Autism Research

Avoiding direct eye contact with others is one of the most common characteristics associated with people with autism spectrum disorder. Many non-spectrum folks have traditionally assumed it is a sign of social or personal indifference.Avoiding direct eye contact with others is one of the most common characteristics associated with people with autism spectrum disorder. Many non-spectrum folks have traditionally assumed it is a sign of social or personal indifference.

Not so, says a new study published this month in the journal Scientific Reports.

According to the study, looking someone in the eye can result in unpleasant overstimulation of the brain for people with autism.

“The findings demonstrate that, contrary to what has been thought, the apparent lack of interpersonal interest among people with autism is not due to lack of concern,” said Nouchine Hadjikhani, a study author and a Harvard associate professor of radiology. “Rather, our results show that this behavior is a way to decrease an unpleasant excessive arousal stemming from overactivation in a particular part of the brain.”

In other words, when people with autism don’t look others in the eye, it doesn’t mean they don’t care, said Hadjikhani.

“It’s because it’s too much for them,” she said.

The results of the study may be useful for educators and others who work with people on the autism spectrum.

Hadjikhani and her fellow researchers with the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital focused on the brain’s subcortical system, which is responsible for newborn babies’ natural focus on faces and is instrumental in emotional perceptions. The system can be activated by eye contact.

Using the technology of functional magnetic resonance imaging, the researchers measured differences in subcortical system activation in about two dozen people with autism and about the same number of neurotypical people as they viewed faces freely as well as focusing on the eye region. Brain overactivation was found in the subjects with autism when they had to concentrate on the eye region. This was true with various facial expressions, but particularly fearful faces.

Overall, the findings suggest an imbalance between the neurotransmitters that stimulate the brain and those that tend to calm it, according to the researchers.  In people with autism, the imbalance may favor the excitatory subcortical signaling involved in face perception. That, in turn, can result in an aversion to direct eye contact.


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A deficiency in the levels of serotonin, a key brain chemical, may lead to the development of certain symptoms of autism, suggests a new animal study.

In particular, low serotonin levels may contribute to a lack of sociability, which is one of the hallmarks of autism spectrum disorder (ASD), reports a group of researchers from the Riken Brain Science Institute in Japan.

In the current study, the researchers discovered that giving young mice with low levels of the brain chemical a serotonin boost during the first three weeks of life led to improved social behavior in adulthood.

They also found that administering serotonin via medicinal means — that is, treating the mice with a selective serotonin reuptake inhibitor (SSRI), a drug commonly used to treat depression — improved the balance of the mice’s response to external stimulus.

“Our work shows that early serotonergic intervention rescues regional excitatory/inhibitory abnormalities in the brain as well as behavioral abnormalities,” said corresponding author Toru Takumi with the Riken Brain Science Institute in Japan.

Building on Past Research

An emerging body of research has linked serotonin levels to symptoms of autism. For example, a 2016 study from Vanderbilt University found an association between serotonin levels and sensory dysfunction, or “unusually strong reactions to touch, sound or visual stimuli, or diminished or absent reactions to stimuli.”

While the Vanderbilt study focused on hyperserotonemia, or elevated levels of the chemical neurotransmitter, the new Japanese study adds an important new layer of understanding of the role and resultant behavior of serotonin deficiency.

“Although abnormalities in the serotonin system have been thought to be part of the pathophysiology in patients with ASD, the functional impact of serotonin deficiency in ASD was totally unknown,” said Takumi.

As many as one in 68 children is affected by an autism disorder, according to the Centers for Disease Control and Prevention (CDC), and prevalence has been rising in recent years.

Low serotonin levels are tied to mood disorders, such as anxiety and depression, and the neurotransmitter also plays a key role in bodily functions that encompass digestion, sleep, blood clotting and sexual health.

In the current study, the researchers used brain-mapping techniques among the mice to identify abnormal neural activity, leading them to focus on serotonin.

“Because the sensory region was receiving abnormally low serotonin input, we reasoned that giving infant mice serotonin therapy might reduce the imbalance and also rescue some of the behavioral abnormalities,” said first author Nobuhiro Sakai, a fellow researcher at the Riken Brain Science Institute.


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For many people with autism, avoiding eye contact isn't a sign that they don't care – instead, it's a response to a deeply uncomfortable sensation.

Researchers have discovered a part of the brain responsible for helping newborns turn towards familiar faces is abnormally activated among those on the autism spectrum, suggesting therapies that force eye contact could inadvertently be inducing anxiety.

Autism spectrum disorder is a term used to describe a variety of conditions that make communicating and socialising a challenge, and is often accompanied by restricted and repetitive behaviours.

A defining characteristic of autism spectrum disorder is a difficulty in making or maintaining eye contact, a behaviour that not only makes social interactions harder, but can lead to miscommunication among cultures where eye contact is taken as a sign of trust and respect.

Those with the condition typically claim it feels "unnatural" or express anxiety over making eye contact, but psychologists have been uncertain if the discomfort is sensory or stems from conflict over the social importance of looking a person in the eye when you communicate.

Previous research suggested the latter, but a team of neurologists from the Massachusetts General Hospital in the US suspected the problem might be over-sensitivity of the parts of the brain responsible for emotional perception.


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Forcing them to stay still is counterproductive.

Children with attention deficit hyperactive disorder (ADHD) are always being told to sit still and concentrate, but new research has revealed that they actually need to move in order to learn.

In fact, small movements such as fidgeting, squirming, leg-swinging, foot-tapping and chair-scuffling may be vital to remembering information and working out complex tasks. The new research contradicts the long-term guidelines for how to deal with children with ADHD, and suggests that incorporating things such as activity balls or treadmill desks to the classroom could help certain students perform better.

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For all those who've declared the autism-vaccine debate over - a new scientific review begs to differ. It considers a host of peer-reviewed, published theories that show possible connections between vaccines and autism.

The article in the Journal of Immunotoxicology is entitled "Theoretical aspects of autism: Causes--A review." The author is Helen Ratajczak, surprisingly herself a former senior scientist at a pharmaceutical firm. Ratajczak did what nobody else apparently has bothered to do: she reviewed the body of published science since autism was first described in 1943. Not just one theory suggested by research such as the role of MMR shots, or the mercury preservative thimerosal; but all of them.

Ratajczak's article states, in part, that "Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis [brain damage] following vaccination [emphasis added]. Therefore, autism is the result of genetic defects and/or inflammation of the brain."

The article goes on to discuss many potential vaccine-related culprits, including the increasing number of vaccines given in a short period of time. "What I have published is highly concentrated on hypersensitivity, Ratajczak told us in an interview, "the body's immune system being thrown out of balance."

University of Pennsylvania's Dr. Brian Strom, who has served on Institute of Medicine panels advising the government on vaccine safety says the prevailing medical opinion is that vaccines are scientifically linked to encephalopathy (brain damage), but not scientifically linked to autism. As for Ratajczak's review, he told us he doesn't find it remarkable. "This is a review of theories. Science is based on facts. To draw conclusions on effects of an exposure on people, you need data on people. The data on people do not support that there is a relationship. As such, any speculation about an explanation for a (non-existing) relationship is irrelevant."

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It's still not known whether people with autism have more or less connections in parts of their brains that normally work in together.

Now a new study suggests the lack of common ground in this area reflects the fact that people with autism have connections that are uniquely their own.

The groundbreaking research could help lead to better diagnosis of autism and improve treatments, the scientists claim.

'It opens up the possibility that there are many altered brain profiles all of which fall under the umbrella of 'autism','' said Dr Marlene Behrmann at Carnegie Mellon University in Pittsburgh.

The researchers studied data taken from functional magnetic resonance imaging (fMRI) conducted while the participants were at rest.

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Scientists find that the hormone improves sociability in a mouse model of autism.

Mutant mice that exhibit many of the characteristics of human autism spectrum disorders, including social deficiency, have more interactions with fellow mice when given a dose of oxytocin, according to a report published today (January 21) inScience Translational Medicine. The beneficial effect was also apparent when the mice’s own oxytocin production was increased—which may be important for translating such a treatment to humans.

“It’s very exciting. They created a mouse model of autism . . . that had social deficits, and they found that if they gave oxytocin, it would rescue those social deficits,” said Larry Young who studies social neuroscience at Emory University and was not involved in the work.

The model mouse lacks a functional gene for contactin-associated protein-like 2 (Cntnp2). In humans, mutation of this gene causes cortical dysplasia and focal epilepsy (CDFE) syndrome; at least 70 percent of CDFE patients also display symptoms of autism spectrum disorders. Importantly, the characteristics of the mice—including their deficiencies in social behavior—are highly similar to those of humans with the CNTNP2 mutation.

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Each autistics' brain is distinct; non-autistics' brains are remarkably uniform.

The New York Times Magazine recently ran a cover article about mapping the connectome, all of the connections that link all of the neurons in someone's brain. Many of these connections are formed and reinforced as a result of our experiences, and their sum total constitutes everything about our personalities: the memories we've formed, the skills we've learned, the passions that drive us.

There is even data suggesting that some neurological disorders are in fact "connectopathies," characterized by either aberrant connections or an unusual extent of connections among neurons. Some studies have found that autism spectrum disorder (ASD) is associated with decreased functional connectivity in the brain, but other experiments have foundincreasedconnectivity in autistic brains. A new study may have reconciled these contradictory findings. Researchers at the Weizmann Institute of Science in Israel determined that brain regions with high interconnectivity in controls have reduced connectivity in ASD, and regions with lower connectivity in controls have elevated connectivity in people with ASD.

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Story by Pat Bailey, video and photos by Joe Proudman

Just a few hours after its birth, the long-legged brown foal stands in its stall, appearing on first glance to be sound, sturdy and healthy. But something is very wrong with this newborn horse.

The foal seems detached, stumbles towards people and doesn’t seem to recognize its mother or have any interest in nursing. It even tries to climb into the corner feeder.

The bizarre symptoms are characteristic of a syndrome that has puzzled horse owners and veterinarians for a century. But recently, UC Davis researchers have discovered a surprising clue to the syndrome and intriguing similarities to childhood autism in humans.

Resembles children with autism

“The behavioral abnormalities in these foals seem to resemble some of the symptoms in children with autism,” said John Madigan, a UC Davis veterinary professor and an expert in equine neonatal health.

“There are thousands of potential causes for autism, but the one thing that all autistic children have in common is that they are detached,” said Isaac Pessah, a professor of molecular biosciencesat the UC Davis School of Veterinary Medicineand a faculty member of the UC Davis MIND Institute, who investigates environmental factors that may play a role in the development of autism in children.

Pessah, Madigan and other researchers in veterinary and human medicine recently formed a joint research group and secured funding to investigate whether abnormal levels of neurosteroids — a group of chemicals that modulate perception — may play a role in both disorders.

They hope their efforts will help prevent and treat the disorder in foals and advance the search for the causes of autism, which affects more than 3 million individuals in the United States.


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The Long Ride Home

The long awaited sequel of the Horse Boy.


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