Links for Keyword: Autism

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by Jonathan Moens Conversations between an autistic and a typical person involve less smiling and more mismatched facial expressions than do interactions between two typical people, a new study suggests1. People engaged in conversation tend to unconsciously mimic each other’s behavior, which may help create and reinforce social bonds. But this synchrony can break down between autistic people and their neurotypical peers, research shows. And throughout an autistic person’s life, these disconnects can lead to fewer opportunities to meet people and maintain relationships. Previous studies have looked at autistic people’s facial expressions as they react to images of social scenes on a computer screen2. The new work, by contrast, is one of a growing number of experiments to capture how facial expressions unfold during ordinary conversation. Changes in facial expressions are easy to observe but notoriously hard to measure, says lead investigator John Herrington, assistant professor of psychiatry at the Children’s Hospital of Philadelphia in Pennsylvania. He and his colleagues devised a new method to quantify these changes over time in an automated and granular way using machine-learning techniques. Atypical facial expressions are in part a manifestation of difficulties with social coordination, Herrington says. So tracking alterations in facial expression may be a useful way to monitor whether interventions targeting these traits are effective. The new study included 20 autistic people and 16 typical controls, aged 9 to 16 years and matched for their scores on intelligence and verbal fluency. Each participant engaged in two 10-minute conversations — first with their mother and then with a research assistant — to plan a hypothetical two-week trip. © 2020 Simons Foundation

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 27440 - Posted: 08.29.2020

by Angie Voyles Askham A new study pinpoints genes and cell types that may account for the atypical brain structure in people with genetic conditions related to autism1. The work offers insight into how the brain develops differently in people with these conditions and identifies new potential therapeutic targets, says Mallar Chakravarty, associate professor of psychiatry at McGill University in Montreal. Chakravarty has collaborated with the researchers previously but was not involved in the new work. The analysis considered people with six genetic conditions associated with atypical brain development, including syndromes associated with deletions in the chromosomal regions 11p13 and 22q11.2, both of which increase the likelihood of autism2. “We used known genetic conditions as a kind of foothold into the complex biology of neurodevelopmental disorders,” says lead researcher Armin Raznahan, chief of the Developmental Neurogenomics section at the U.S. National Institute of Mental Health intramural research program. Previous studies of mice with autism-linked genetic conditions have shown that brain structure changes tend to crop up in regions where the relevant genes are ordinarily expressed3. The same holds true for people, Raznahan and his colleagues found after comparing measurements from brain scans with existing data from postmortem brains. “It’s wildly creative,” Chakravarty says of the method. Raznahan and his colleagues used magnetic resonance imaging to scan the brains of 231 adolescents and adults with one of the six genetic conditions and 287 controls. Each of the six conditions results from a deletion or duplication of a chromosome or set of genes within a chromosome. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27430 - Posted: 08.22.2020

by Laura Dattaro Extra repeating bits of DNA may account for nearly 3 percent of the genetic architecture of autism, according to a new study1. The work is the first to examine such genetic variants in autism on a large scale. About half of the identified repeating sections occur in genes that have not been previously linked to autism, suggesting new lines of inquiry for geneticists. “These genes are involved in autism, absolutely,” says study investigator Steve Scherer, professor of medicine at the University of Toronto in Canada. “Those [genes] will become diagnostic tests for the autism screening panel.” The researchers looked at areas of the genome with tandem repeats — stretches of 2 to 20 nucleotides, which are the ‘building blocks’ of DNA, that are repeated two or more times in one spot. These repeats can expand when they are passed down from parents to children: If a nucleotide, or combination of them, is repeated 10 times in a parents’ DNA, it may be repeated hundreds of times in their child, for example. The more a repeat expands, the more likely it is that it will disrupt the gene’s function. Some specific repeats are already associated with autism: About 5 percent of autistic people have fragile X syndrome, which is nearly always caused by the expansion of a particular repeat in the FMR1 gene. But less than a quarter of people with autism have a known genetic cause, even though twin studies suggest that autism is highly heritable2. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27410 - Posted: 08.11.2020

by Peter Hess / Infants with particular patterns of electrical activity in the brain go on to have high levels of autism traits as toddlers, a new study shows1. Specifically, babies who have unusually high or low synchrony between certain brain waves — as measured by electroencephalography (EEG) — at 3 months old tend to score high on a standardized scale of autism-linked behaviors when they are 18 months old. These levels of synchrony reflect underlying patterns of connectivity in the brain. The findings suggest that EEG could help clinicians identify autistic babies long before these children show behaviors flagged by standard diagnostic tests. The work “reinforces the concept and the truism that brain development is affected before autism diagnoses are made,” says lead researcher Shafali Spurling Jeste, associate professor of psychiatry and neurology at the University of California, Los Angeles. “We believe that we could work to start rewiring the brain if we intervene effectively and early enough. That message, quite simply, is a very important one.” The study involved ‘baby sibs,’ the younger siblings of autistic children. Baby sibs are 10 to 20 times more likely to have autism than the general population. Previous research showed similar patterns of altered connectivity in functional magnetic resonance imaging (MRI) data from infants who were later diagnosed with autism, but MRI is costly and prone to errors. EEG measurements, on the other hand, are relatively inexpensive and simple to perform, which makes them more practical for clinical use, says Charles Nelson, professor of pediatrics and neuroscience at Harvard University, who was not involved in the study. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27380 - Posted: 07.25.2020

by Angie Voyles Askham The autism gene SHANK3 is crucial for the development and function of muscles and the motor neurons that control them, according to a new study1. This relationship may explain why some people with mutations in the gene have low muscle tone, says co-lead investigator Maria Demestre, senior researcher at the Institute for Bioengineering of Catalonia in Barcelona. “It opens an avenue for treatment.” Between 1 and 2 percent of people with autism have a mutation in SHANK3. Deletions of the chromosomal region containing SHANK3 lead to Phelan-McDermid syndrome, characterized by intellectual disability, speech delay and, often, autism. One of the earliest signs of the syndrome in infants is hypotonia, or low muscle tone, which can result in difficulty feeding and a delay in reaching developmental milestones such as crawling and walking. SHANK3 encodes a protein that helps neurons communicate throughout the brain. But studies have shown that the gene is also found in other parts of the body and that mutations or deletions of genes in peripheral cells can contribute to autism traits2. SHANK3 is heavily expressed throughout the motor system of both mice and people, the new work shows. Muscle cells derived from people with Phelan-McDermid syndrome fail to mature, and mice deficient in SHANK3 have poor muscle function. The results add to “the growing appreciation of the role of autism-associated genes — in this case, SHANK3 — outside of the brain,” says David Ginty, professor of neurobiology at Harvard Medical School, who was not involved in the study. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27375 - Posted: 07.21.2020

by Jonathan Moens / Autistic people with deletions in the chromosomal region 22q11.2 have a brain structure that’s distinct from that of autistic people without the deletions, according to a new brain imaging study1. The findings suggest that brain changes related to autism vary depending on the condition’s etiology, says study investigator Carrie Bearden, professor of clinical psychology at the University of California, Los Angeles. “[Autism is] really not one thing.” Deletions in 22q11.2 cause a syndrome characterized by heart defects, learning difficulties and an increased risk of psychiatric conditions such as schizophrenia. About 16 percent of people with the syndrome have autism2. Brain anatomy differs between people with the syndrome who have autism and those who do not, past studies by the same team show3. The new work is the first to compare these two groups with people who have ‘idiopathic’ autism, meaning its etiology is unknown. Disentangling these brain differences may be key to understanding if clinicians should treat autistic people with 22q deletions differently than people with autism without the deletions, Bearden says. “Maybe we’re treating these [conditions] as all the same at one level when we really need to dissect this a bit more.” Some experts say these findings could also be a first step toward dividing autism’s broad spectrum of traits into smaller sets of genetic conditions. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27372 - Posted: 07.18.2020

by Sarah DeWeerdt The amygdala is a deep brain structure about the size and shape of an almond — from which it gets its name. It is commonly described as a center for detecting threats in the environment and for processing fear and other emotions. Researchers who study the region argue that its function is broader — and that it plays a crucial role in autism. “Emotion is such a big part in social function,” says Wei Gao, associate professor of biomedical sciences at Cedars-Sinai Medical Center in Los Angeles, California. “So I think the amygdala has got to have a big role in the emergence or development of autism-related traits.” The amygdala is the brain’s surveillance hub: involved in recognizing when someone with an angry face and hostile body language gets closer, tamping down alarm when a honeybee buzzes past, and paying attention when your mother teaches you how to cross the street safely and points out which direction traffic will be coming from — in other words, things people should run away from, but also those they should look toward, attend to and remember. In that sense, researchers say, this little knot of brain tissue shows just how tangled up emotion and social behavior are for humans. “Important events tend to be emotional in nature,” as do most aspects of social behavior, says John Herrington, assistant professor of psychiatry at the Children’s Hospital of Philadelphia in Pennsylvania. As a result, the amygdala has long been a focus of autism research, but its exact role in the condition is still unclear. © 2020 Simons Foundation

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 27363 - Posted: 07.15.2020

by Angie Voyles Askham Toddlers with autism have unusually strong connections between sensory areas of the brain, according to a new study1. And the stronger the connections, the more pronounced a child’s autism traits tend to be. Overconnectivity in sensory areas may get in the way of an autistic child’s brain development, says lead investigator Inna Fishman, associate research professor at San Diego State University in California. “Their brain is busy with things it shouldn’t be busy with.” The findings add to a complicated field of research on brain connectivity and autism, which has shown weakened connectivity between some brain areas, strengthened connectivity between others, or no difference in connectivity at all. Previous brain-imaging studies have found that babies and toddlers with autism have altered connectivity in various brain areas and networks, including sensory areas. But most of these data come from ‘baby sibs’ — the younger siblings of autistic children, who are about 20 times more likely to have autism than the general population. “A lot of our early knowledge is from these high-risk samples of infant siblings,” says Benjamin Yerys, assistant professor of psychology in psychiatry at the University of Pennsylvania, who was not involved with the study. “If their behaviors and genetics are different, then all of this early brain work may also be different.” By contrast, the new work focused on autistic children who were newly diagnosed. “There are very, very few studies focused on this age, right around the time the diagnosis can be made,” says Christine Wu Nordahl, associate professor at the University of California, Davis MIND Institute. “I think that is the major strength of the study.” © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27345 - Posted: 07.06.2020

by Peter Hess / Inherited mutations in a gene called ACTL6B lead to autism, epilepsy and intellectual disability, according to a new study1. The mutations are recessive, which means that they lead to autism only if a person inherits them in both copies of the gene — one from each parent, who are silent carriers. Most other mutations implicated in autism are spontaneous, or ‘de novo,’ mutations, which are not inherited. The study suggests that recessive mutations in ACTL6B could be a relatively common cause of autism, says co-lead researcher Joseph Gleeson, professor of neurosciences and pediatrics at the University of California, San Diego. ACTL6B helps to control the expression of other genes in brain cells by encoding part of a protein complex called BAF. This complex tightens and loosens chromatin, the bundle of DNA and protein crammed inside a cell’s nucleus, during transcription. Scientists have linked autism to mutations in many other chromatin regulation genes — including several that encode other parts of the BAF complex. ACTL6B mutations have previously been associated with neurodevelopmental conditions, but the new study makes a strong case that they are tied to autism, says Gaia Novarino, professor of neuroscience at the Institute of Science and Technology in Klosterneuburg, Austria, who was not involved in the study. The work also provides a comprehensive look at how mutations in ACTL6B affect the brains of people, mice and flies, and suggests that the gene plays a common role across species. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27325 - Posted: 06.26.2020

by Laura Dattaro Children with autism are more likely than typical children to have had problems falling asleep as infants, according to a new study1. These infants also have more growth in the hippocampus, the brain’s memory hub, from age 6 to 24 months. The study is the first to link sleep problems to altered brain development in infants later diagnosed with autism. Sleep difficulties are common in autistic children: Nearly 80 percent of autistic preschoolers have trouble sleeping2. But little is known about the interplay between sleep and brain development in early life, says lead investigator Annette Estes, director of the UW Autism Center at the University of Washington in Seattle. The researchers examined the sleep patterns and brain scans of infants who have autistic older siblings, a group known as ‘baby sibs.’ Baby sibs are 20 times as likely to be diagnosed with autism as are children in the general population, and they often show signs of autism early in life. The study shows an association between sleep problems and brain structure in babies who have autism. But it is too early to say whether sleep troubles contribute to brain changes and autism traits or vice versa, or whether some common factor underlies all three, Estes says. It is also not clear what, if any, connection exists between these findings and the well-documented sleep problems in older autistic children. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 27314 - Posted: 06.22.2020

by Tessa van Leeuwen, Rob van Lier Have you ever considered what your favorite piece of music tastes like? Or the color of Tuesday? If the answer is yes, you might be a synesthete. For people with synesthesia, ordinary sensory events, such as listening to music or reading text, elicit experiences involving other senses, such as perceiving a taste or seeing a color. Synesthesia is not to be confused with common metaphors — such as saying someone ‘sees red’ to describe anger. Instead, synesthetic associations are perceptual, highly specific and idiosyncratic, and typically stable beginning in childhood. And many types exist: A taste can have a shape, a word can have a color, the months of the year may be experienced as an array around the body. In the general population, the phenomenon is relatively rare: Only 2 to 4 percent of people have it. But as much as 20 percent of people with autism experience synesthesia1,2. Why would two relatively rare conditions occur together so often? Over the past few years, researchers have found that people with synesthesia or autism share many characteristics. Synesthetes often have sensory sensitivities and attention differences, as well as other autism traits3,4. The two conditions also share brain connectivity patterns and possibly genes, suggesting they have common biological underpinnings. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27304 - Posted: 06.17.2020

by Peter Hess Early behavioral signs predict seizures in autistic children, according to a new study1. Previous work has shown that 5 to 46 percent of people with autism experience seizures. And autistic adults with epilepsy have, on average, less cognitive ability and weaker daily living skills than their autistic peers who do not have seizures2. The new study shows that people with autism who begin having seizures during childhood show small but significant behavioral differences before they ever experience a seizure, compared with those who do not develop epilepsy. They score lower than their peers on measures of quality of life and adaptive behaviors, which include communication, daily living skills, socialization and motor skills. They score higher on a measure of hyperactivity. The results suggest that seizures and certain behavioral issues in autism could have common origins, says co-lead investigator Jamie Capal, associate professor of pediatrics and neurology at the University of North Carolina at Chapel Hill. “I think it really does show us that in individuals with autism who eventually have epilepsy, there is some shared mechanism early on that we just haven’t been able to identify,” Capal says. Early signs: To investigate the relationship between childhood behaviors in autism and the development of seizures, the researchers analyzed data on 472 autistic children aged 2 to 15 from the Autism Treatment Network, a medical registry that includes 12 clinics in the United States and Canada. None of the children had experienced seizures before enrolling in the network, but 22 developed seizures two to six years after enrollment. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27294 - Posted: 06.09.2020

by Emily Anthes The overproduction of proteins in brain cells called microglia causes social impairments, cognitive deficits and repetitive behavior in male mice, a new study has found.1 These behavioral differences are not present in female mice, or in mice that produce excess protein in other brain cells, including neurons or star-shaped support cells known as astrocytes. Microglia help eliminate excess synapses — connections between brain cells — that form early in life; this pruning process is crucial to healthy brain development. But male mice that have been engineered to overproduce proteins in these cells have enlarged microglia. That, in turn, lowers the cells’ mobility and may prevent them from migrating to synapses that need eliminating. In support of that idea, the mice have too many synapses, the researchers found — a result that mirrors evidence that certain brain regions may be overconnected in people with autism. “Increased protein synthesis in microglia is sufficient to cause autism phenotypes in mice,” says lead investigator Baoji Xu, professor of neuroscience at the Scripps Research Institute in Jupiter, Florida. “Problems in microglia could be an important pathological mechanism for autism.” Malfunctioning microglia: The researchers studied mice that produce excess levels of EIF4E, a protein that facilitates the synthesis of other proteins. Mutations in several genes linked to autism — including TSC1, TSC2, PTEN and FMR1 — are associated with elevated levels of an active form of EIF4E and, as a result, many other proteins in the brain. Mice that overproduce EIF4E also display autism-like behavior, researchers have previously found. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27273 - Posted: 06.01.2020

by Laura Dattaro Correcting a mutation in the autism gene SHANK3 in fetal mice lessens some autism-like behaviors after birth, according to a new study1. The work adds to evidence that gene therapy may help some people with SHANK3 mutations. In people, mutations in SHANK3 can lead to Phelan-McDermid syndrome, a condition that causes developmental delays and often autism. Up to 2 percent of people with autism have a mutation in SHANK32. “Our findings imply that early genetic correction of SHANK3 has the potential to provide therapeutic benefit for patients,” lead investigator Craig Powell, professor of neurobiology at the University of Alabama at Birmingham, wrote in an email. A 2016 study showed that correcting mutations in SHANK3 in both young and adult mice can decrease excessive grooming, which is thought to correspond to repetitive behaviors in people with autism. Last year, Powell and his team also showed that correcting SHANK3 mutations in adult mice eliminates some autism-like behaviors3. But the results were difficult to interpret. The team reversed the mutation using an enzyme called Cre-recombinase that could edit SHANK3 if the animals were given a drug called tamoxifen. Control mice in that study that did not receive tamoxifen but had the gene for Cre still showed behavior changes, raising the possibility that the enzyme affected their brains. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27270 - Posted: 05.29.2020

Peter Hess The relative contributions of genetic and environmental factors to autism and traits of the condition have held steady over multiple decades, according to a large twin study. Among tens of thousands of Swedish twins born over the span of 26 years, genetic factors have consistently had a larger impact on the occurrence of autism and autism traits than environmental factors have. The study suggests that genetics account for about 93 percent of the chance that a person has autism, and 61–73 percent of the odds she shows autism traits. The figures fall in line with previous work that shows genetics exert an outsized influence on autism odds. The findings also indicate that environmental factors are unlikely to explain the rise in autism prevalence. Otherwise, their contribution to autism among the twins would have also risen over time. “I think the relative consistency of the genetic and environmental factors underlying autism and autism traits is the most important aspect of this work,” says Mark Taylor, senior research specialist at the Karolinska Institutet in Stockholm, Sweden, who led the study. “Prior to our study, there had been no twin studies examining whether the genetic and environmental factors underlying autism had changed over time.” Family factors: The researchers analyzed data from two sources: 22,678 pairs of twins in the Swedish Twin Registry, who were born from 1982 to 2008; and 15,280 pairs of twins from the Child and Adolescent Twin Study in Sweden, born from 1992 to 2008. © 1986–2020 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27262 - Posted: 05.28.2020

by Peter Hess The relative contributions of genetic and environmental factors to autism and traits of the condition have held steady over multiple decades, according to a large twin study 1. Among tens of thousands of Swedish twins born over the span of 26 years, genetic factors have consistently had a larger impact on the occurrence of autism and autism traits than environmental factors have. The study suggests that genetics account for about 93 percent of the chance that a person has autism, and 61 to 73 percent of the odds she shows autism traits. The figures fall in line with previous work that shows genetics exert an outsized influence on autism odds. The findings also indicate that environmental factors are unlikely to explain the rise in autism prevalence. Otherwise, their contribution to autism among the twins would have also risen over time. “I think the relative consistency of the genetic and environmental factors underlying autism and autism traits is the most important aspect of this work,” says Mark Taylor, senior research specialist at the Karolinska Institutet in Stockholm, Sweden, who led the study. “Prior to our study, there had been no twin studies examining whether the genetic and environmental factors underlying autism had changed over time.” The researchers analyzed data from two sources: 22,678 pairs of twins in the Swedish Twin Registry, who were born from 1982 to 2008; and 15,280 pairs of twins from the Child and Adolescent Twin Study in Sweden, born from 1992 to 2008. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27256 - Posted: 05.20.2020

by Peter Hess Low levels of the hormone vasopressin in early infancy may presage an autism diagnosis in childhood, according to a new study1. Although preliminary, the results suggest that testing vasopressin levels — particularly in infants with high odds of having autism — could flag the condition in the first few months of life. Early identification would allow autistic children to start therapies far sooner than is currently possible, says co-lead investigator Karen Parker, associate professor of psychiatry and behavioral sciences at Stanford University in California. “By the time a child receives an autism diagnosis, they’re pretty far along the path of having these robust social impairments,” Parker says. Previous work has shown that autistic children have, on average, 66 percent less vasopressin in their cerebrospinal fluid than their neurotypical peers, and that low levels of vasopressin track with poor social skills. The new study found a similar trend in infants aged 3 months and younger. “The surprising thing is that this relationship extends to infancy,” before any observable autism traits have emerged, says Larry Young, chief of behavioral neuroscience and psychiatric disorders at Emory University in Atlanta, Georgia, who was not involved with the study. The results, if confirmed, suggest there is a direct biological connection between vasopressin release and autism, Young says. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 8: Hormones and Sex
Link ID: 27243 - Posted: 05.12.2020

by Giorgia Guglielmi More than half of the genes expressed in the prefrontal cortex, a brain region that is implicated in autism, begin to change their expression patterns in late fetal development, according to a new study1. Previous studies have looked at how DNA variants can influence gene expression at specific developmental periods. This is the first to map their effects in a specific region over the full span of human brain development, says co-senior investigator Stephan Sanders, associate professor of psychiatry at the University of California, San Francisco. “If we ever really want to understand what autism is, understanding human fetal development of the brain is going to be absolutely critical,” Sanders says. Some of the changes in expression patterns vary depending on individual differences in neighboring DNA sequences, the study found. Some of that variation occurs in stretches of the genome linked to neurodevelopmental outcomes, such as how much schooling a person completes (a proxy for intelligence) or whether she develops schizophrenia. “This study creates a resource for trying to understand neurodevelopment and neuropsychiatric disorders,” Sanders says. Fetal expression: The researchers analyzed the prefrontal cortex of 176 postmortem brains from donors ranging in age from 6 weeks post-conception to 20 years. None had any known neuropsychiatric conditions or large-scale genetic anomalies. The team identified 23,782 genes expressed during brain development in the dorsolateral prefrontal cortex, a region implicated in many developmental conditions, including autism. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27239 - Posted: 05.08.2020

A small study funded by the National Institutes of Health suggests that sleep problems among children who have a sibling with autism spectrum disorder (ASD) may further raise the likelihood of an ASD diagnosis, compared to at-risk children who do not have difficulty sleeping. Previous research has shown that young children who have a sibling with ASD are at a higher risk for also being diagnosed with the condition. The study appears in The American Journal of Psychiatry. If confirmed by other studies, the findings may give clinicians a tool to identify sleep problems early and provide interventions to reduce their effects on the health and development of children with autism. The findings may also provide insights into the potential role of sleep problems in the development of ASD. The study was conducted by Annette M. Estes, Ph.D., of the University of Washington Autism Center in Seattle, and colleagues in the NIH Autism Centers of Excellence Infant Brain Imaging Study Network. NIH funding was provided by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health. “The results are a promising lead,” said Alice Kau, Ph.D., of NICHD’s Intellectual and Developmental Disabilities Branch. “If confirmed by more in-depth studies, patterns of sleep disturbance in early life might be used to pinpoint increased risk for ASD among young children already at risk because they have a sibling with ASD.” The researchers analyzed data from a long-term study of children who do and do not have siblings with ASD. When the children were 6 and 12 months of age, parents were asked to respond to an infant temperament questionnaire that asks how much difficulty their child has falling asleep at bedtime and falling back to sleep after waking up during the night. At these time intervals, the children also received MRI scans to track their brain development. At 24 months, the children were assessed for ASD.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 10: Biological Rhythms and Sleep
Link ID: 27238 - Posted: 05.08.2020

by Laura Dattaro / Autistic people have atypical activity in a part of the brain that regulates attention, according to a new study1. The researchers measured pupil responses as a proxy for brain activity in a brain region known as the locus ceruleus. Located in the brain stem, the region plays a key role in modulating activity throughout the brain, in part by controlling attention. It can broaden and narrow pupils to adjust how much visual information a person receives, for example. Because of this, researchers can use pupil size to infer activity in the region and gauge a person’s focus on a task; a wider pupil indicates increased focus. The locus ceruleus may also be key to regulating the balance between excitatory and inhibitory brain signals. Some research indicates this equilibrium is disrupted in autism, suggesting the region plays a role in the condition’s underlying biology. In the new study, researchers compared autistic and typical people’s pupil responses when performing a task with and without a distracting sound. Typical people’s pupils grew larger when hearing the sound, suggesting a boost in focus directed by the locus ceruleus. By contrast, the pupils of autistic people did not widen, indicating they do not modulate their attention in the same way. This might have profound consequences for autistic people’s sensory experience, the researchers say. © 2020 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 14: Attention and Higher Cognition
Link ID: 27231 - Posted: 05.05.2020