for the child,” said the study’s first author, Karen Pierce, PhD, professor of neurosciences and co-director of the UC San Diego Autism Center of Excellence. She led the study with senior author Eric Courchesne, PhD, also a professor of neurosciences.

Multiple studies, including research conducted by Pierce, have found that simple parent checklists performed at the child’s first birthday can identify symptoms of ASD. And yet the mean age of ASD diagnoses in the United States, write the researchers, is “often years later, generally between ages three and four.”

Pierce said the lag between the first signs of ASD and diagnosis represents a missed opportunity, particularly given the accelerated pace of brain development in the first years of life.

“Synaptic density or connections between neurons in the prefrontal and temporal cortex, brain regions centrally involved in higher-order social behavior, doubles between birth and one to two years in age,” said Pierce. “It’s conceivable that outcomes for children with autism could be improved if treatment occurred during this period of rapid brain growth, rather than after, which is more commonly the case.”

To conduct their study, Pierce and colleagues assessed 1,269 toddlers from the general population (441 ASD, 828 non-ASD) who received their first diagnostic evaluation between 12 and 36 months and at least one subsequent evaluation, all by licensed psychologists. Diagnoses ranged from ASD and features of ASD to language and developmental delay or other developmental issues.

The overall diagnostic stability for ASD was 0.84, higher than for any other diagnostic group. Only 2 percent of toddlers initially considered to have ASD transitioned to later diagnoses of typical development. Within the group diagnosed with ASD, the most common transition was from ASD to ASD features at 9 percent.

Diagnostic stability of ASD was weakest at 12 to 13 months, just 0.50, but increased to 0.79 by 14 months and 0.83 by 16 months. Twenty-four percent of toddlers were not designated as ASD at their first evaluations, but later identified. The most common transition in this group was an initial designation of developmental delay (25 percent) or language delay (16 percent), transitioning to later-onset ASD.

“Our findings suggest that an ASD diagnosis becomes stable starting at 14 months, and overall is more stable than other diagnoses, such as language or developmental delay,” said Pierce.

“Once a toddler is identified as ASD, there is an extremely low chance that he or she will test within typical levels at age three or four, so it is imperative that we use every effective tool as early as we can to begin treating diagnosed children.”


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Autistic adults thought they were ‘bad people’

Neuroscience News | Nov 7 2019

Summary: Many people on the autism spectrum who were not diagnosed until later in life grew up believing they were “bad people.”

Many over-50s who were diagnosed with autism late in life had grown up believing they were bad people, according to a new study published in the journal Health Psychology and Behavioural Medicine.

Researchers from Anglia Ruskin University interviewed nine adults about their experiences of being diagnosed with autism in their 50s. The participants were aged between 52 and 54.

As children, some participants recounted having no friends and being isolated from others, and as adults they could not understand why people treated them differently. Several had been treated for anxiety and depression.

Participants also highlighted the lack of support available to adults with a new diagnosis.

It is thought to be the first study of its kind that examines the phenomenon of receiving a diagnosis exclusively in middle age.

Dr Steven Stagg, Senior Lecturer in Psychology at Anglia Ruskin University (ARU) and lead author of the study, said: “One aspect of the research I found heart-wrenching was that the participants had grown up believing they were bad people. They referred to themselves as ‘alien’ and ‘non human.’

“The research also suggests that receiving a diagnosis in middle age can be positive. The participants often described it as a eureka moment that brought relief into their lives. It allowed them to understand why others had reacted negatively towards them."

“Clinicians and health workers need to be aware of the possible signs of autism. Often people are diagnosed with depression, anxiety or other mental health conditions and the autism is missed. More work also needs to be done to support older people after they receive a diagnosis.”

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mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

New brain-based test enables rapid, more accurate autism diagnosis

Science News | May 20, 2019

Scientists at Wake Forest School of Medicine have taken the first step in developing an objective, brain-based test to diagnose autism.

Using functional magnetic resonance imaging (fMRI), the team was able to measure the response of autistic children to different environmental cues by imaging a specific part of the brain involved in assigning value to social interactions.

Findings from the study are published in the current online edition of the journal Biological Psychology.

"Right now, a two- to four-hour session by a qualified clinician is required to diagnose autism, and ultimately it is a subjective assessment based on their experience," said the study's principal investigator, Kenneth Kishida, Ph.D., assistant professor of physiology and pharmacology at Wake Forest School of Medicine.

"Our test would be a rapid, objective measurement of the brain to determine if the child responds normally to social stimulus versus non-social stimulus, in essence a biomarker for autism."

Autism spectrum disorder (ASD) is a developmental disorder that affects communication and interaction with other people. The National Institutes of Health estimates that 1 in 60 children in the United States are autistic.

In the study, the team led by Kishida and P. Read Montague, Ph.D., of Virginia Tech, tested the responsiveness of the brain's ventral medial prefrontal cortex (vmPFC) to visual cues that represented highly-valued social interaction in children diagnosed with ASD compared to typically developing (TD) children. The study included 40 participants ranging in age from 6 to18; 12 had ASD and 28 were TD.

First, the study participants were scanned in an fMRI while viewing eight images of either people or objects, each one multiple times. Included in each set of images were two self-selected pictures of a favorite person and object from each participant. The other six were standardized images of three faces and three objects, each representing pleasant, neutral or unpleasant aspects from a data base widely used in psychological experiments.

After completing the 12- to 15-minute MRI scan, the children viewed the same set of images on a computer screen and ranked them in order from pleasant to unpleasant with a self-assessing sliding scale. In addition, pairs of images were viewed and ranked as to which one they liked better.

According to the study, the average response of the vmPFC was significantly lower in the ASD group than in the TD group. Using images as a single stimulus to capture 30 seconds of fMRI data was sufficient to differentiate the ASD and TD groups, Kishida said.

"How the brain responded to these pictures is consistent with our hypothesis that the brains of children with autism do not encode the value of social exchange in the same way as typically developing children," he said.

"Based on our study, we envision a test for autism in which a child could simply get into a scanner, be shown a set of pictures and within 30 seconds have an objective measurement that indicates if their brain responds normally to social stimulus and non-social stimuli."

He added that this approach could also help scientists better understand the brain mechanisms involved in autism disorder as a whole as well as the many variations on the disorder's spectrum.

Kishida's team plans to do follow-up studies to identify which additional areas of the brain are involved in the different facets of the disorder to help personalize treatments for patients.


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Early statin treatment may help children with Fragile X

Neuroscience News | May 29, 2019

Children with an inherited form of intellectual disability and autism could be helped by a medicine commonly used to lower cholesterol, if used early in life.

The drug – called lovastatin – corrected learning and memory problems in rats with a form of Fragile X Syndrome, tests revealed.

Rats were treated with lovastatin for four weeks during infancy but the benefits persisted for months afterwards.

Researchers say this suggests learning problems in children with Fragile X might be prevented by a similar treatment in early life.

Fragile X Syndrome is one of the most common genetic causes of intellectual disability. It is often associated with autism and attention deficit and hyperactivity disorder, or ADHD. Many affected individuals also have seizures.

The condition occurs when a particular gene is disrupted leading to altered communication between brain cells.

Previous studies in mice and rats have shown that this disruption can be treated with drugs, but it was not known how long treatment might be effective for.

Researchers at the University of Edinburgh studied rats with a genetic alteration similar to that found in people with Fragile X Syndrome. These rats have problems completing certain memory tasks when compared with typical rats.

Treatment with lovastatin between five and nine weeks of age – the precise window when they are developing these memory abilities – restored normal development in the rats.

The animals were able to complete the memory tasks more than three months after treatment ended, indicating the effects of the drug were long-lasting.

Children with Fragile X Syndrome are usually diagnosed around the age of three, typically because they are late in learning to speak. Genetic tests have enabled earlier diagnosis, which raises the possibility of starting treatments sooner.

Current medications help manage specific symptoms – such as hyperactivity and seizures – but there are not yet any treatments that tackle the underlying brain changes leading to Fragile X Syndrome.

Statins are widely prescribed to both children and adults to control high blood cholesterol and to reduce the risk of heart disease.

The study, published in Science Translational Medicine, was led by researchers at the University of Edinburgh’s Patrick Wild Centre and the Simons Initiative for the Developing Brain.

Professor Peter Kind, Director of the Patrick Wild Centre and Simons Initiative for the Developing Brain at the University of Edinburgh, said: “Children with Fragile X Syndrome need special education and, although some will live semi-independently, most require some form of lifelong support."

“We have found that early intervention for a limited period during development can lead to persistent beneficial effects, long after treatment ends, in a rat model of Fragile X Syndrome. Our future experiments will focus on whether there is a critical time-window during development when treatment is more effective.”


CBD Gel a promising treatment for Fragile X

by Susan Ward | May 21, 2019

A clear transdermal cannabidiol (CBD) gel (ZYN002, Zynerba Pharmaceuticals) improved emotional and behavioral symptoms experienced by children and adolescents with fragile X syndrome in a phase 2 open-label study, the company reports.

ZYN002 met its primary endpoint, with patients demonstrating a 46% improvement in the total score on the Anxiety, Depression, and Mood Scale (ADAMS) at week 12 compared to baseline.

ZYN002 also led to meaningful improvements in all measures of the Aberrant Behavior Checklist for Fragile X (ABC-FXS), which addresses the key symptoms of fragile X syndrome, including social avoidance, temper tantrums, repetitive movements, and hyperactivity.

“These open-label findings highlight both the short- and long-term positive impact of ZYN002 on emotional and behavioral symptoms experienced by children and adolescents with fragile X syndrome,” Donna Gutterman, PharmD, of Zynerba Pharmaceuticals, told Medscape Medical News.

The results of the FAB-C study were presented here at the American Psychiatric Association (APA) 2109 annual meeting.

Transdermal gel

Fragile X syndrome is a genetic condition caused by a mutation in the fragile X mental retardation 1 gene, located on the X chromosome. This mutation causes dysregulation of the endocannabinoid system, resulting in significant social, behavioral, and cognitive deficits.

“There is a logic to why CBD might work in kids with fragile X,” Gutterman said.

The FAB-C study evaluated the safety, tolerability, and efficacy of ZYN002, a permeation-enhanced, pharmaceutically produced CBD gel formulated for transdermal delivery. The study included 20 patients with fragile X syndrome. Most patients were male; the median age was 9 years (range, 6 to 17 years).

Treatment with ZYN002 was initiated at a dose of 50 mg daily. The dose could be titrated up to 250 mg daily during the first 6 weeks. The initial 6 weeks of therapy were followed by a maintenance dosing period, which lasted through week 12 and was followed by an extension period of up to 24 months.

The gel is rubbed on the upper arm and takes 30 to 45 seconds to dry. Eighteen of 20 patients completed the initial 6-week phase. Safety and efficacy were analyzed at week 12. Thirteen patients continued into the 24-month extension study. Only the 12-month results were reported at the APA meeting.

The study met the primary endpoint for change from baseline to week 12 in the total score of the ADAMS scale. That scale has been validated in patients with fragile X syndrome. The ADAMS score was 33.4 at baseline and 18.1 at week 12, an improvement of 45.8% (P < .0001), Gutterman reported.

The CBD gel also led to improvements in scores on the general anxiety, social avoidance, compulsive behavior, manic/hyperactive behavior, and depressed mood subscales of the ADAMS.

Treatment with the CBD gel also led to significant improvements in social avoidance, irritability, and social unresponsiveness/lethargy on the ABC-FXS.

ZYN002 was well tolerated. No serious adverse events were reported, and there were no clinically meaningful trends in vital signs, ECG results, or laboratory findings, including liver function test results. The most common treatment-emergent adverse events were mild to moderate gastroenteritis and upper respiratory infections.

A randomized, double-blind, placebo-controlled trial to extend these findings is currently enrolling patients in Australia, New Zealand, and the United States, Gutterman said.

Compelling mechanism

“This is an interesting study with promising results,” Alex Kolevzon, MD, professor of psychiatry and pediatrics and clinical director of the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai, New York City, told Medscape Medical News.

“CBD has a compelling mechanism with relevance to fragile X syndrome. While open-label studies must be interpreted with caution, these data support the need for larger, controlled studies,” said Kolevzon.


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Gut bacteria transplanted from autistic children cause autistic behavior in mice

Neuroscience News | May 30, 2019

Researchers transplanted fecal bacteria from autistic children, and neurotypical children. Mice who received the transplants from the autistic children began to exhibit autism-like behaviors, whereas the mice who received transplants from typically developing children did not.

Autism spectrum disorder (ASD) affects an estimated one in 59 people in the United States, causing a variety of difficulties with social communication and repetitive behavior. Many factors, including genetic and environmental effects, are believed to influence symptoms, and there are no approved treatments. Now, using mouse models, Caltech researchers have discovered that gut bacteria directly contribute to autism-like behaviors in mice.

The work was done primarily in the laboratory of Sarkis Mazmanian, Luis B. and Nelly Soux Professor of Microbiology and Heritage Medical Research Institute (HMRI) Investigator. A paper describing the research appears online in the journal Cell on May 30.

“In recent years, numerous studies have revealed differences in the bacterial composition of the gut microbiome between individuals with ASD and neurotypical subjects,” says Mazmanian. “However, while this previous research identifies potentially important associations, it is unable to resolve whether observed microbiome changes are a consequence of having ASD or if they contribute to symptoms.”

“Our study shows that the gut microbiota is sufficient to promote autism-like behaviors in mice. However, these findings do not indicate that the gut microbes cause autism,”
emphasizes Gil Sharon, senior postdoctoral scholar in the Mazmanian lab and the study’s first author. “Additional studies are needed to address the impact of gut bacteria in humans.”

The communities of microorganisms that inhabit the human gut are called the microbiota, and their collective genomes are known as the microbiome. These organisms live in a symbiotic state with humans. In exchange for a warm and nutrient-rich environment, bacteria help us digest food, affect metabolism, and educate our immune system.

To examine the microbiota’s role in autism-like behavior in mice, the team used “germ-free” mice–laboratory animals that are grown in the absence of microorganisms. Gut microorganisms from children with autism were transferred into these mice via fecal transplantation, and samples from people without autism were transplanted into other groups of animals.

The mice with microbiota from individuals with ASD exhibited autism-like behaviors, whereas the mice harboring microbiota from typically-developing individuals did not show these symptoms. Specifically, they spent less time socially interacting with other mice, vocalized less, and exhibited repetitive behaviors. These symptoms are analogous to behavioral characteristics of people with ASD.

In addition to the behavioral differences, mice colonized with human ASD microbiota also showed altered gene expression in their brains and differences in the types of metabolites present (metabolites are the molecules produced as byproducts of digestion and microbial metabolism). Two metabolites in particular were found in lower amounts in these mice: 5-aminovaleric acid (5AV) and taurine. ASD is sometimes characterized by an imbalance in the ratio of excitation and inhibition in the brain, so the researchers were intrigued by the lower amounts of 5AV and taurine, as both affect certain inhibitory neural receptors called GABA receptors.

“We were surprised to see how profound the effects were,” says Sharon.

The team then turned to mice that offer a different model of autism. This strain of mice, called BTBR mice, naturally exhibits autism-like behaviors. The researchers wanted to see if treating these mice with 5AV or taurine would reduce these behavioral symptoms. Notably, treated mice did indeed show decreases in autism-like behaviors. Further, brain examinations showed that 5AV, in particular, decreased neural excitability.

“There are many factors that make autism more complicated in humans than in mice. In mice, we can model the symptoms of the disorder but not reproduce it,” says Mazmanian. “However, this research provides clues into the role that the gut microbiota plays in neural changes that are associated with ASD. It suggests that ASD symptoms may one day be remedied with bacterial metabolites or a probiotic drug. Further, it opens the possibility that ASD, and perhaps other classical neurologic conditions, may be treated by therapies that target the gut rather than the brain, a seemingly more tractable approach.”


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

‘I understand exactly who he is’ : Moms discover they share autism with their children

by Isabela Dias | The Washington Post | June 11, 2019

Maria Mercado always knew she was different. Growing up in a boisterous Puerto Rican family in the Bronx, Mercado rarely spoke unless challenged or angry. To the outside world, she came across as a smart but shy girl, who learned to read at age 4 and couldn’t keep eye contact. For most of her school years, she had little trouble with academics — despite a severe stutter and constant daydreaming — but struggled in social settings.

Even into adulthood, Mercado sometimes had a hard time verbalizing her thoughts. “Can I say this?” she asked herself. Yet only she appeared to be aware of the problem. She just didn’t understand why.

The answer came in 2009 when Mercado was 28. Her son, Jackson, who was then 13 months old, began to regress in his development.

Abruptly, Jackson no longer seemed attuned to his surroundings. He stopped saying “mama” and “dada” and responding to his name when called. Five months later, following a 40-minute home interview with a psychologist and a speech therapist, Jackson was diagnosed with pervasive developmental disorders, now known as autism spectrum disorder.

At first, Mercado felt overwhelmed. But when she laid out flashcards and watched Jackson successfully match the words with the corresponding pictures, she knew “he was in there,” as she puts it, just the same as she had always been.

It isn’t uncommon for women with autism to receive a late diagnosis, or none at all. In the United States, autism is about four times more prevalent in boys than in girls — so much that, for decades, doctors didn’t even look for it in the latter.

Researchers now believe, however, that many girls have gone overlooked. Sometimes, they went on to be mothers of children with autism and, only then, did they find both the tools to navigate their own lives better and to care for their children in ways that perhaps no one else could.

After almost three decades without an explanation for her challenges growing up, Mercado didn’t need an official diagnosis to know that she was also on the spectrum. “It made me feel so much better that I can help him because I understand exactly who he is,” she said. “It’s not that I know him too well, it is that I know myself.”

When Jackson was young and couldn’t sleep, she turned him horizontally on the bed in the same way she had done herself on many restless nights. In a heartbreaking effort to get him to speak, Mercado would take away his toys and they sat together, crying, until Jackson made a sound.

“I knew that to get him to communicate I had to push him because that’s how I was able to break out of it,” she said. And because, like Jackson, Mercado is extremely sensitive to loud noises, she keeps headphones handy at all times for him to shut the world outside when it becomes too overwhelming.

The reason Mercado is so mindful of Jackson’s special needs is because hers were never addressed.

Gender differences in autism are little understood. But, in recent years, a growing body of research suggests that males and females exhibit their symptoms in different ways.

Girls tend to be better at masking their challenges with social interactions, for instance. And that they are obsessed with the color pink or collecting stuffed animals might not raise a flag about their development because these are expected from girls. Like Mercado, they are often labeled as introverted and their symptoms attributed to anxiety or attention-deficit/hyperactivity disorder.

“The way our culture thinks of autism is a 4-year-old boy who can’t talk,” said Julia Bascom, the executive director of the Autistic Self Advocacy Network. “So whoever doesn’t fit that picture is swept under the rug.”

When Jennifer Malia took her 2-year-old daughter to the family practitioner and to a developmental pediatrician for consultation, they wrote off the child’s communication issues as a language disorder. Her daughter wasn’t on the autism spectrum because she was able to keep eye contact, Malia was told.

But Malia wasn’t convinced. She had witnessed the 45-minute emotional meltdowns during which her daughter would go from angry to nonverbal. She knew it because she had experienced such episodes herself.

So after hours of research, Malia, an author and associate professor of English at Norfolk State University, concluded that she was also on the autism spectrum and, at 39, received a diagnosis on the same day as her daughter. A year later, her son was also diagnosed, following an evaluation with a clinical psychologist and formal testing.

“It was really frustrating because my daughter didn’t have the stereotypical autism traits,” Malia said. “If I hadn’t pushed for that, we would have never been diagnosed.”

That early detection allowed her daughter to undergo 35 to 40 hours of speech, occupational and behavioral therapy per week and, eventually, overcome her language delay.

“She’s still on the spectrum, but she has manageable challenges,” Malia said.

Missing that critical intervention may have lasting effects on women, including depression and anxiety caused by a persistent feeling of failure. But a diagnosis, even later in life, means being part of a community and having access to a much-needed support network. For some, it even means finding a mission.

Dena Gassner, 60, used to blame herself for forgetting to buy tickets for her daughter’s Halloween party or for her inability to manage daily chores, such as being on time for church every week or doing laundry. (“The way I describe it is: I can do what you’re doing but I’m wearing an 80 pound backpack,” Gassner said.)

Everything changed when her 4-year-old son, Patrick, was diagnosed — and that prompted her own discovery at 38. Gassner immersed herself in the autism community and started attending conferences and reading biographies by other women on the spectrum, such as Valerie Paradiz’s “Elijah’s Cup” and Liane Holliday Willey’s “Pretending to Be Normal.”

Following three decades of self-doubt and 15 different medications for clinical depression and bipolar disorder, she found her own way both as a parent and a professional — Gassner is a PhD candidate in social work at Adelphi University and a board member of The Arc, an organization serving people with intellectual and developmental disabilities.

“Getting my own diagnosis has helped me liberate from the social pressures and enabled me to help my son become his own personal best,” Gassner said. “The journey was necessary, and now I can look back and say ‘thank God,’ because his autism has resulted in me finding out my identity.”

Maria Mercado said she was terrified when she became a public advocate appointee to the Citywide Council on Special Education in February 2018. At school meetings, Jackson’s father, from whom she has separated, always introduced the family because she couldn’t bring herself to speak in public. So Mercado didn’t know how to address dozens of parents who had been advocating for years, some of whom were even in charge of their own nonprofit groups.

But confronting her fear, Mercado faced a crowd to say: “This is who I am. I didn’t just parent, I lived this life. I live in my head just like our children.”

When it was over, she went to the bathroom and cried.

“If I expect Jackson to push himself, then I have to do the same thing,” she said recently. “I can’t expect him to be the best if I’m not pushing myself to be the best.”

Because of Jackson, Mercado has learned a lot about herself and what she can do.

Today, besides being a full-time mother and an advocate, she’s also a filmmaker. Her first short documentary is called “Apple of My Tree,” about her relationship with Jackson and being on the spectrum together.

Even without an official diagnosis, Mercado finds comfort in the special connection she has with her son. In her living room, surrounded by portraits of Jackson and “Breakfast at Tiffany’s” and “I Love Lucy” books and vintage dolls, Mercado dwells on the same uncertainties as any other parent. She wishes she could guarantee Jackson’s future after she is gone. She wishes she could ensure his happiness and safety.

But it all goes away when she lies in bed with him at night and he looks at her and says: “Don’t worry, mommy.”


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Ketamine may hold potential as a treatment for autism, Tourette's

Health Europa | 10 Dec 2019 | Lancaster University | Dec 16 2019

To this day there is no known cure for either autism or Tourette’s syndrome, however, new research has revealed how a common anaesthetic could open up pathways to new treatments.

Lancaster University researchers have discovered, for the first time, how a genetic alteration that increases the risk of developing autism and Tourette’s impacts on the brain.

Based on the revelations, published in Cerebral Cortex, the researchers suggest that ketamine may hold the potential as a useful treatment for both autism and Tourette’s.

The researchers have shown how genetic deletion of a chromosome – known as chromosome 2p16.3 – can cause developmental delay and learning difficulties. They have also shown that people who have this deletion are around 15 times more likely to develop autism, and 20 times more likely to develop Tourette’s Syndrome.

Currently, the mechanisms involved are not completely understood.

Autism affects an estimated 2.8 million people in the UK while Tourette’s Syndrome affects an estimated 300,000 people in the UK. Recent research has shown that these disorders are genetically linked.

Treatments available for both disorders are limited, and new ones are urgently required.

Deletion of 2p16.3

Neuroscientists have shown that 2p16.3 deletion (Neurexin1) impacts on the function of brain regions involved in both conditions – this genetic deletion disrupts a brain area known as the thalamus, compromising its ability to communicate with other brain areas.

Lead researcher Dr Neil Dawson of Lancaster University said: “We currently have a very poor understanding of how the 2p16.3 deletion dramatically increases the risk of developing these disorders."

“However, we do know that the 2p16.3 deletion involves deletion of the Neurexin1 gene, a gene that makes a protein responsible for allowing neurons to communicate effectively.”

Ketamine as potential therapy

In the study the researchers found that the ability of the thalamic brain regions to communicate with other brain areas was impaired by the genetic deletion.

They tested the ability of a low dose of the drug ketamine, a drug used clinically at higher doses as an anaesthetic, to normalise the alterations in brain function induced by the genetic deletion.

“Intriguingly our data suggest that ketamine can restore some aspects of the brain dysfunction that results from 2p16.3 deletion and suggests that ketamine, or other related drugs, may be useful in treating some of the symptoms seen in autism and Tourette’s," said Dr Dawson.

“The brain circuits affected suggest that these drugs may be particularly useful for the cognitive and motor problems experienced by people with these disorders."

“Ketamine was shown to normalise activity in the thalamic regions found to be hyperactive as a result of the genetic deletion, and re-established the ability of these regions to communicate with other brain areas.”

This suggests that ketamine may be a useful treatment for people with 2p16.3 deletion or with autism and Tourette’s Syndrome, although more research is needed.

Dr Dawson continued: “While this data gives us important new information on the brain circuits affected by 2p16.3 deletion, and of the potential usefulness of ketamine to help people with autism and Tourette’s, much more research needs to be conducted to prove its clinical potential."

“The findings of this study give us important clues regarding the types of drugs that may be useful in the treatment of these disorders, and we are using this information to actively pursue the validation of these drugs for the potential treatment of these disorders.”

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mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

LSD as a therapeutic agent for autism

Treatment of children with autism in the 1960s included shock therapies and many different psychotropic drugs. The results were bad: there was no positive change in those children although the treatments were occasionally maintained for years. Under these circumstances, more powerful drugs were sought and a new substance was considered: LSD had been synthesized by the Swiss chemist Albert Hofmann in 1938 and five years later, in 1943, in an example of serendipity, he discovered its psychedelic properties. It was an enormously powerful substance and produced an unleashed imagination consisting of “fantastic images, extraordinary shapes and an intense set of colors, as if it were a kaleidoscope.”

Between 1959 and 1974 different groups used LSD in children with autism. A detailed study by Freedman and his group appeared in 1962. These researchers gave LSD to 12 children with autism, 10 children and 2 girls, ranging in age from 5 years and 11 months to 11 years and 10 months. They administered the drug orally, in varying doses (50, 100 or 200 μg) at the first hour, upon arrival at school. The study authors noted that the effects of LSD intoxication were patent from 15-30 minutes and lasted from 4 to 5 hours. Some children became flush and their pupils dilated, but neither pulse nor blood pressure showed much change. Other children seemed to be catatonic (strange postures, hands in fixed and strange positions, waxy flexibility of arms). No child ate lunch until the drug effects were over. Freedman’s description included references to greater physical contact, disappearance of mannerisms, and a development of what appeared to be new bodily sensations. Seeing what happened in adults, the authors hoped that LSD would promote some loquacity in nonverbal children but “the hoped for change from muteness to speech did not occur.”

Comparing their results with what was known about adults with schizophrenia – autism was then considered childhood schizophrenia -, and despite this rather positive description, the authors concluded “little hope for its [i.e., LSD’s] success in the treatment of children.” However, other authors were much more positive and, overall, reviewers concluded that the effects of LSD treatment were very promising and could even be considered excellent for the majority of children with autism.

New research began to make things clearer and to break those expectations. Different studies on children with autism saw no improvement in them. In addition, the vast majority of these studies, with our current criteria, which are much more demanding, left much to be desired. There were no controls, variables to be analyzed were not well defined nor were there any objective ways of evaluating possible improvements. The children were observed, without much estimation of their conditions and circumstances, and their reactions recorded in a narrative way. Observers knew that these children had received the medication – it was not a blind study – and no one was evaluating the reliability of their descriptions. Therefore, the data were purely qualitative, the descriptions were subjective, there were possible biases by the expectations of the observers and the reliability, accuracy and validity of such descriptions are unknown. In addition, some of these narratives are difficult to interpret. Neutral or negative results were often exposed in a more favorable light than they possibly deserved. For example, an increase in aggressiveness was described by Bender and her group as “an improvement in that it represented a contact with the environment that was previously ignored.” At present these studies would most likely not be approved for their completion and their results would not pass a peer review and would not be accepted for publication, but that is because science is improving day by day and fifty years have passed.

In those papers ethical issues regarding LSD use in children received barely a mention. Even statements concerning the procurement of parental consent were glaringly brief, or even absent, leaving the question open as to whether the parents of the children involved in those studies were even informed as to the effects of LSD.

In 1969 there were enough studies to publish a first review but the clinical picture of LSD was already severely damaged. The use as recreational drug had generated a very negative publicity and an important social alarm. The patent expired in 1963 and Sandoz ceased manufacturing in 1965, but although samples could still be obtained from the National Institutes of Mental Health (NIMH), bureaucratic barriers were important and the scope of the substance was notorious. The main reason given by researchers working with LSD in children with autism was sad: “all known forms of treatment have been tried unsuccessfully.” The truth is that evidence-based treatments simply did not exist. Pharmacological methods, shock therapies, and psychoanalytic strategies did not make any headway and behavior modification techniques were in their first steps. Today the situation is fortunately different: we have effective procedures for many of the deficits and excesses present in autism including problems of dreams, anxiety, depression or attention deficit. Behavior modification techniques are useful in many children and the best training of therapists and teachers makes clear and definite progress.

A recent paper by Bogenschutz and Ross 4 reviews what is known about the therapeutic uses of LSD. In addition to those studies on children with autism, it has been used in the treatment of alcoholism and other addictions, to relieve existential distress concerning death, particularly in the face of terminal cancer, and, with more limited evidence, to treat mood and anxiety disorders.

Contrary to what was observed for autism, the research that was conducted in the three decades after its discovery strongly suggests that LSD has some clinically relevant effects, particularly in the case of treatment of alcoholism. The studies that have been completed to date are not sufficient to establish efficacy, but the outcomes have been very encouraging, and larger trials are now underway or being planned. Nevertheless, the mechanisms of clinically relevant effects remain poorly understood and we have to remember previous mistakes, do not forget the lessons of those shameful studies and do our work under the highest quality standards.


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

A study led by University of Waterloo
researchers characterized how children
with ASD scan a person’s face differently
than a neuro-typical child.

New technique developed to detect autism in children

Neuroscience News | July 9, 2019

Researchers have developed a new technique to help doctors more quickly and accurately detect autism spectrum disorder (ASD) in children.

In a study led by the University of Waterloo, researchers characterized how children with ASD scan a person’s face differently than a neuro-typical child. Based on the findings, the researchers were able to develop a technique that considers how a child with ASD gaze transitions from one part of a person’s face to another.

According to the developers, the use of this technology makes the diagnostic process less stressful for the children and if combined with existing manual methods could help doctors better avoid a false positive autism diagnosis.

“Many people are suffering from autism, and we need early diagnosis especially in children,” said Mehrshad Sadria, a master’s student in Waterloo’s Department of Applied Mathematics. “The current approaches to determining if someone has autism are not really child-friendly. Our method allows for the diagnosis to be made more easily and with less possibility of mistakes.
The new technique can be used in all ASD diagnosis, but we believe it’s particularly effective for children.”

In developing the new technique, the researchers evaluated 17 children with ASD and 23 neuro-typical children. The mean chronological ages of the ASD and neuro-typical groups were 5.5 and 4.8, respectively.

Each participant was shown 44 photographs of faces on a 19-inch screen, integrated into an eye-tracking system. The infrared device interpreted and identified the locations on the stimuli at which each child was looking via emission and reflection of wave from the iris.

The images were separated into seven key areas of interest (AOIs) in which participants focussed their gaze: under the right eye, right eye, under the left eye, left eye, nose, mouth and other parts of the screen. The researchers wanted to know more than how much time the participants spent looking at each AOI, but also how they moved their eyes and scan the faces. To get that information, the researchers used four different concepts from network analysis to evaluate the varying degree of importance the children placed on the seven AOIs when exploring the facial features.

The first concept determined the number of other AOIs that the participant directly moves their eyes to and from a particular AOI. The second concept looked at how often a particular AOI is involved when the participant moves their eyes between two other AOIs as quickly as possible. The third concept is related to how quickly one can move their eyes from a particular AOI to other AOIs. The fourth concept measured the importance of an AOI, in the context of eye movement and face scanning, by the number of important AOIs that it shares direct transitions with.

Currently, the two most favored ways of assessing ASD involve a questionnaire or an evaluation from a psychologist.

“It is much easier for children to just look at something, like the animated face of a dog, than to fill out a questionnaire or be evaluated by a psychologist,” said Anita Layton, who supervises Sadria and is a professor of Applied Mathematics, Pharmacy, and Biology at Waterloo. “Also, the challenge many psychologists face is that sometimes behaviors deteriorate over time, so the child might not display signs of autism, but then a few years later, something starts showing up."


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Psilocybin and Aspergers – Life changing*


I usually don’t post to the internet, but this is just too important.

I set up this website as it may just help others in my position, and there really needs to be more research done on this subject.

I removed many aspects of autism and literally fixed my brain! I can now understand emotions & social interaction, eliminated depression, and now actually have a future.

The beginning

I’m a 20-something guy with Aspergers Syndrome. I can’t leave the house alone, I feel totally lost and freeze up in social situations, I often glitch and get stuck on my words when trying to talk, and I literally can’t function around unknown people or in busy places without help. My life kinda sucks.

However, I can fix and repair most computers, build complicated electronics projects, absorb an entire service manual in one reading, solve problems logically, and remember the layout of every building I’ve ever been in, but I can’t even answer the phone or go and buy my own food.

I’m intelligent enough to realize these issues which have basically ruined my life, and now I’ve had enough. There’s literally no reason why I cannot do these things except for my own mind getting in the way and worrying/over-thinking everything & causing so much stress.

Something had to change.

The backstory

2016 was a bad year for everyone, myself included. I had to move house (twice), had a difficult break-up from my first ever boyfriend, and ended a large project I’d run for almost a decade (all within a 2-month period). This was the lowest point of my life. I couldn’t possibly see how it could get better, and thought about just ending it then and there.

I did not.

Since 2016, I’ve been suffering from depression, lack of energy and sleep, and lack of motivation (on top of the autism), but I refuse to take any kinds of pharmaceuticals as they come with extensive lists of side-effects often worse than the very thing they’re supposed to help with.

All these issues are in the mind, and the mind is what has to fix them, not mask the symptoms with pills in the way that air fresheners mask bad odors, and especially not trying to hide from and ignore the issues for as long as I have done.

The Third Option

At this point, I was between a life stuck on anti-depressants, or death. I did not want either of these. I want a life where I look forward to waking up in the morning, not one where I waste my days on YouTube, alone, at a computer.

At the beginning of 2017 I discovered the existence of psychedelics (shows how little contact I have with the outside world..), and I quickly became obsessed with reading other people’s reports of using them, articles on psilocybin (Magic Mushrooms) & depression, and what little there is, on people with autism using things like mushrooms or LSD to reduce or totally erase the issues they’ve been facing all their lives. I decided I had to find out what it could do for me. I had nothing left to lose.

I first started by contacting The Psychedelic Society and applying for one of their Experience Weekends, but sadly I didn’t hear anything back from them for weeks.

I also got in contact with www.psilohuasca.com about their 1:1 ceremonies, but was sadly declined due to my condition.

I knew I couldn’t wait any longer, and decided I just had to do it myself.

So last week I went to Amsterdam.

I can’t even go out alone, yet I went to a foreign country to stay in a strange new place and eat some plants.

Trip #1. Testing testing.

One morning, I took a small ~8g dose of Psilocybe Atlantis truffles, made as a tea. What followed was one of the best experiences of my life.

I spent about 5 hours giggling (so much so that my face muscles started to ache in the end), and lecturing the camera about politics/life/YouTube/magnets/CRT monitors/or whatever else popped into my head at the time.

There were absolutely ZERO negative thoughts at all during the event. The constant over-thinking and feelings of being shit/broken/useless/inferior to other people were literally gone for about 4 hours (I even suggested going out to get some lunch, though never left the couch), and my assistant also noticed things that I did not, such as, for the first time in my life, I was able to look directly at another person, if only for a few seconds.

All too soon the effects wore off and I was back to how I was before, though now I had a plan.

This first test was only a small dose to see if psychedelics were something I could even stand. As it turns out, not only can I tolerate it (I actually really enjoyed it!), but it was one of the least stressful events of my life.

The future

I’m now planning more trips. First a 15g “medium” dose to compare, then I’m going all-out Heroic Dose to try and achieve the so-called “ego death”, which is, as far as I’ve been able to work out, where you literally lose connection with reality entirely and your brain kind of “reboots” so to speak.

The description of that alone appeals to me so much, it sounds like a more intense version of what the vacbed does, where most senses are removed. (EDIT: I was right!!)

I guess its like Marmite, you either love it or hate it. I have a theory that bad trips are caused by people trying to hold on to reality, which is why it can go so wrong for people who don’t like that idea of not being in control.

To me it just sounds like something I have to do. As to why? I guess I’ll find out.

…Three weeks later…

Trip #2. Medium dose.

This time with 15g of Atlantis truffles.

It came up a lot faster this time, within 15 minutes or so, and again started with giggles and laughter, which continued for most of the event. (I’d not laughed as much in my life!)

It didn’t *seem* too much more intense than the previous trip, though I did notice (and was told) the following:

- I was able to speak my mind a hell of lot easier (But some things I still got stuck on).

- I was able to make actual eye contact for the first time in my life, and for more than just a few seconds! – Though the ability to do so ended with the trip.

- All feelings of shittyness and depression were GONE for another 5 hours, though they did return later, as I knew they would.

- Everything felt amplified – I noticed some nice changes to sound/light/touch.

Some hours after the trip had ended; I was sitting on the couch with friends and had a sort of emotional overload. I got stuck on my words a lot and felt really fucking bad. This has happened at other times in my life exactly the same, nothing to do with the psilocybin, though I imagine that’s what bought it all up.

I was able to work through it and talk about the issues and problems, and it was another 100% positive experience overall.

Now comes the real work.

In the next trip I will attempt to achieve the ego death. 45g Hollandia, in the dark, with no distractions. That should do it.

I fully expect this to not be in any way pleasant, but the only way to get past these issues is to face them and to fucking destroy them.

I just hope that my brain isn’t of the type that psilocybin just won’t help (EDIT: It wasn’t!). I have much more testing to do but so far its been the best thing I’ve ever done.

Time will tell.

…One week later…

Trip #3. Heroic Dose.

Time to get some real work done.

I made a tea of 45g of Hollandia truffles (supposedly stronger than Atlantis ones I had last time), and sat down on the couch ready to drink it.

Something physically blocked me. I could barely move the cup to my mouth, it was like something inside was preventing me from doing it, the same exact thing that blocks my words and makes me freeze up in social situations.

I managed to override it, and with huge effort drank the foul tea. I then sat back and waited.

Nothing much happened for a while. Open-eye visuals (EDIT: I’ve had almost no closed-eye visuals, at any dose), but nothing very “big”, considering the amount I took.

After some time though, I noticed that all logical thought, the constant thought process, and all stress and worry were entirely gone. In fact even looking up words from long-term memory was hard to do, and at some point I couldn’t tell the difference between reality and memory. None of this bothered me though; it was all kind of nice.

I still don’t think I experienced “ego loss” or anything like reality/sense of self ceasing to exist, but what happened was better than I could ever have imagined:

It started as I was listening to the Chicken Run soundtrack at about ~120 mins into the trip.

Then something strange began to happen.

I started to literally feel the music instead of just hearing it. Like, I could detect the emotion behind it all.

This has never happened before and was a totally new thing for me. Usually music either has a good tune or it doesn’t..

When the soundtrack ended, another song, Warning Call by CHVRCHES came on and I felt more emotion than I’ve ever felt before in my life.

I was almost overloaded. I tried to tell my assistant but was getting stuck on words and getting quite stressed. They noticed and came over and sat down on the couch beside me.

The moment they did this, my internal brain filter that’s always running literally shut itself down, and seconds later more than a decade’s worth of emotions, troubles, hidden feelings, and bullshit all came out at once.

The next few hours were very intense, impossible to describe, emotional, but in no way bad. It was a huge release of everything. The entire trip was more “feeling” than “thinking”. No giggly funny times here.

I felt a huge amount of a feeling I’ve never had before. It was a sort of warm, nice, comforting feeling, like how I imagine cats must feel when in someone’s lap.

The closest I can describe it to is like laying in bed next to a boyfriend while he strokes my hair sort of thing.

Over the next 2 hours, with its help, and only with its help, was I able to talk through everything that had been stuck in my head for so long, and many more things that were totally new to me.

I know I wouldn’t have been able to do all this without the mushrooms help, even if logic was turned off by any other means. I needed that feeling more than I can ever explain in words.

After everything had been said (The trip had been about ~4 hours), I felt it slowly begin to leave me, and tried to sit up on the couch – it was about 1AM.

I drank some milk, and then stood up. I was covered in sweat, tears, and blocked nose, but I felt SO MUCH more energy at that point than ever I’d felt for years.

So then we went out to get some chips! Sadly everywhere was closed and we ended up coming back home, eating a huge bowl of mash potato, and talking about the trip and my life in huge detail until about 5:30AM. Many things were worked out during this time. Talking before & after the trip is essential!

The next day I woke up very early (without an alarm) even though I only got about ~4 hours sleep, yet I still had tons of energy throughout the day!

Then we went to a pub for lunch. That alone would have been literally impossible prior to this.

The following things have changed in the 1 week since the trip:

- I can now do natural non-forced eye contact with anyone
- I now know more than ever before what I’m looking for in a relationship, my specific role in the relationship, and why previous ones had all failed.
- I don’t glitch or get stuck on my words nearly as much – And don’t care when it happens!
- Stress and worry are greatly reduced – I was even able to use the phone today without help!
- I called the waiter over and asked for a 2nd portion of chips!
- I could also talk to the barman and dynamically generate conversation about the food and payment, without freezing, or even feeling shit or that I might fuck it up!
- And didn’t mind waiting for others to finish their meal before we went home
- The constant headache I’ve had since 2016 has finally GONE!
- And I can sleep quite a bit better, I’m waking up at ~9:00AM even without an alarm
- Today I went into a shop alone to speak with the manager (an old friend) – Usually I need help with this sort of social event
- A few days later I walked into another store to post a parcel, buy a chocolate bar, and not give a shit!
- Oh and I talked to about 6 people at once at a friend’s company
- Tonight I looked at myself in the mirror and, for the first time ever, didn’t hate what I saw.

I just can’t get over how positively I’ve changed in only a few days; I only hope it stays this way! I’ll definitely be exploring my mind further in future trips, to find out what other abilities remain locked and unknown to me. I think the term is Psychonaut.

The mushrooms have helped me more in 8 hours than anything else in my whole life ever has.

They showed me that I could do social skills, and how to understand emotions for the first time.

The ability was there all along, I just needed to see it. By shutting out the logical mind and its constant chatter and endless worrying, the real emotional side of my brain was able to take control for the first time.

There NEEDS TO BE more research on the subject of psychedelics and autism. If they helped me so much, I know they can help others too.

*From the article here:


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

One therapy bests others at motivating kids with autism to speak, study finds

by Stanford University Medical Center

Pivotal Response Treatment involving parents works better than other existing therapies at motivating children with autism and significant speech delays to talk, according to the results of a large study by researchers at the Stanford University School of Medicine.

Because children with autism are less socially motivated than typically developing children, parents' instincts about how to engage them often don't succeed, said Grace Gengoux, Ph.D., clinical associate professor of psychiatry and behavioral sciences. PRT gives parents a way to breach this barrier.

"We were teaching parents how to set up situations where their child would be motivated to communicate," Gengoux said. "The results of our study are exciting because we found that children in the PRT group improved not just in their communication skills, but also in their broader social abilities."

Heidi Pim of Palo Alto, California, participated in the study with her son, James, who was diagnosed as a toddler with autism and speech delays.

"I was really worried and anxious about not knowing if he would ever be able to talk," Pim said. She was impressed by the changes she saw in James, who was 3 at the time of the study. "I feel so grateful now to see how many words and phrases he knows," she said. "He's able to speak clearly and socialize as well, to go up to people and ask them questions."

A paper describing the study will be published online Aug. 5 in Pediatrics. Gengoux is the lead author. The senior author is Antonio Hardan, MD, professor of psychiatry and behavioral sciences.

Six-month study

The six-month study enrolled 48 children who were 2 to 5 years old and had autism and significant language delays. Half the children received PRT treatment from therapists and their parents, while the remaining children continued to receive whatever autism treatments they had been getting before the study began, which included other types of applied behavior analysis and conventional speech therapy.

For the first 12 weeks of the study, children in the PRT group underwent 10 hours per week of PRT from a trained therapist, and their parents received training for one hour per week in how to use the treatment's techniques during everyday interactions with their children. For the second 12 weeks of the study, children in the PRT group received five hours per week of therapist treatment, and their parents had monthly instruction sessions.

In PRT, the therapist or parent notes what the child is interested in, and uses the object to encourage speech. For example, if James wanted a toy car, Pim, his mother, learned to pick up the car, hold it where he could see it and encourage him to say "car." When he tried to say the word, he was rewarded with the toy.

At first, James learned single words. He then progressed to phrases such as "green car" and "ready, set, go." Pim also used PRT to help James learn to express his needs, such as by saying "bottle" if he was thirsty.

"He used to not be able to point to something or ask," Pim said. "PRT really improved his vocabulary skills and communication back and forth. It helped us understand what he needs and wants."

As the trial progressed, Pim also saw James' frustration levels decrease. "Before, he didn't know how to express his feelings," she said. "When I would leave for the day and come back, he didn't know how to say 'Mommy, I missed you,' so instead he would hit me or cry. That has lessened."

Today, James, now 8, is a happy kid who attends school in a mainstream classroom and enjoys playing with his twin sister, Jessica. Pim still uses PRT techniques to engage James in conversation on his favorite topics, such as elevators.

Speaking more

At the end of the study, the children in the PRT group spoke more than those in the comparison group, and were using common words that could be recognized by others, an important marker of progress given that many children spoke unintelligibly at the start of the trial. The children in the PRT group also showed greater improvement in a measure of their overall social communication, which is critical for an optimal long-term outcome, the researchers reported.

They also found that children who began with lower developmental abilities benefited more from the intervention, a surprising finding since many autism therapies are of greater benefit to higher-functioning children.

"It's discouraging for parents of lower-functioning kids if we tell them that higher-functioning kids do better, because higher-functioning kids are already doing better," Gengoux said. "The new findings suggest that parents can play an especially valuable role in assisting children who have the greatest needs," she said, adding, "This provides a lot of hope."

Stanford researchers believe that findings from this trial are promising but that they need to be replicated in larger investigations. They are also currently recruiting young children with autism for a new study of how the brain changes in PRT. Interested parents can call (650) 736-1235 or e-mail [email protected] for more information.

Parents and teachers who want to learn PRT techniques can attend a one-day conference being held at Stanford in September. More information about the conference is available at http://med.stanford.edu/autismcenter.html.


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

80% of autistic children treated with CBD saw improvement

Israeli researchers have found compelling evidence that medical cannabis is an effective therapy for children on the autism spectrum. In this soon-to-be-published study in the journal Neurology, researchers treated autistic children with high concentrations of CBD, a non-intoxicating cannabinoid found in the cannabis plant.

Conditions in 80% of the children improved. Alternatively, the children had not shown improvement with conventional drug therapies.

The study was led by the director of pediatric neurology at Jerusalem’s Shaare Zedek Hospital, Dr. Adi Aran, who treated the 60 children with a high-CBD cannabis oil (20% CBD and 1% THC). The children were treated for at least seven months with the oil.

After the treatment period, parents answered assessment questionnaires to characterize their child’s condition. Questions were asked about behavioral changes, anxiety levels and ability to communicate.

Here’s what they reported:

- 80% of parents noted a decrease in problematic behaviors, with 62% reporting significant improvements.
- Half of the children had improved communication.
- 40% reported significant decreases in anxiety. (Note: one-third of the study participants began the study with no anxiety.)

Just as Israel is a pioneer in medical cannabis research, Aran is a pioneer in cannabinoid therapy for autism. Aran originally began a 2017 project to test 120 autistic children. It was the first study of its kind worldwide, and was made possible by the Israeli government’s funding and progressive approach to cannabis research.

Aran said that when word of the study got out, his waiting lists were soon full with many families from all over Israel who wanted to participate.

Autism spectrum disorders are neurodevelopmental in nature, usually appearing in infancy or early childhood and lasting a lifetime. More severe cases have debilitating symptoms including compulsive, repetitive behaviors and impaired social skills and communication. Some children cannot speak at all. Autism affects around 1% of people worldwide.

The causes of autism are not understood and there is no cure—and the prevalence is climbing. In April 2018, the CDC updated its autism prevalence estimates to 1 in 59 children, up from 1 in 166 children in 2004. Doctors traditionally treat symptoms with antipsychotic medications, which have harmful side effects. Some children do not respond to these medications.

Aran began small autism research studies after similar cannabis studies on epilepsy, a disease that affects about 20% of autistic children. While studying epilepsy, researchers discovered that certain cannabis compounds would likely also help some autism symptoms. Less than 2% of the general population has epilepsy, but up to 33% of people with autism also suffer from epilepsy.

Neuroscientist Dr. Thomas Deuel of the Swedish Hospital in Seattle says there is definitely a connection. While scientists do not clearly understand the reasons behind the relationship, they suspect that the different brain development that occurs in autistic children is more likely to create circuits that cause epileptic seizures.

That link has caused many parents to seek out cannabis treatments for their autistic children. Parents certainly have anecdotal evidence of the effectiveness of CBD oils on their autistic children, but mainstream medicine has remained skeptical due to the lack of data. With most conditions treated with cannabis, anecdotal evidence and personal experience far outweigh actual peer-reviewed scientific research.

Now, New York University (NYU) neurologist Dr. Orrin Devinsky, the same scientist who did research on Epidiolex, is now conducting two studies on CBD effects on children aged 5 to 18 with moderate to severe autism. The only other doctor who is currently doing studies like this is Aran.

Since autism and epilepsy go hand in hand, CBD is showing promise for treating both conditions.

Perhaps as doctors begin to see the effects of Epidiolex, and review research like that of Aran’s and Devinsky’s autism studies, many more will begin to delve further into use of medical cannabis.


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

Wearable device can predict aggressive outbursts in people with autism a minute in advance

Neuroscience News | Aug 27 2019

What would you do if you could predict the future a minute in advance? That might not seem like a long time, but for caretakers of people with autism, knowing what will happen 60 seconds from now could be enough time to prevent an aggressive outburst.

To alert caretakers when stress levels are nearing the point of an aggressive episode, Northeastern behavioral scientist Matthew Goodwin has created a wearable wrist device for people with autism that monitors physiological indicators of stress.

People with autism are prone to aggressive outbursts because their resting levels of stress are much higher than someone without autism. “Their arousal levels are already at the ceiling,” says Goodwin, an associate professor with joint appointments in Bouvé College of Health Sciences and the Khoury College of Computer and Sciences. “It takes very little to cross the tipping point.”

On top of that, it’s often difficult, if not impossible, for people with autism to communicate what’s distressing them. This makes it especially hard for caretakers to act preemptively, which is why an automatic warning signal such as Goodwin’s would be helpful, even if it’s only a 60-second head start.

“If we could give caregivers advance notice, it would prevent them from getting caught off guard and potentially allow them to relax the individual and make sure everyone in the environment is safe,” Goodwin says.

During a study, Goodwin and his team of researchers observed 20 children with autism who have aggressive episodes. Over the course of 87 hours, they tracked each episode and the corresponding physiological changes.

That information was then synchronized with a clock in the biosensors the children wore. This allowed researchers to match each aggressive episode with the bodily changes that occurred before, during, and after.

The device monitors heart rate, sweat production, skin surface temperature, and arm movements. The image is adapted from the Northeastern news release.

Based on these 20 samples, Goodwin can predict an aggressive outburst a minute in advance with 84 percent accuracy.

“But those aren’t magic numbers. Those are just limitations of our data set,” Goodwin says. “As our data set grows and we use more sophisticated machine learning models, I think we might get more than 60 seconds.”

With the help of funding from the Department of Defense, the Simons Foundation and the Nancy Lurie Marks Family Foundation, Goodwin will expand his sample size to 240 individuals with autism who behave aggressively.

“Families with children who act aggressively tell us that they don’t know what causes these outbursts, and they’re fearful it could happen anytime, so they self-impose house arrest,” Goodwin says. “They don’t go to the movies. They don’t go to the grocery store with their kids. They don’t go to parks.”

Goodwin hopes to eliminate these fears by providing some clarity of the future. “Some parents say that even if we can only give them 60 percent accuracy, that’s better than chance, which is what they’ve got now,” Goodwin says. “They say that would be priceless.”


mr peabody

Moderator: PM
Staff member
Aug 31, 2016
Frostbite Falls, MN

High levels of estrogen in the womb linked to autism

University of Cambridge | Jul 29 2019

Scientists have identified a link between exposure to high levels of oestrogen sex hormones in the womb and the likelihood of developing autism. The findings are published today in the journal Molecular Psychiatry.

The discovery adds further evidence to support the prenatal sex steroid theory of autism first proposed 20 years ago.

In 2015, a team of scientists at the University of Cambridge and the State Serum Institute in Denmark measured the levels of four prenatal steroid hormones, including two known as androgens, in the amniotic fluid in the womb and discovered that they were higher in male foetuses who later developed autism. These androgens are produced in higher quantities in male than in female foetuses on average, so might also explain why autism occurs more often in boys. They are also known to masculinise parts of the brain, and to have effects on the number of connections between brain cells.

Today, the same scientists have built on their previous findings by testing the amniotic fluid samples from the same 98 individuals sampled from the Danish Biobank, which has collected amniotic samples from over 100,000 pregnancies, but this time looking at another set of prenatal sex steroid hormones called oestrogens. This is an important next step because some of the hormones previously studied are directly converted into oestrogens.

All four oestrogens were significantly elevated, on average, in the 98 foetuses who later developed autism, compared to the 177 foetuses who did not. High levels of prenatal oestrogens were even more predictive of likelihood of autism than were high levels of prenatal androgens (such as testosterone). Contrary to popular belief that associates oestrogens with feminisation, prenatal oestrogens have effects on brain growth and also masculinise the brain in many mammals.

Professor Simon Baron-Cohen, Director of the Autism Research Centre at the University of Cambridge, who led this study and who first proposed the prenatal sex steroid theory of autism, said: "This new finding supports the idea that increased prenatal sex steroid hormones are one of the potential causes for the condition. Genetics is well established as another, and these hormones likely interact with genetic factors to affect the developing foetal brain."

Alex Tsompanidis, a Ph.D. student in Cambridge who worked on the study, said: "These elevated hormones could be coming from the mother, the baby or the placenta. Our next step should be to study all these possible sources and how they interact during pregnancy."

Dr. Alexa Pohl, part of the Cambridge team, said: "This finding is exciting because the role of oestrogens in autism has hardly been studied, and we hope that we can learn more about how they contribute to foetal brain development in further experiments. We still need to see whether the same result holds true in autistic females."

However, the team cautioned that these findings cannot and should not be used to screen for autism. "We are interested in understanding autism, not preventing it," added Professor Baron- Cohen.

Dr. Arieh Cohen, the biochemist on the team, based at the State Serum Institute in Copenhagen, said: "This is a terrific example of how a unique biobank set up 40 years ago is still reaping scientific fruit today in unimagined ways, through international collaboration."

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mr peabody

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Aug 31, 2016
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Pilot study finds MDMA-assisted psychotherapy significantly reduces social anxiety in autistic adults

Experiencing repeated social rejection and abuse from family and friends is a difficult part of childhood for many people, but it’s especially traumatic (and common) for children on the autism spectrum. Many of these children later develop into adults who suffer from diagnosed conditions like anxiety, post-traumatic stress disorder (PTSD), and depression, in addition to enduring challenges with interpersonal connection and social adaptability.

Conventional medications have been mostly ineffective at treating stress-related issues among the autistic population, and traditional psychotherapy is largely unsuccessful because it is typically difficult for people with autism to develop rapport with therapists. Due to these issues, effectively reducing stress for those with autism has remained a lofty goal that so far hasn’t borne many practical solutions—until now.

A new study published earlier this month in Psychopharmacology explored whether psychotherapy combined with MDMA (the primary ingredient in the street drug known as “ecstasy”) was safe and effective at treating social anxiety in autistic adults.

Rather than attempt to treat autism itself, the study aimed to find out whether the treatment method was able to relieve symptoms (such as social fear and avoidance) that contribute to the sociability and quality of life that this population commonly experiences.

The Phase 2 pilot study, sponsored by the Multidisciplinary Association for Psychedelic Studies (MAPS), marks the first time clinical research has ever been conducted on treating autistic adults with MDMA—or any other psychedelic substance, for that matter.

Giving ecstasy to adults with autism in an attempt to address their social anxiety may sound a bit foolish to some—perhaps even dangerously reckless. However, other studies have found MDMA to be effective in treating other anxiety disorders and the researchers took measures to ensure the safety of all participants.

Prior to designing the study, interviews were conducted and survey data was collected from autistic adults about their experiences with using MDMA in non-medical settings. This data showed that a majority of survey participants reported experiencing an ease of communication and heightened feelings of empathy and connectedness, both during their (unsupervised) MDMA sessions and after.

That’s because MDMA is capable of engendering benefits such as increased feelings of well-being and cultivating qualities like interpersonal trust and empathy, while also decreasing feelings of fear. So even if people use MDMA outside of the medical model, it’s possible to experience lasting benefits from safe experimentation. This assumes that they are employing tried-and-true harm reduction techniques like drug checking, avoiding dangerous drug combinations, and accurately weighing their doses, of course.

By taking part in this innovative scientific study, these autistic adults did imbibe MDMA within the modern psychedelic therapy framework.

Study Design

The randomized, placebo-controlled, double-blind single-site study occurred over the course of nearly three years—from February 2014 through April 2017. Twelve autistic adults with marked to very severe social anxiety were recruited through Internet advertisements, word of mouth, and clinician referrals. All participants were required to be 21 or older, MDMA-naive (by self-report), physically healthy, and psychologically stable.

After three 60- to 90-minute non-drug preparatory psychotherapy sessions, participants underwent two eight-hour experimental sessions, receiving either MDMA or the placebo (lactose). These experimental sessions were spaced roughly one month apart.

Eight participants received MDMA, and the remaining four participants received the placebo. As this was a double-blind study, neither the participants nor the researchers knew whether the dose was active or placebo until the blind was broken during a six-month follow-up session. Surprisingly (compared to other psychedelic research studies), it was not always apparent (to both the participants and the researchers) whether MDMA or the placebo was administered.

Following each experimental session, the volunteers participated in three additional 60- to 90-minute non-drug integrative psychotherapy sessions over the course of three weeks. Each session included mindfulness-based therapeutic techniques, which have been previously found to be useful for autistic adults and other populations experiencing issues with emotional regulation, relationships, and tolerance of distress.

This study design was similar to the methods used in researching MDMA-assisted psychotherapy for the treatment of PTSD in otherwise healthy adults, but it employed a few variations that were intended to meet the needs of the autistic population. The first four participants received MDMA in the initial session at a dose lower (75mg) than the typical full dose in PTSD trials (100-125mg), and after verifying that there weren’t any issues with the 75mg dose, the dose was increased to 100-125mg for the rest of the sessions and participants.

Also different from the MDMA-assisted psychotherapy PTSD studies, this study’s participants were not required to stay overnight in the clinic after the experimental MDMA sessions. Instead, they left with a trusted “Study Support Partner” who remained with them at home. This protocol change was made to best accommodate the needs of the autistic adults, who may have experienced elevated anxiety from staying in a clinical setting overnight.

Participants who received the placebo during the study were eligible to return for two optimal open-label treatment sessions with MDMA. Data for those additional experimental sessions were not included in the published study results.

The Results

Data from the study showed that not only is clinically-administered MDMA safe and well-tolerated in adults on the autism spectrum—there were also considerable improvements in social anxiety and improved sociability for the group that received MDMA.

Several participants and Study Support Partners described accounts of improved interpersonal interactions with family members, and some participants reported benefits like being able to start dating for the first time and becoming more comfortable with exploring and expressing gender identity.

The improvements were significantly greater for the MDMA group compared to the placebo group. More importantly, six months after the study’s conclusion, these therapeutic effects were still holding strong—social anxiety remained the same or continued to improve slightly for those participants who received MDMA.


Although the sample size was limited, this Phase 2 pilot study still provided more evidence supporting the idea that MDMA is capable of treating anxiety-related issues. As the first study to administer a psychedelic-related compound to the autistic population, this is truly groundbreaking research.

Due to the current legality surrounding substances like MDMA and other psychedelics, MDMA-assisted psychotherapy is not legally available to the vast majority of people who really need it. Until the laws shift, it can be helpful to research ways to access psychedelic therapy without using illegal substances. And experimenting with mindfulness techniques like meditation, yoga, and breathwork can be extremely beneficial at addressing anxiety symptoms.

Through psychedelic research studies like this one, we continue to learn more about how psychedelic substances can improve our mental health. This revolutionary research goes a long way toward finding treatments that can help the autistic population live easier, more enjoyable lives.


mr peabody

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Aug 31, 2016
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I have autism (+ depression/anxiety). I have tried psychedelics, and I definitely think something about them helps people with autism.

More and more people seem to be sharing stuff about this online. A couple years ago there were few personal anecdotes about this when I was searching for it (e.g. googling autism+psilocybin/psychedelics), but now there's tons.

Personal effects (not necessarily all from "treating" autism, but these are definitely different than what most people experience)
  • Intuitively understand body language, way more capable of empathy. Normally empathy is a logical process, mushrooms make it emotional.
  • Verbal fluency increases dramatically, to the point where others notice that I'm suddenly better at talking about things
  • Improved memory (recalling things I know, specifically)
  • More appreciation/love for people I care about
  • Drastically improved coordination. Improve a ton at things like slackline, darts, etc. Also my handwriting goes from sort of sloppy to being pretty nice.
  • Improved energy
  • Improved sleep
  • Drastically improved anxiety. Being truly calm from psychedelics made me realize just how absurd my anxiety levels normally are.
  • They make me feel standard "happy" emotions where not much else has. Normally am either blank or annoyed or excited, but happy and sad occur very rarely. I feel both on mushrooms.
For me, mushrooms are the only psychedelic that does this. Have also tried LSD. I have another friend with autism who says that psychedelics are the only time she feels regular emotions. For her, both mushrooms and LSD have this effect.

I've tried to recreate the effect with 20+ nootropics, ADHD meds, and antidepressants/benzos, but nothing else has a similar effect for me at all. (microdosing .3-.5g 1-3x/day)


mr peabody

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Aug 31, 2016
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My autism journey: how I learned to stop trying to fit in

by Eloise Stark | AEON | Oct 4 2019

My name is Eloise and I am many things at once: I am a graduate student at the University of Oxford; I am a tutor, a rower, a feminist, a granddaughter, a daughter, a sister, a stepsister, a friend. I am also autistic.

I was diagnosed several years ago, aged 27. But, looking back, the signs were always there. I have always harboured intense ‘special interests’ that form something between a passion and an obsession. For instance, as a child, I was obsessed with collecting Barbie dolls, not to play with, but to create the ‘perfect’ Barbie doll home, complete with furniture made from cardboard cereal boxes and copious amounts of glue and glitter. Most neurotypical people have favourite interests, but theirs are more akin to hobbies, which they can put on hold if life is busy. For autistic individuals such as me, the opposite is true. We often need these special interests to stay sane in a world that can be so bafflingly complex – such interests can provide predictability, focus and great reward.

My interest in plastic people has since morphed into a deep fascination with understanding real people. Today I feel fortunate to study psychology as part of my PhD. Another of my special interests is literary fiction. Since I was small, I’ve read voraciously. What I found most enticing about literature was the possibility of learning social rules, expectations, how to cope with challenges and much more, all from the comfort of my armchair without the risk of saying the wrong thing or making a mistake. Again, this is typical for many autistic people, particularly women but also many men, who learn about the social world explicitly through pursuits such as literature, but also soap operas, films and closely watching significant others. We then use what we have learnt in social situations, to ‘camouflage’ our lack of social instinct, and behave according to the social rules of the specific situation.

Unfortunately, immersing myself in literature did not equip me with all the understanding and skills I needed to cope with the complex social rules of teenage life. When I turned 13 and moved to senior school, that’s when things went wrong for me. I didn’t understand the social rules in the enormous concrete monolith that became my hell, and I began to be badly bullied. For instance, a girl once spat at me in the corridor, at which point I informed her that spitting on someone is considered an offence of common assault under the Criminal Justice Act. This prompted a lot of laughter from the girl and her friends, only escalating the situation. I thought it would deter them at the time, but looking back I didn’t understand how to ‘keep my head down’ and stay out of harm’s way.

The bullying left me highly anxious, constantly feeling as if the bullies were about to burst out of my wardrobe. I wouldn’t go out in public if I could help it, and nightmares plagued my sleep.

The American author Paul Collins, whose son is autistic, wrote in Not Even Wrong: Adventures in Autism (2004) that: ‘Autists are the ultimate square pegs, and the problem with pounding a square peg into a round hole is not that the hammering is hard work. It’s that you’re destroying the peg.’ I can say from my own experience that the social pressure of growing up can be a toxic environment for us autists as we are forced to conform to the norms or stand out and risk bullying and trauma.

With hindsight, the next warning sign that I was autistic was my first experience of university, at a place I’d like to forget, to study English literature. I arrived with a car-full of books, and was shocked at the person who parked next to us unloading crates of alcohol. I struggled immensely with the social side of university including the loud bars and clubs, which assaulted my senses and left my ears ringing for days afterwards. I left after two terms.

Fast-forward a few years and I tried again, this time to study experimental psychology at Oxford. It was glorious to feel intellectually stimulated by the subject of the human mind, and I could work passionately for all hours and avoid the clubbing and the more socially overwhelming aspects of university without anyone thinking it strange. I had found my intellectual niche: I could pursue my special interest – people – and I even found a new special interest in rowing. The neurotypical world can be jarring, but I learnt at Oxford that autistic people, like orchids, can flourish in an environment that suits us. For instance, I know of a successful autistic man who loves boardgames, and he works in a boardgame café. I would like to believe that there is a niche out there for every autistic individual, even if it might require a little understanding from others and some adjustments such as removing bright lights to reduce sensory overload.

At this stage, my mental health was the best it had been for a long time. However, bad things can happen unexpectedly. I was walking across Magdalen Bridge in Oxford with my good friend Tess in 2012. We were carefree, chatting about our gap year together and enjoying the sunshine. A man walking past us suddenly jumped on me with his hands around my neck and tried to strangle me. I struggled, and eventually got away. I thought how bizarre it was that this awful thing had happened, and yet I still found myself conscious and breathing. Nothing had changed, but everything had changed too.

Following the attack, I developed a recurrence of mental-health problems from my youth. I grew more and more unwell. I was anxious, obsessive, depressed, and began to have suicidal feelings. I was overwhelmed by the world, by just being, and didn’t know how to cope with it.

I poured my limited mental energy into my academic studies to hide my growing unhappiness, and I won a competitive scholarship to begin a PhD at Oxford. But I still felt ‘different’ and had never truly dealt with my mental-health problems. The stress mounted. In one desperate moment, I went online and bought every self-help book I could find. I spent a week huddled in my room trying to cure myself through education. When the realisation hit me that this was unlikely, I reached rock-bottom. I was admitted to hospital, yet every clinician disagreed on my diagnosis. Most remarked that they felt they were ‘missing something’.

Eventually, I had an appointment with a top psychiatrist in Oxfordshire. I spent three hours with him talking in depth about my life, my mental health and my feelings of being different. After this mammoth session, he turned to me and said: ‘Eloise, I believe that you are autistic.’ He informed me that female autism is more difficult to detect because we tend to be better at ‘camouflaging’ our social difficulties. At the same time, he explained how the pressure of relentlessly trying to fit in can have an understandable toll on our mental health.

Receiving this diagnosis was a huge relief. Finally, someone was sure about something – to an extent, I didn’t care what it was, I just wanted an answer. Now I had an explanation for why I had always felt different.

Being me, I gathered every book I could find on autism in women, and read them all. I went to conferences about autism and autism in women, and I spoke to experts. I wrote about my experiences, I spoke to friends and family. I used my love of learning to learn to love myself.

I eventually returned to studying for my PhD. I love my studies and it has probably become one of my special interests. I look forward to every single day spent in the lab, whether I’m analysing neuroimaging data or writing academic papers. Eventually, I began to apply my critical mind to the question of autism. You could say that it has become one of my special interests. I mused upon my own situation with the goal of helping others like me too. I can’t rewind the past and make up for all of the bad experiences I have had. But I can use them to help me to help others. Autism fascinates me for its scientific conundrums, but also because I’ve lived it and I know how it feels.

Early on, I felt a huge resistance to being different. But I’ve grown to realise that it’s not about being different for the sake of being different, it’s about being the most authentic version of yourself, particularly in relationships, because sharing and expressing one’s true self with others can increase openness, sincerity and trust. I think a large part of my journey has been to accept myself the way I am and to stop trying desperately to ‘fit in’. I am who I am, I’m autistic and proud, I’m different, and for the first time in my life, I’m okay with that.

Eloise Stark is a DPhil student in psychiatry at the University of Oxford. She blogs for Student Minds and The Mental Elf, and writes for The Psychologist.

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mr peabody

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Aug 31, 2016
Frostbite Falls, MN

Possible link between autism and the use of antidepressants during pregnancy*

Neuroscience News | Apr 30 2019

A new study in mice reveals a possible link between the use of SSRI antidepressants during pregnancy and an increased risk of autism-like symptoms in offspring. Offspring exposed to fluoxetine (Prozac) in utero were more likely to exhibit impaired neurotransmission caused by an overactive serotonin receptor in the prefrontal cortex, an area of the brain implicated in modulating social behaviors. However, treating the mice with a compound that blocks the receptor alleviated the behavioral problems and improved working memory.

An international team led by Duke-NUS Medical School has found a potential link between autistic-like behaviour in adult mice and exposure to a common antidepressant in the womb. They also identified a treatment that helped improve memory loss and social interactions, according to the new study published in the journal Molecular Brain.

Antidepressants are commonly prescribed for treating major depression and post-traumatic stress disorder, including in pregnant women. One of the most commonly prescribed antidepressants is fluoxetine, a serotonin reuptake inhibitor. Fluoxetine can cross the placenta and is also detected in breast milk. Little is known about its safety during pregnancy, and not enough studies have been conducted on its long-term effects on offspring.

“Many human association studies have been conducted to investigate connections between antidepressant exposure during pregnancy and children with autism and attention deficit disorder (ADHD). But they have not been able to pinpoint a causal relationship,” stated Associate Professor Hyunsoo Shawn Je, from Duke-NUS’ Neuroscience and Behavioural Disorders (NBD) Programme, a senior and corresponding author of the study.

The team from Duke-NUS and their collaborators in South Korea and Singapore investigated adult mice born to mothers treated with fluoxetine (sold under the brand names Prozac and Sarafem) over a 15-day time period that corresponds to the second trimester in humans, in comparison with those born to mothers given normal saline as controls. They found key differences in behaviour. For example, the unexposed mice normally explored all three arms of a Y-shaped maze over a ten-minute time period and, over the courses of multiple arm entries, mice usually enter a less recently visited arm, while the fluoxetine-exposed ones were less inclined to explore unvisited arm.

In a second experiment, the mice were introduced to two juvenile mice, one after the other. When the second new mouse was introduced, mice that were not exposed to fluoxetine were more likely to only sniff the newly introduced mouse, recognizing that they had already met the first mouse. But the fluoxetine-exposed group sniffed both mice, indicating that they had impaired social novelty recognition.

The team then examined nerve signal transmission in the prefrontal cortex, a part of the brain involved in moderating social behaviour. They found impaired transmission caused by an overactive serotonin receptor. Treating fluoxetine-exposed mice with a compound that blocks the receptor alleviated their behavioural problems and improved their working memory.

The team next wants to examine autistic children born to mothers treated with antidepressants using positron emission tomography (PET) scans, an imaging technique used to observe metabolic processes in the body. If they also show enhanced serotonin receptor activity in the same area of the brain, the team plans to test whether FDA-approved serotonin receptor blockers can normalize their behaviours.

“The consensus among experts is that the rise in the number of people diagnosed with autism around the world is likely due to more awareness and testing rather than an increase in the prevalence of autism,” noted Professor Patrick Casey, Senior Vice Dean for Research at Duke-NUS. “This collaborative study by our researchers offers a compelling case for a link between autism and antidepressant exposure in the womb in an animal model, and a possible mechanism that could potentially be exploited for future therapies.”

*From the article here:

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mr peabody

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Aug 31, 2016
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Can autism be detected by observing children as they watch videos?*

Neuroscience News | Oct 28 2019

Tracking gaze patterns in children as they watch videos of social interactions is an accurate way to detect almost 50% of autism cases, a new study reports.

Measuring children’s gaze patterns as they watch movies of social interactions is a reliable way to accurately identify nearly half of autism spectrum disorder (ASD) cases, according to a new study just published in Autism Research by Ben-Gurion University of the Negev (BGU) researchers.

“Eye tracking is likely to be one of the first technologies that will be incorporated into clinical use for assessment of ASD symptoms, but it needs to be optimized to identify and quantify specific ASD symptoms,” explains Prof. Ilan Dinstein, of BGU’s Departments of Psychology and Cognitive and Brain Sciences and director of Israel’s National Autism Research Center. “This new study takes a first important step in this direction using eye tracking technology to compare different movies and measures within the same group of children.”

The research was presented at the Breaking the Barriers of Brain Science symposium sponsored by American Associates, Ben-Gurion University of the Negev (AABGU) on Sunday, October 27 at the InterContinental New York Times Square.

According to the United States Center for Disease Control (CDC), one in 59 children in the U.S. has ASD. Generally, when typically developing children watch movies of social interactions, they do so in a reliable and predictable manner, observing faces, gestures, body movements, and objects that are relevant to the social interaction and its narrative. In the new study, the researchers demonstrate that children with ASD watch such movies with significantly more variable and idiosyncratic gaze patterns.

Previous eye tracking studies have reported that children with ASD fixate less on faces in comparison to control groups. However, children must also gaze at actions, gestures, body movements, contextual details, and objects that are part of the social narrative, thereby creating complex gaze patterns to properly understand social interactions.

In the current study, the researchers presented ASD and control children with three short movies, each shown twice. Two of the movies were animated and one was a realistic home video; all contained social interactions between at least two individuals. This experimental design allowed comparisons across movies, presentations and different eye tracking measures to identify what is the best technique for identifying ASD children based on differences in gaze behavior.

Since children watch movies in a predictable manner, the gaze pattern of individual children is remarkably similar to the mean gaze pattern of their group. In other words, typically developing children agree on where and when to look at specific locations in the frame.

In contrast, children with ASD exhibited significantly more variable/idiosyncratic gaze patterns that differed from the mean gaze pattern of the typically developing children. Moreover, their gaze patterns were remarkably inconsistent not only between individuals, but also across movie presentations. Hence, when children with ASD watch the same movie repeatedly, they have more variable and inconsistent gaze patterns.

“Quantifying this gaze idiosyncrasy in individual children enabled separation of ASD and control children with higher sensitivity and specificity than traditional measures such as time gazing at faces,” Dinstein says. “It was also strongly correlated with their social symptom’s severity.”

The largest differences across ASD and control groups were apparent when using a realistic video containing a social interaction between two sisters (two and five years-old) in a messy room with everyday objects. This suggests that abnormal, idiosyncratic gaze patterns were most pronounced when ASD children observed real-life unedited interactions of other children. This makes the findings particularly relevant to real-life social situations.

“Taken together, these results demonstrate that ASD children with more severe symptoms exhibit larger gaze idiosyncrasy,” Dinstein says. “This can aid not only in early detection of autism, but also in assessing changes in ASD severity over time and in response to treatments. Such measures, which objectively measure symptoms directly from the child, are critically lacking in today’s clinical trials of autism treatments.”

*From the article here:

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