Links for Keyword: Autism

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 795

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 BN8e: 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, Learning, and Development; 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; 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 BN8e: 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, Learning, and Development; 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 BN8e: 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, Learning, and Development; Chapter 3: 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 BN8e: 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, Learning, and Development; Chapter 2: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 27231 - Posted: 05.05.2020

By Emily Willingham Professional burnout is all too familiar: Go at something too hard for too long, and the motivational tank empties. But burnout for an autistic person isn’t always about overwork, Dora Raymaker, an autistic systems scientist at Portland State University (PSU), found in a study of autistic workers. Instead, the need to mask autistic behaviors through a workday with nonautistic people can cause chronic exhaustion, reduced ability to tolerate stimuli like light or sound, and loss of skills, the study showed through interviews and a survey of social media comments. The work, which Raymaker’s team published last month, highlights a new trend in autism research. Raymaker and colleagues are part of a small but growing number of research teams with autistic members. These groups are shifting the focus in autism research from cause and cure to practical steps, including ones that help autistic people in settings such as the workplace. And they’re publishing some of their findings in a new journal, Autism in Adulthood, which is dedicated to including the perspectives of autistic people in what it publishes. Interest in those perspectives is “skyrocketing,” says Christina Nicolaidis, a co-author on the burnout study. Nicolaidis, a professor in the School of Social Work at PSU, has an adult son who is autistic. Although much research on autism has focused on children, autistic adults who came of age in the 1990s and early 2000s are joining the field and bringing a focus on their own experience. One member of that cohort is TC Waisman, a doctoral candidate at the University of Calgary studying how faculty and staff can improve autistic students’ college experiences. Waisman says she sees researchers increasingly “respecting us as our own self-determined culture and foregrounding our needs in studies.” © 2020 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27223 - Posted: 04.30.2020

By Neil Genzlinger Mel Baggs, whose forthright writings and films about being a nonverbal person with autism made an impact in the fields of neurodiversity and disability rights, died on April 11 in Burlington, Vt., at age 39. Anna Baggs, Mx. Baggs’s mother, said the cause was believed to be respiratory failure, though numerous health problems may also have played a part. Mx. Baggs, a vigorous blogger, used the term “genderless” as a self-description. “I like that it just means lack of gender, and has no spoken or unspoken secondary meaning,” read a 2018 entry on the blog “Cussin’ and Discussin’: Mel being human in a world that says I’m not.” Many friends and admirers posting about Mx. Baggs’s death on social media used gender-neutral pronouns, while others used the traditional feminine ones. Gender issues, though, were not Mx. Baggs’s major concern. Of more urgency was conveying that people who think and communicate in nontraditional ways are fully human, and that humanness is a spectrum, not something that can be reduced to a normal/abnormal dichotomy. Many people were introduced to these ideas through Mx. Baggs’s short film “In My Language,” posted on the internet in 2007 and given wide exposure through coverage on CNN. For three minutes it shows Mx. Baggs fiddling with the knob on a dresser drawer, rubbing against a book and more. Then it offers “a translation,” as the film puts it. “The previous part of this video was in my native language,” a synthesized voice says. “Many people have assumed that when I talk about this being my language, that means that each part of the video must have a particular symbolic message within it designed for the human mind to interpret. But my language is not about designing words or even visual symbols for people to interpret. It is about being in a constant conversation with every aspect of my environment.” By the time “In My Language” was posted, Mx. Baggs had already drawn considerable attention in the autism world for creating the website “Getting the Truth Out,” a response to an awareness campaign by the Autism Society of America called “Getting the Word Out,” which Mx. Baggs thought made autistic people objects of pity. Part of that attention was skepticism about Mx. Baggs’s claims. Autism online forums can be caustic, with sharp divisions among various factions, and the harshest detractors have accused Mx. Baggs of being a fake. © 2020 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27218 - Posted: 04.29.2020

by Peter Hess The mood-stabilizing drug lithium eases repetitive behaviors seen in mice missing SHANK3, an autism gene, according to a new study1. The findings suggest lithium merits further study as a treatment for some people with autism, even though the drug has troublesome side effects, including tremors and impaired memory. “Lithium is, of course, a rather difficult, non-ideal treatment,” says lead investigator Gina Turrigiano, professor of vision science at Brandeis University in Waltham, Massachusetts. “It’s really hard to get people on a lithium regimen that they can tolerate well.” But understanding why lithium works may set the stage for better treatments, she says. About 1 percent of people with autism have mutations in SHANK3. Deletion or mutation of the gene can also lead to Phelan-McDermid syndrome, which is characterized by intellectual disability, delayed speech and, often, autism. Case studies of people with Phelan-McDermid syndrome also suggest that lithium eases behavior problems associated with the condition2. Previous work has shown that SHANK3 helps stabilize neuronal circuits by adjusting excitatory and inhibitory signaling like a thermostat. This process, called homeostatic plasticity, allows neurons to respond to changes in sensory input. © 2020 Simons Foundation

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27215 - Posted: 04.27.2020

by Lauren Schenkman Mice with mutations in a gene called DLG2 are anxious and asocial; they also sleep poorly and overgroom themselves, according to a new study1. These characteristics resemble those seen in some people with autism. The results offer the first evidence that mutations in DLG2 may account for some of the condition’s behavioral traits. “This study is a baby step indicating DLG2’s implication in [autism’s] core behavioral symptoms,” says lead investigator Soo Young Kim, assistant professor of pharmacy at Yeungnam University in Gyeongsan, South Korea. A 2013 study reported that mice and people with DLG2 mutations have differences in learning, attention and other cognitive processes2. Last year, a study of nearly 500 families with two or more autistic children identified DLG2 as a candidate gene for autism3. The new work offers “a more full picture” of DLG2’s effect on behavior, says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland. Grant led the 2013 work but was not involved in the new study. “It’s a useful contribution.” Kim and her colleagues bred male mice that have two mutant copies of DLG2. The animals lack the corresponding protein, which forms part of a neuron’s scaffolding. DLG4, another gene implicated in autism, has a similar role. © 2020 Simons Foundation

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27212 - Posted: 04.24.2020

by Peter Hess Early sleep problems predict repetitive behaviors later in childhood1. And toddlers who overreact or underreact to sensory stimuli have more repetitive behaviors and other autism traits later on2. Together, the findings from two independent studies suggest that early behavioral differences may set the stage for restricted and repetitive behaviors, a core characteristic of autism also associated with other conditions of brain development. The studies also highlight areas for early intervention, particularly if further research identifies causal links between these traits. “Addressing sleep problems might be able to improve trajectories,” says Annette Estes, director of the University of Washington Autism Center in Seattle, who led the sleep study. Autistic children are twice as likely to have trouble sleeping as typical children. Their poor sleep has been linked to severe traits including severe repetitive and restricted behaviors. The new study is unusual in that it links sleep problems with a subset of ‘higher-order’ restrictive and repetitive behaviors that include restricted interests, rituals or routines and an insistence on sameness. The study involved 38 autistic children aged 2 to 6 years and 19 children with developmental delay aged 2 to 4. Parents completed a standardized questionnaire about their children’s sleep problems at age 4 — including difficulty falling asleep, short sleep duration and parasomnias such as sleepwalking and night terrors. Clinicians assessed autism traits, including repetitive behaviors, around age 2 and at two or three later points in time. © 2020 Simons Foundation

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 27208 - Posted: 04.22.2020

by Laura Dattaro Children with autistic older siblings have bigger neural responses than controls do in the brain networks that process faces, according to a new study1. The researchers followed these children from infancy to age 7, looking for relationships between neural signals and the children’s face-processing abilities that remained consistent during this period of development. The work is the first to track face processing in so-called ‘baby sibs’ — children who have autistic older siblings. Baby sibs are 20 times as likely to be diagnosed with autism as typical children are, and they often show autism traits early in life. For this reason, researchers frequently study them to get new clues about autism’s underlying biology. The new study shows the importance of monitoring neural activity and behavior over time to better understand autism, says lead investigator Tony Charman, chair of clinical child psychology at King’s College London in the United Kingdom. “If you measure both the neurocognitive abilities and the behaviors at multiple time points, maybe you get a better handle on the causal mechanisms,” Charman says. “If you understand the mechanisms, you’ve got at least a basis for talking about mechanistic-based interventions” — targeted therapies that might help ease autism traits. The team used electroencephalography (EEG) to measure the brain’s responses to faces and objects. One distinctive response, called the P1, occurs about 100 milliseconds after seeing any visual stimulus and is usually larger and faster when looking at a face. The N170 follows about 70 milliseconds later, mostly in the brain’s right hemisphere. This response is thought to mark the moment when the brain distinguishes a face from an object, or one face from another. In autistic children, the N170 is slower than in typical children2. © 2020 Simons Foundation

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 27204 - Posted: 04.17.2020

by Alla Katsnelson Several regions in the outer layer of the brain are thicker in children and young adults with autism than in their typical peers, a new study finds. The differences are greatest in girls, in children aged 8 to 10 years, and in those with a low intelligence quotient (IQ)1. During typical development, the brain’s outer layer, called the cerebral cortex, thickens until about age 2 and then grows gradually thinner into adolescence as the brain matures. The new study, one of the largest to investigate cortical thickness in autism, aligns with others that indicate this trajectory differs in people with the condition. The findings suggest that brain structure does not change in a uniform way in autism, but instead varies with factors such as age, gender and IQ, says lead researcher Mallar Chakravarty, assistant professor of psychiatry at McGill University in Montreal, Canada. These variations could help explain the inconsistent findings about cortical thickness and autism seen in earlier studies that did not consider such factors, says Christine Wu Nordahl, associate professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute, who was not involved in the work. “I think this is the type of study we need to be doing as a field, more and more,” she says. The researchers began with unprocessed magnetic resonance imaging (MRI) brain scans of 3,145 participants from previous studies conducted at multiple institutions. © 2020 Simons Foundation

Related chapters from BN8e: 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, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27188 - Posted: 04.14.2020