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

Keyword: Autism; Epilepsy
Link ID: 27294 - Posted: 06.09.2020

Amber Dance They told Marcelle Girard her baby was dead. Back in 1992, Girard, a dentist in Gatineau, Canada, was 26 weeks pregnant and on her honeymoon in the Dominican Republic. When she started bleeding, physicians at the local clinic assumed the baby had died. But Girard and her husband felt a kick. Only then did the doctors check for a fetal heartbeat and realize the baby was alive. The couple was medically evacuated by air to Montreal, Canada, then taken to the Sainte-Justine University Hospital Center. Five hours later, Camille Girard-Bock was born, weighing just 920 grams (2 pounds). Babies born so early are fragile and underdeveloped. Their lungs are particularly delicate: the organs lack the slippery substance, called surfactant, that prevents the airways from collapsing upon exhalation. Fortunately for Girard and her family, Sainte-Justine had recently started giving surfactant, a new treatment at the time, to premature babies. After three months of intensive care, Girard took her baby home. Today, Camille Girard-Bock is 27 years old and studying for a PhD in biomedical sciences at the University of Montreal. Working with researchers at Sainte-Justine, she’s addressing the long-term consequences of being born extremely premature — defined, variously, as less than 25–28 weeks in gestational age. Families often assume they will have grasped the major issues arising from a premature birth once the child reaches school age, by which time any neurodevelopmental problems will have appeared, Girard-Bock says. But that’s not necessarily the case. Her PhD advisers have found that young adults of this population exhibit risk factors for cardiovascular disease — and it may be that more chronic health conditions will show up with time.

Keyword: Development of the Brain
Link ID: 27279 - Posted: 06.04.2020

By Laura Sanders The heart has its own “brain.” Now, scientists have drawn a detailed map of this little brain, called the intracardiac nervous system, in rat hearts. The heart’s big boss is the brain, but nerve cells in the heart have a say, too. These neurons are thought to play a crucial role in heart health, helping to fine-tune heart rhythms and perhaps protecting people against certain kinds of heart disease. But so far, this local control system hasn’t been mapped in great detail. To make their map, systems biologist James Schwaber at Thomas Jefferson University in Philadelphia and colleagues imaged male and female rat hearts with a method called knife-edge scanning microscopy, creating detailed pictures of heart anatomy. Those images could then be built into a 3-D model of the heart. The scientists also plucked out individual neurons and measured the amount of gene activity within each cell. These measurements helped sort the heart’s neurons into discrete groups. Most of these neuron clusters dot the top of the heart, where blood vessels come in and out. Some of these clusters spread down the back of the heart, and were particularly abundant on the left side. With this new view of the individual clusters, scientists can begin to study whether these groups have distinct jobs. The comprehensive, 3-D map of the heart’s little brain could ultimately lead to targeted therapies that could treat or prevent heart diseases, the authors write online May 26 in iScience. © Society for Science & the Public 2000–2020.

Keyword: Development of the Brain
Link ID: 27274 - Posted: 06.03.2020

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

Keyword: Autism; Glia
Link ID: 27273 - Posted: 06.01.2020

By Tina Hesman Saey A genetic variant that raises one’s risk of developing Alzheimer’s disease may also make people more susceptible to COVID-19. People with two copies of a version of the APOE gene called APOE4 are 14 times as likely to develop Alzheimer’s disease as people with two copies of the APOE3 version of the gene (SN: 9/22/17). Those people were also more than twice as likely to test positive for the coronavirus than people with two copies of the APOE3 version, researchers report May 26 in the Journals of Gerontology: Series A. The results come from a study of more than 600 people in England diagnosed with COVID-19 from March 16 to April 26. Two previous studies showed that people with dementia were more likely to have severe cases or to die of COVID-19. This new study found that even people with no signs of dementia or other diseases associated with having APOE4 were still more susceptible to COVID-19 than people with the APOE3 version. Among nearly 400,000 participants in the large genetic database called the UK Biobank, only 3 percent have two copies of APOE4, while 69 percent have two copies of APOE3. The remainder have one of each version. But the APOE4 version was more common than expected among people diagnosed with COVID-19, the study found. Of 622 people who tested positive for the coronavirus, 37 had two copies of APOE4. On a population scale, that means about 410 of every 100,000 people with two copies of that version of the gene would test positive, the researchers calculate. That compares with 179 of every 100,000 people with two copies of APOE3 testing positive. © Society for Science & the Public 2000–2020.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27271 - 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

Keyword: Autism; Genes & Behavior
Link ID: 27270 - Posted: 05.29.2020

A team of researchers has generated a developmental map of a key sound-sensing structure in the mouse inner ear. Scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health, and their collaborators analyzed data from 30,000 cells from mouse cochlea, the snail-shaped structure of the inner ear. The results provide insights into the genetic programs that drive the formation of cells important for detecting sounds. The study also sheds light specifically on the underlying cause of hearing loss linked to Ehlers-Danlos syndrome and Loeys-Dietz syndrome. The study data is shared on a unique platform open to any researcher, creating an unprecedented resource that could catalyze future research on hearing loss. Led by Matthew W. Kelley, Ph.D., chief of the Section on Developmental Neuroscience at the NIDCD, the study appeared online in Nature Communications(link is external). The research team includes investigators at the University of Maryland School of Medicine, Baltimore; Decibel Therapeutics, Boston; and King’s College London. “Unlike many other types of cells in the body, the sensory cells that enable us to hear do not have the capacity to regenerate when they become damaged or diseased,” said NIDCD Director Debara L. Tucci, M.D., who is also an otolaryngology-head and neck surgeon. “By clarifying our understanding of how these cells are formed in the developing inner ear, this work is an important asset for scientists working on stem cell-based therapeutics that may treat or reverse some forms of inner ear hearing loss.”

Keyword: Hearing; Development of the Brain
Link ID: 27268 - Posted: 05.29.2020

Jef Akst The APOE ε4 gene variant that puts people at a greater risk of developing Alzheimer’s disease also has a link to COVID-19. According to a study published today (May 26) in The Journals of Gerontology, Series A, carrying two copies of the variant, often called APOE4, makes people twice as likely to develop a severe form of the disease, which is caused by the SARS-CoV-2 coronavirus currently spreading around the world. David Melzer of Exeter University and colleagues used genetic and health data on volunteers in the UK Biobank to look at the role of the APOE4 variant, which affects cholesterol transport and inflammation. Of some 383,000 people of European descent included in the study, more than 9,000 carried two copies. The researchers cross-referenced this list with people who tested positive for COVID-19 between March 16 and April 26—the assumption being that most such cases were severe because testing at the time was largely limited to hospital settings. The analysis suggested that the APOE4 homozygous genotype was linked to a doubled risk of severe disease, compared with people who had two copies of another variant called ε3. The result isn’t due to nursing home settings or to a greater likelihood of having a diagnosis of dementia, which none of the 37 people with two copies of APOE4 who tested positive for COVID-19 had. “It is pretty bulletproof—whatever associated disease we remove, the association is still there,” Melzer tells The Guardian. “So it looks as if it is the gene variant that is doing it.” © 1986–2020 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27267 - Posted: 05.29.2020

R. Douglas Fields Discoveries that transcend boundaries are among the greatest delights of scientific research, but such leaps are often overlooked because they outstrip conventional thinking. Take, for example, a new discovery for treating dementia that defies received wisdom by combining two formerly unrelated areas of research: brain waves and the brain’s immune cells, called microglia. It’s an important finding, but it still requires the buy-in and understanding of researchers to achieve its true potential. The history of brain waves shows why. In 1887, Richard Caton announced his discovery of brain waves at a scientific meeting. “Read my paper on the electrical currents of the brain,” he wrote in his personal diary. “It was well received but not understood by most of the audience.” Even though Caton’s observations of brain waves were correct, his thinking was too unorthodox for others to take seriously. Faced with such a lack of interest, he abandoned his research and the discovery was forgotten for decades. Flash forward to October 2019. At a gathering of scientists that I helped organize at the annual meeting of the Society for Neuroscience in Chicago, I asked if anyone knew of recent research by neuroscientists at the Massachusetts Institute of Technology who had found a new way to treat Alzheimer’s disease by manipulating microglia and brain waves. No one replied. I understood: Scientists must specialize to succeed. Biologists studying microglia don’t tend to read papers about brain waves, and brain wave researchers are generally unaware of glial research. A study that bridges these two traditionally separate disciplines may fail to gain traction. But this study needed attention: Incredible as it may sound, the researchers improved the brains of animals with Alzheimer’s simply by using LED lights that flashed 40 times a second. Even sound played at this charmed frequency, 40 hertz, had a similar effect. All Rights Reserved © 2020

Keyword: Alzheimers; Glia
Link ID: 27264 - Posted: 05.28.2020

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.

Keyword: Autism; Genes & Behavior
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

Keyword: Autism; Genes & Behavior
Link ID: 27256 - Posted: 05.20.2020

By Nicholas Bakalar Eating foods high in flavonoids — a group of nutrients found in many fruits and vegetables — may lower your risk for dementia, researchers report. The study, in the American Journal of Clinical Nutrition, looked at 2,801 men and women who were 50 and older and free of dementia at the start. Over an average of 20 years of follow-up, researchers gathered diet information at five periodic health examinations; during that time, 193 of the participants developed Alzheimer’s disease or other forms of dementia. Compared with those in the 15th percentile or lower for flavonoid intake, those in the 60th or higher had a 42 to 68 percent lower risk for dementia, depending on the type of flavonoid consumed. Intake of one type of flavonoid, anthocyanins, abundant in blueberries, strawberries and red wine, had the strongest association with lowered risk. Apples, pears, oranges, bananas and tea also contributed. The study controlled for many health and behavioral characteristics, including how strongly participants adhered to the government’s Dietary Guidelines for Americans, which in addition to fruits and vegetables emphasize whole grains, lean meats and other heart-healthy foods. The senior author, Paul F. Jacques, a scientist with the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, said that the amount consumed by those who benefited the most was not large. Their monthly average was about seven half-cup servings of strawberries or blueberries, eight apples or pears, and 17 cups of tea. “It doesn’t take much,” he said. “A couple of servings of berries a week, maybe an apple or two.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27255 - Posted: 05.20.2020

By Ellen Ruppel Shell My first day in Mexico City was tough. The smog was so thick that I gasped for breath while climbing the stairs to my hotel room. I had braced for headaches from the high altitude and thin air, but I was not prepared for how dirty that air was or for the bloodshot eyes and burning lungs. Declared the world's most polluted metropolis by the United Nations in 1992, greater Mexico City has worked hard to clean up its act. To some degree it has: the city is rightfully proud of its miles of bike paths and lush parks. Yet a casual glance at the smudged horizon shows that those efforts are not enough. Most days the area has levels of airborne sooty particles that greatly exceed standards set by the World Health Organization, as well as elevated amounts of other pollutants. Clogged with more than 9.6 million vehicles and an estimated 50,000 smokestacks, Mexico City stews in a toxic brew known to corrode human lungs and hearts. Now many scientists agree that this pollution also damages the brain. In 2018 a study found lesions known to be hallmarks of Alzheimer's disease in the brains of Mexico City residents in their 30s and 40s—decades before signs of the disease normally can be detected—and tied this damage to exposure to the city's bad air. The researchers who did that work, who are from institutions in Mexico and the U.S., have also found early forms of this frightening damage in infants and young children. And Mexico City is not the only place where bad air has been linked to Alzheimer's. Just a few years ago a team of Harvard scientists released data from a large study of 10 million Medicare recipients ages 65 and older living in 50 different cities in the northeastern U.S. The researchers reported a strong correlation between exposure to specific air pollutants and a number of neurodegenerative disorders, including Alzheimer's. © 2020 Scientific American

Keyword: Alzheimers; Neurotoxins
Link ID: 27247 - Posted: 05.14.2020

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

Keyword: Autism; Hormones & Behavior
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

Keyword: Autism; Genes & Behavior
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.

Keyword: Autism; Sleep
Link ID: 27238 - Posted: 05.08.2020

Ashley Yeager In the spring of 2019, neuroscientist Heather Cameron set up a simple experiment. She and her colleagues put an adult rat in the middle of a plastic box with a water bottle at one end. They waited until the rat started drinking and then made a startling noise to see how the animal would respond. The team did this repeatedly with regular rats and with animals that were genetically altered so that they couldn’t make new neurons in their hippocampuses, a brain region involved in learning and memory. When the animals heard the noise, those that could make new hippocampal neurons immediately stopped slurping water and looked around, but the animals lacking hippocampal neurogenesis kept drinking. When the team ran the experiment without the water bottle, both sets of rats looked around right away to figure out where the sound was coming from. Rats that couldn’t make new neurons seemed to have trouble shifting their attention from one task to another, the researchers concluded. “It’s a very surprising result,” says Cameron, who works at the National Institute of Mental Health (NIMH) in Bethesda, Maryland. Researchers studying neurogenesis in the adult hippocampus typically conduct experiments in which animals have had extensive training in a task, such as in a water maze, or have experienced repetitive foot shocks, she explains. In her experiments, the rats were just drinking water. “It seemed like there would be no reason that the hippocampus should have any role,” she says. Yet in animals engineered to lack hippocampal neurogenesis, “the effects are pretty big.” The study joins a growing body of work that challenges the decades-old notion that the primary role of new neurons within the adult hippocampus is in learning and memory. More recently, experiments have tied neurogenesis to forgetting, one possible way to ensure the brain doesn’t become overloaded with information it doesn’t need, and to anxiety, depression, stress, and, as Cameron’s work suggests, attention. Now, neuro-scientists are rethinking the role that new neurons, and the hippocampus as a whole, play in the brain. © 1986–2020 The Scientist.

Keyword: Neurogenesis; Learning & Memory
Link ID: 27236 - Posted: 05.06.2020

Michael Marshall In 2018, psychiatrist Oleguer Plana-Ripoll was wrestling with a puzzling fact about mental disorders. He knew that many individuals have multiple conditions — anxiety and depression, say, or schizophrenia and bipolar disorder. He wanted to know how common it was to have more than one diagnosis, so he got his hands on a database containing the medical details of around 5.9 million Danish citizens. He was taken aback by what he found. Every single mental disorder predisposed the patient to every other mental disorder — no matter how distinct the symptoms1. “We knew that comorbidity was important, but we didn’t expect to find associations for all pairs,” says Plana-Ripoll, who is based at Aarhus University in Denmark. The study tackles a fundamental question that has bothered researchers for more than a century. What are the roots of mental illness? In the hope of finding an answer, scientists have piled up an enormous amount of data over the past decade, through studies of genes, brain activity and neuroanatomy. They have found evidence that many of the same genes underlie seemingly distinct disorders, such as schizophrenia and autism, and that changes in the brain’s decision-making systems could be involved in many conditions. Researchers are also drastically rethinking theories of how our brains go wrong. The idea that mental illness can be classified into distinct, discrete categories such as ‘anxiety’ or ‘psychosis’ has been disproved to a large extent. Instead, disorders shade into each other, and there are no hard dividing lines — as Plana-Ripoll’s study so clearly demonstrated. © 2020 Springer Nature Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27235 - Posted: 05.06.2020

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

Keyword: Autism; Attention
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

Keyword: Autism
Link ID: 27223 - Posted: 04.30.2020