Chapter 7. Life-Span Development of the Brain and Behavior

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By Nancy Clanton, Studies have shown COVID-19 can cause brain complications in some patients’ brains, from memory problems to strokes. A new study has found the brains of people who died from COVID-19 were remarkably similar to the brains of people who die from Alzheimer’s and Parkinson’s, showing inflammation and disrupted circuitry, researchers reported. “The brains of patients who died from severe COVID-19 showed profound molecular markers of inflammation, even though those patients didn’t have any reported clinical signs of neurological impairment,” study co-senior author Tony Wyss-Coray, a professor of neurology and neurological sciences at Stanford University, said in a press release. According to Wyss-Coray, about a third of hospitalized COVID-19 patients report neurological symptoms, such as fuzzy thinking, forgetfulness, difficulty concentrating and depression, and these problems continue for long haul patients even when they’ve recovered from COVID. For their study, his team analyzed brain tissue from eight people who died of COVID-19 and 14 who died of other causes. The researchers found significant inflammation in the brains of the deceased COVID-19 patients. However, their brain tissue showed no signs of SARS-CoV-2, the virus that causes COVID-19. Wyss-Coray added that scientists disagree about whether the virus is present in COVID-19 patients’ brains. © 2021 The Atlanta Journal-Constitution.

Keyword: Parkinsons; Alzheimers
Link ID: 27871 - Posted: 06.23.2021

by Charles Q. Choi Mutations in CUL3, a leading autism gene, may disrupt the movements of neurons during development and interrupt the precise assembly of the brain, a new study suggests. Correcting this misdirection could lead to a therapy for autism in people with CUL3 mutations, the researchers say. Mutations that knock CUL3 out of commission are linked not only with autism, but also with varying levels of intellectual disability, movement problems, attention deficit hyperactivity disorder, epilepsy and sleep disturbances. Scientists have thoroughly explored how the protein that CUL3 encodes helps tag and break down other, expendable proteins in cells, but much remains unknown about its role in the developing brain. For the new work, researchers made mice that have only one functioning CUL3 gene instead of the usual two. These mice have movement problems, diminished sociability and poor memory — traits reminiscent of those in people with CUL3 mutations. The team also engineered mice in which they could knock out one copy of CUL3 by giving the rodents the cancer drug tamoxifen. Turning off CUL3 in 30-day-old juvenile mice had little effect, which suggests that CUL3 mutations contribute to autism-like behaviors during brain development, the researchers say. Identifying this window “is critical to consider for future critical trials,” says lead investigator Gaia Novarino, professor of neuroscience at the Institute of Science and Technology in Klosterneuburg, Austria. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27870 - Posted: 06.23.2021

By Diana Kwon Long before the earliest animals swam through the water-covered surface of Earth’s ancient past, one of the most important encounters in the history of life took place. A primitive bacterium was engulfed by our oldest ancestor — a solo, free-floating cell. The two fused to form a mutually beneficial relationship that has lasted more than a billion years, with the latter providing a safe, comfortable home and the former becoming a powerhouse, fueling the processes necessary to maintain life. That’s the best hypothesis to date for how the cellular components, or organelles, known as mitochondria came to be. Today, trillions of these bacterial descendants live within our bodies, churning out ATP, the molecular energy source that sustains our cells. Despite being inextricably integrated into the machinery of the human body, mitochondria also carry remnants of their bacterial past, such as their own set of DNA. The DNA that constitutes the human genome is contained within the nucleus of our cells. But mitochondria possess their own set of circular DNA, which is likely a remnant of their ancient bacterial past. These features make mitochondria both a critical element of our cells and a potential source of problems. Like the DNA inside the nuclei of our cells that makes up the human genome, mitochondrial DNA can harbor mutations. Age, stress and other factors may disrupt mitochondria’s many functions. On top of that, mitochondrial injury can release molecules that, due to their similarities to those made by bacteria, can be mistaken by our immune system as foreign invaders, triggering a harmful inflammatory response against our own cells. © 2021 Annual Reviews, Inc

Keyword: Schizophrenia; Alzheimers
Link ID: 27863 - Posted: 06.19.2021

Christopher M. Filley One of the most enduring themes in human neuroscience is the association of higher brain functions with gray matter. In particular, the cerebral cortex—the gray matter of the brain's surface—has been the primary focus of decades of work aiming to understand the neurobiological basis of cognition and emotion. Yet, the cerebral cortex is only a few millimeters thick, so the relative neglect of the rest of the brain below the cortex has prompted the term “corticocentric myopia” (1). Other regions relevant to behavior include the deep gray matter of the basal ganglia and thalamus, the brainstem and cerebellum, and the white matter that interconnects all of these structures. On page 1304 of this issue, Zhao et al. (2) present compelling evidence for the importance of white matter by demonstrating genetic influences on structural connectivity that invoke a host of provocative clinical implications. Insight into the importance of white matter in human behavior begins with its anatomy (3–5) (see the figure). White matter occupies about half of the adult human brain, and some 135,000 km of myelinated axons course through a wide array of tracts to link gray matter regions into distributed neural networks that serve cognitive and emotional functions (3). The human brain is particularly well interconnected because white matter has expanded more in evolution than gray matter, which has endowed the brain of Homo sapiens with extensive structural connectivity (6). The myelin sheath, white matter's characteristic feature, appeared late in vertebrate evolution and greatly increased axonal conduction velocity. This development enhanced the efficiency of distributed neural networks, expanding the transfer of information throughout the brain (5). Information transfer serves to complement the information processing of gray matter, where neuronal cell bodies, synapses, and a variety of neurotransmitters are located (5). The result is a brain with prodigious numbers of both neurons and myelinated axons, which have evolved to subserve the domains of attention, memory, emotion, language, perception, visuospatial processing, executive function (5), and social cognition (7). © 2021 American Association for the Advancement of Science.

Keyword: Development of the Brain; Attention
Link ID: 27862 - Posted: 06.19.2021

Scientists studied the brain activity of school-aged children during development and found that regions that activated upon seeing limbs (hands, legs, etc.) subsequently activated upon seeing faces or words when the children grew older. The research, by scientists at Stanford University, Palo Alto, California, reveals new insights about vision development in the brain and could help inform prevention and treatment strategies for learning disorders. The study was funded by the National Eye Institute and is published in Nature Human Behaviour. “Our study addresses how experiences, such as learning to read, shape the developing brain,” said Kalanit Grill-Spector, Ph.D., a professor at Stanford University’s Wu Tsai Neurosciences Institute. “Further, it sheds light on the initial functional role of brain regions that later in development process written words, before they support this important skill of reading.” Grill-Spector’s team used functional MRI to study areas in the ventral temporal cortex (VTC) that are stimulated by the recognition of images. About 30 children, ages 5 to 12 at their first MRI, participated in the study. While in the MRI scanner, the children viewed images from 10 different categories, including words, body parts, faces, objects, and places. The researchers mapped areas of VTC that exhibited stimulation and measured how they changed in intensity and volume on the children’s subsequent MRI tests over the next one to five years. Results showed that VTC regions corresponding to face and word recognition increased with age. Compared to the 5-9-year-olds, teenagers had twice the volume of the word-selective region in VTC. Notably, as word-selective VTC volume doubled, limb-selective volume in the same region halved. According to the investigators, the decrease in limb-selectivity is directly linked to the increase in word- and face-selectivity, providing the first evidence for cortical recycling during childhood development.

Keyword: Vision; Development of the Brain
Link ID: 27860 - Posted: 06.19.2021

Andrew Anthony David Eagleman, 50, is an American neuroscientist, bestselling author and presenter of the BBC series The Brain, as well as co-founder and chief executive officer of Neosensory, which develops devices for sensory substitution. His area of speciality is brain plasticity, and that is the subject of his new book, Livewired, which examines how experience refashions the brain, and shows that it is a much more adaptable organ than previously thought. For the past half-century or more the brain has been spoken of in terms of a computer. What are the biggest flaws with that particular model? It’s a very seductive comparison. But in fact, what we’re looking at is three pounds of material in our skulls that is essentially a very alien kind of material to us. It doesn’t write down memories, the way we think of a computer doing it. And it is capable of figuring out its own culture and identity and making leaps into the unknown. I’m here in Silicon Valley. Everything we talk about is hardware and software. But what’s happening in the brain is what I call livewire, where you have 86bn neurons, each with 10,000 connections, and they are constantly reconfiguring every second of your life. Even by the time you get to the end of this paragraph, you’ll be a slightly different person than you were at the beginning. In what way does the working of the brain resemble drug dealers in Albuquerque? It’s that the brain can accomplish remarkable things without any top-down control. If a child has half their brain removed in surgery, the functions of the brain will rewire themselves on to the remaining real estate. And so I use this example of drug dealers to point out that if suddenly in Albuquerque, where I happened to grow up, there was a terrific earthquake, and half the territory was lost, the drug dealers would rearrange themselves to control the remaining territory. It’s because each one has competition with his neighbours and they fight over whatever territory exists, as opposed to a top-down council meeting where the territory is distributed. And that’s really the way to understand the brain. It’s made up of billions of neurons, each of which is competing for its own territory. © 2021 Guardian News & Media Limited

Keyword: Development of the Brain; Stroke
Link ID: 27855 - Posted: 06.16.2021

By Carolyn Wilke Scientists have long sought to prevent sharp memories from dulling with age, but the problem remains stubborn. Now research published in Scientific Reports suggests virtual reality might help older people recall facts and events based on specific details. The study involved 42 healthy older adults from the San Francisco Bay Area. Half spent a dozen hours over four weeks playing a virtual-reality game called Labyrinth; they strapped on headsets and walked in place, roaming virtual neighborhoods while completing errands. The other half, in the control group, used electronic tablets to play games that did not require navigating or recalling details. After 15 sessions, the latter performed roughly the same as before on a long-term memory test based on picking out objects they had seen about an hour earlier. But the Labyrinth players' scores rose, and they were less frequently tricked by objects that resembled ones they had viewed. Those improvements “brought them back up to the level of another group of younger adults who did the same memory tests,” says cognitive neuroscientist Peter Wais of the University of California, San Francisco. He and his colleagues designed the VR game, which they say likely stimulates the hippocampus—a brain area important for long-term memory. The team did not observe improvement on two other tests, which measured autobiographical memory and spatial memory capability. © 2021 Scientific American,

Keyword: Learning & Memory; Alzheimers
Link ID: 27853 - Posted: 06.16.2021

By Pam Belluck and Rebecca Robbins In a powerful statement of disagreement with the Food and Drug Administration’s approval of Biogen’s controversial Alzheimer’s drug, three scientists have resigned from the independent committee that advised the agency on the treatment. “This might be the worst approval decision that the F.D.A. has made that I can remember,” said Dr. Aaron Kesselheim, a professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, who submitted his resignation Thursday after six years on the committee. He said the agency’s approval of the drug, aducanumab, which is being marketed as Aduhelm, a monthly intravenous infusion that Biogen has priced at $56,000 per year, was wrong “because of so many different factors, starting from the fact that there’s no good evidence that the drug works.” Two other members of the committee resigned earlier this week, expressing dismay at the approval of the drug despite the committee’s overwhelming rejection of it after reviewing clinical trial data in November. The committee had found that the evidence did not convincingly show that Aduhelm could slow cognitive decline in people in the early stages of the disease — and that the drug could cause potentially serious side effects of brain swelling and brain bleeding. None of the 11 members of the committee considered the drug ready for approval: Ten voted against and one was uncertain. “Approval of a drug that is not effective has serious potential to impair future research into new treatments that may be effective,” said Dr. Joel Perlmutter, a neurologist at Washington University School of Medicine in St. Louis, who was the first to resign from the committee. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 27849 - Posted: 06.11.2021

By Laurie McGinley The Food and Drug Administration on Monday approved the first Alzheimer’s treatment intended to slow cognitive decline, a move hailed by patients and advocates but sharply criticized by others who argued there was not sufficient evidence that the drug works. The medication, called aducanumab, is the first drug cleared for Alzheimer’s that is designed to alter the course of the disease by slowing the deterioration of brain function — not just to ease symptoms. No Alzheimer’s treatment has been approved since 2003, reflecting the extraordinarily high failure rate of drugs developed for the illness. But in an explicit acknowledgment of the uncertainties about the effectiveness of the drug, the FDA did not grant the medication full approval. Instead, the agency cleared the drug — its brand name will be Aduhelm — based on its ability to reduce clumps of amyloid beta in the brain, a hallmark of the disease. It ordered the drug’s maker, the biotech giant Biogen, to conduct a post-approval study confirming the medicine actually slows cognitive deterioration. If the medication does not provide such a clinical benefit, the FDA’s approval could be withdrawn. Patrizia Cavazzoni, director of the FDA’s Center for Drug Evaluation and Research, said officials believe it is “reasonably likely” that the reduction in amyloid clumps will confer “important benefits to patients.” Monday’s FDA decision was the most contentious in years and followed prolonged debate among researchers, doctors, patients and advocates about whether the medication works — a consequence of the drug’s complicated history. One of the biggest points of disagreement is whether a reduction in amyloid beta, a sticky compound that many scientists believe damages communication between brain cells and eventually kills them, results in a slowdown in cognitive decline. © 1996-2021 The Washington Post

Keyword: Alzheimers
Link ID: 27846 - Posted: 06.08.2021

Laurie McGinley When Phil Gutis was diagnosed with early-stage Alzheimer’s disease at 54, he immediately enrolled in a clinical trial for an experimental drug but had little hope of being helped. Over time, though, he started feeling better, his brain less cloudy. “There was just a fogginess I remember having a couple of years ago that I don’t really feel I have now,” said Gutis, who has received monthly infusions of a medication called aducanumab for five years, except for a short interruption. Now, he is hoping others with the disease will have a chance to try the drug. But he is worried that the Food and Drug Administration, which is weighing whether to approve the drug, will reject it, derailing the medication and jeopardizing his ability to get the treatment. “Would my world become fuzzy again?” said Gutis, who lives in New Hope, Pa., with his husband and is a former reporter. “I don’t want to go backward.” By June 7, the FDA is expected to make one of its most important decisions in years: whether to approve the drug for mild cognitive impairment or early-stage dementia caused by Alzheimer’s. It would be the first treatment ever sold to slow the deterioration in brain function caused by the disease, not just to ease symptoms. And it would be the first new Alzheimer’s treatment since 2003. The medication is a monoclonal antibody, a protein made in the laboratory that can bind to substances — in this case, clumps of amyloid beta, a sticky plaque compound that many scientists believe damages communication between brain cells and eventually kills them. The treatment is designed to trigger an immune response that removes the plaques.

Keyword: Alzheimers
Link ID: 27839 - Posted: 06.02.2021

Amanda Heidt A damaged drainage system in the brain might be behind the spotty performance of some Alzheimer’s therapies, according to a study published April 28 in Nature. Mice modeling the neurodegenerative disorder that received plaque-busting antibodies along with a treatment to stimulate the growth of lymphatic vessels in the brain saw many of their symptoms reversed. Mice with damaged lymphatics, on the other hand, didn’t respond as well to the antibodies. This suggests that dysfunctional lymphatics might hinder the performance of antibody-based immunotherapy, an approach that has had mixed results in clinical trials among Alzheimer’s patients. “Whenever a paper provides us with a novel way to look at Alzheimer’s, such as this one does . . . it opens up a world of possibilities,” says Gabrielle Britton, a neuroscientist at the Instituto de Investigaciones Científicas y Servicios de Alta Tecnología in Panama who was not involved in the research. “The methods are sound, and [the fact] that they use several different approaches that converge on the same findings suggests a very strong paper.” The buildup of amyloid-β plaques in the brain is a hallmark of the disease, and one of the most promising immunotherapies has been a monoclonal antibody called aducanumab that breaks them up. But two clinical trials were discontinued after they yielded contradictory results, and scientists have been working ever since to figure out why as the companies continue to move forward with new trials of the therapy. The working hypothesis, Britton tells The Scientist, is that the discrepancy stems from some unexplained variation among participants. © 1986–2021 The Scientist.

Keyword: Alzheimers
Link ID: 27835 - Posted: 05.29.2021

By Mitch Leslie For the past 3 years, about 6000 middle-aged and elderly Australians have pumped iron, loaded up on greens and whole grains, strived to quell stress, and challenged their wits with computer exercises, all in an effort to preserve their cognition. They’re part of a clinical trial called Maintain Your Brain, one of about 30 current or planned studies that eschew pharmaceutical interventions and test whether altering multiple aspects of participants’ lives improves brain health. Such multidomain studies may finally reveal whether modifying diet, exercise, and other factors can slow cognitive decline as people age—or even prevent dementia. “There’s a lot of hope for multidomain trials,” says psychologist Kaarin Anstey of the University of New South Wales, Sydney, one of the principal investigators of the Maintain Your Brain trial, which will finish by the end of this year. Although people can’t escape some mental decline as they get older, lifestyle exerts a powerful influence over the risk of developing dementia—the type of severe cognitive impairment seen in conditions such as Alzheimer’s disease. Last year, an international committee of scientists and psychiatrists known as the Lancet Commission on dementia prevention, intervention, and care estimated that so-called modifiable factors account for 40% of dementia risk. Their report highlighted a dozen factors, including many familiar villains—diabetes, high blood pressure, smoking, obesity, and lack of exercise. Researchers are still probing exactly how these risk factors steal people’s faculties, but they’ve identified some likely mechanisms. Lack of physical activity may impair cognition, for instance, because exercise stimulates formation of new neurons and soothes brain inflammation. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers; Obesity
Link ID: 27834 - Posted: 05.29.2021

By Bill Hathaway A massive genome-wide association study (GWAS) of genetic and health records of 1.2 million people from four separate data banks has identified 178 gene variants linked to major depression, a disorder that will affect one of every five people during their lifetimes. The results of the study, led by the U.S. Department of Veterans Affairs (V.A.) researchers at Yale University School of Medicine and University of California-San Diego (UCSD), may one day help identify people most at risk of depression and related psychiatric disorders and help doctors prescribe drugs best suited to treat the disorder. The study was published May 27 in the journal Nature Neuroscience. For the study, the research team analyzed medical records and genomes collected from more than 300,000 participants in the V.A.’s Million Veteran Program (MVP), one of the largest and most diverse databanks of genetic and medical information in the world. These new data were combined in a meta-analysis with genetic and health records from the UK Biobank, FinnGen (a Finland-based biobank), and results from the consumer genetics company 23andMe. This part of the study included 1.2 million participants. The researchers crosschecked their findings from that analysis with an entirely separate sample of 1.3 million volunteers from 23andMe customers. When the two sets of data from the different sources were compared, genetic variants linked to depression replicated with statistical significance for most of the markers tested. Copyright © 2021 Yale University

Keyword: Depression; Genes & Behavior
Link ID: 27833 - Posted: 05.29.2021

By Peter Mundy Since the modern era of research on autism began in the 1980s, questions about social cognition and social brain development have been of central interest to researchers. This year marks the 20th anniversary of the first annual meeting of the International Society for Autism Research (INSAR), and it is evident in this year’s meeting that the growth of social-cognitive neuroscience over the past two decades has significantly enriched autism science. For those unfamiliar with the term, social-cognitive neuroscience is the study of the brain systems that are involved in the causes and effects of social behaviors and social interaction. Some of these involve brain systems involved in thinking about other people’s thoughts or intentions, empathizing, social motivation and the impact of social attention on an individual’s thinking and emotions. At the same time, research with and for autistic people has also enriched social-cognitive neuroscience and the understanding of how our social minds develop. Autism spectrum disorder (ASD) is a complex and heterogeneous part of the human condition, or neurodiversity. It is associated with a wide range of life outcomes, from “disorder” or the profound challenges that encumber about 30 percent of affected individuals with minimal language and intellectual disability, to “differences” among people who have well-above-average abilities and accomplishments. Regardless of their outcomes, though, people on the autism spectrum travel a different path of social-cognitive neurodevelopment that appears to begin in infancy. For example, many experience some level of difficulty with social-cognitive mentalizing, also known as “theory of mind”—the mental representation of other people’s thoughts, perspectives, beliefs, intentions or emotions, which enables us to understand or predict their behaviors. © 2021 Scientific American

Keyword: Autism
Link ID: 27824 - Posted: 05.19.2021

By Daniela Kaufer, Alon Friedman It was the middle of the night in Jerusalem, and we were watching mice swim. The year was 1994, and the two of us were crouching over a pool of cold water in a laboratory at the Hebrew University. The room was chilly, our hunched backs ached, and we had been repeating this routine over many nights, so we were tired and uncomfortable. So were the mice. Mice really dislike swimming, especially in cold water—but we wanted to stress them out. We humans were on the night shift because both of us had other things to do during the day. Kaufer was working on a doctorate in molecular neurobiology, and Friedman was an Israel Defense Forces physician and was often on call. What brought us together with the mice every evening was an attempt to understand a medical mystery: Gulf War syndrome. After the conflict ended in 1991, there were an increasing number of reports of soldiers from the U.S.-led coalition who were afflicted with chronic fatigue, muscle pain, sleep problems and cognitive deterioration, and those soldiers were hospitalized at higher rates than nondeployed veterans. Some doctors suspected that pyridostigmine, a drug that had been given to soldiers to protect them from chemical weapons, could cause these ailments if it made it into their brains. There was a big problem with this theory, however: pyridostigmine in the bloodstream was not supposed to reach the brain. Blood vessels that course through this vital organ have walls made of specialized cells, packed very closely and with abilities to control what can get in and out. They form a shield that keeps toxins, pathogens such as bacteria, and most drugs safely within the vessels. This structure is called the blood-brain barrier, or BBB for short, and the drug should not have been able to pass through it. © 2021 Scientific American

Keyword: Alzheimers
Link ID: 27816 - Posted: 05.12.2021

by Laura Dattaro Many genes linked to autism, schizophrenia and developmental delay share the same functions: They regulate the expression of other genes and support communication between neurons, according to an unpublished study. Researchers presented the findings virtually today at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Hundreds of genes with diverse functions are linked to autism, but how each contributes to the condition is unclear. In the new work, researchers analyzed the functions of 102 autism-linked genes that previous studies identified by comparing the genetic sequences of thousands of people with autism and those with other conditions, along with their family members and controls. “The genes identified give us an unprecedented opportunity to follow the biology, follow the genetics, to ask the question, where does this converge on function?” said lead investigator Stephan Sanders while presenting the work. Sanders is associate professor of psychiatry at the University of California, San Francisco. Other researchers are studying convergence in 3D brain models called organoids and looking for neuroanatomical similarities and differences across different animal models of autism, including mice and frogs. “Distinguishing causal functions from non-causal functions of these genes is a massive challenge,” Sanders says, and finding points of convergence could help. “The ultimate goal is to identify why disrupting these genes leads to autism.” © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27808 - Posted: 05.08.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27803 - Posted: 05.05.2021

By Jane E. Brody Look and you shall see: A generation of the real-life nearsighted Mr. Magoos is growing up before your eyes. A largely unrecognized epidemic of nearsightedness, or myopia, is afflicting the eyes of children. People with myopia can see close-up objects clearly, like the words on a page. But their distance vision is blurry, and correction with glasses or contact lenses is likely to be needed for activities like seeing the blackboard clearly, cycling, driving or recognizing faces down the block. The growing incidence of myopia is related to changes in children’s behavior, especially how little time they spend outdoors, often staring at screens indoors instead of enjoying activities illuminated by daylight. Gone are the days when most children played outside between the end of the school day and suppertime. And the devastating pandemic of the past year may be making matters worse. Susceptibility to myopia is determined by genetics and environment. Children with one or both nearsighted parents are more likely to become myopic. However, while genes take many centuries to change, the prevalence of myopia in the United States increased from 25 percent in the early 1970s to nearly 42 percent just three decades later. And the rise in myopia is not limited to highly developed countries. The World Health Organization estimates that half the world’s population may be myopic by 2050. Given that genes don’t change that quickly, environmental factors, especially children’s decreased exposure to outdoor light, are the likely cause of this rise in myopia, experts believe. Consider, for example, factors that keep modern children indoors: an emphasis on academic studies and their accompanying homework, the irresistible attraction of electronic devices and safety concerns that demand adult supervision during outdoor play. All of these things drastically limit the time youngsters now spend outside in daylight, to the likely detriment of the clarity of their distance vision. © 2021 The New York Times Company

Keyword: Vision; Development of the Brain
Link ID: 27802 - Posted: 05.05.2021

by Peter Hess Deleting the autism-related gene CHD8 from the intestines induces significant gastrointestinal and behavioral changes in mice, according to a new unpublished study. The results suggest that changes to the gut are involved in some of the behavioral traits seen in people with CHD8 mutations, says lead researcher Evan Elliott, assistant professor of molecular and behavioral neuroscience at Bar-Ilan University in Ramat Gan, Israel. Elliott’s team presented the findings virtually this week at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Up to 90 percent of people with CHD8 mutations report gastrointestinal issues such as constipation, Elliott says. Most also have autism. Mice missing one copy of CHD8 have unusually thin and permeable small intestines, Elliott and his colleagues found. The reason seems to be that these mice have fewer mucus-producing goblet cells than controls, resulting in thinner organ walls and less mucus lining the digestive tract. CHD8 regulates the expression of other genes, so Elliott’s team looked at gene expression levels in the CHD8 mice’s intestinal epithelial cells via RNA sequencing. The mice expressed 920 genes differently than control mice did. These include an increase in the expression of genes involved in inflammatory responses and in antimicrobial activity. The latter set may be the body’s way of compensating for increased microbial populations, Elliott says. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27801 - Posted: 05.05.2021

Jon Hamilton An experimental drug intended for Alzheimer's patients seems to improve both language and learning in adults with Fragile X syndrome. The drug, called BPN14770, increased cognitive scores by about 10% in 30 adult males after 12 weeks, a team reports in the journal Nature Medicine. That is enough to change the lives of many people with Fragile X, says Mark Gurney, CEO of Tetra Therapeutics, developer of the medicine. "People with Fragile X with an IQ of 40 are typically living with their parents or in an institutional setting," Gurney says. "With an IQ of 50, in some cases they're able to ride the bus, they're able to hold a job with some assistance and they're able to function better in their community." But it will take a much larger study to know whether the drug is as good as it seems, says Mark Bear, Picower professor of neuroscience at the Massachusetts Institute of Technology. "This study is certainly not definitive, but it's encouraging," he says. Fragile X syndrome is a genetic disorder that affects about 1 in 4,000 males and a smaller proportion of females. It is the most common inherited cause of intellectual disabilities and autism. The idea of treating Fragile X with an Alzheimer's drug came from Gurney after he learned that both conditions affect a substance called cyclic AMP that helps transmit messages inside cells. © 2021 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 27796 - Posted: 05.01.2021