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

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By William Wan If only Dan Goerke could hold his wife’s hand. Maybe she would talk again. Maybe she would look at him and smile as she used to. Maybe she would eat and stop wasting away. Since the pandemic began, Goerke’s wife, Denise — 63 years old and afflicted with Alzheimer’s disease — had declined dramatically. Left alone in her nursing home, she had lost 16 pounds, could not form the simplest words, no longer responded to the voices of her children. In recent weeks, she had stopped recognizing even the man she loved. Goerke, 61, could tell the isolation was killing his wife, and there was nothing he could do but watch. “Every day it gets a little worse,” he said. “We’ve lost months, maybe years of her already.” Beyond the staggering U.S. deaths caused directly by the novel coronavirus, more than 134,200 people have died from Alzheimer’s and other forms of dementia since March. That is 13,200 more U.S. deaths caused by dementia than expected, compared with previous years, according to an analysis of federal data by The Washington Post. Overlooked amid America’s war against the coronavirus is this reality: People with dementia are dying not just from the virus but from the very strategy of isolation that’s supposed to protect them. In recent months, doctors have reported increased falls, pulmonary infections, depression and sudden frailty in patients who had been stable for years. Social and mental stimulation are among the few tools that can slow the march of dementia. Yet even as U.S. leaders have rushed to reopen universities, bowling alleys and malls, nursing homes say they continue begging in vain for sufficient testing, protective equipment and help.

Keyword: Alzheimers
Link ID: 27478 - Posted: 09.19.2020

by Angie Voyles Askham . Many problems associated with fragile X syndrome stem from a leak in mitochondria, organelles that act as the power stations of the cell, a new study suggests1. Stopping this leak eases some of the autism-like traits of mice that model the syndrome. “The paper is very solid,” says John Jay Gargus, director of the Center for Autism Research and Translation at the University of California, Irvine, who was not involved in the study. And because mitochondrial energy deficiency is seen in other forms of autism, the findings may be relevant beyond fragile X syndrome, Gargus says. Fragile X syndrome results from mutations in the FMR1 gene, which lead to a loss of the protein FMRP. Without FMRP, cells have immature dendritic spines — the bumps along a neuron’s arms that receive input from other neurons — and produce other proteins in excess. These differences are thought to contribute to the syndrome’s characteristic traits, such as developmental delay, intellectual disability and, often, autism. The new study shows that a leak in the mitochondrial membrane, possibly caused by the lack of FMRP, may drive the affected cells’ immaturity and excess protein production. The leak affects a cell’s metabolism, causing it to produce energy quickly but not efficiently, says lead researcher Elizabeth Jonas, professor of internal medicine and neuroscience at Yale University. All cells start out with mitochondrial leaks; the rapid energy production these leaks allow may be useful in early development. As typical cells mature and efficiency becomes more important than speed, however, they seem to close the leaks, Jonas says. Because cells with a fragile X mutation cannot close their leaks, they remain in an immature state. © 2020 Simons Foundation

Keyword: Development of the Brain
Link ID: 27466 - Posted: 09.12.2020

By Nicholas Bakalar Being overweight may be linked to an increased risk for dementia. British researchers used data on 6,582 men and women, age 50 and older, who were cognitively healthy at the start of the study. The analysis, in the International Journal of Epidemiology, tracked the population for an average of 11 years, recording incidents of physician-diagnosed dementia. Almost 7 percent of the group developed dementia. Compared with people of normal weight (body mass index between 18.5 and 24.9), overweight people with a B.M.I. of 25 to 29.9 were 27 percent more likely to develop dementia, and the obese, with a B.M.I. of 30 or higher, were 31 percent more likely to become demented. The researchers also found that women with central obesity — a waist size larger than 34.6 inches — were 39 percent more likely to develop dementia than those with normal waist size. Fat around the middle was not associated with a higher dementia risk in men. The study controlled for age, sex, APOE4 (a gene known to increase the risk of Alzheimer’s disease, the most common form of dementia), education, marital status, smoking and other known dementia risks. The lead author, Yixuan Ma, a student at University College London, said that this observational study does not prove cause and effect. “Being overweight is just a risk,” she said. “It doesn’t mean that an overweight person will necessarily get dementia. But for many reasons, it’s good to maintain a normal weight and engage in vigorous physical activity over a lifetime.” © 2020 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27449 - Posted: 09.05.2020

By Esther Landhuis A researcher slips stickers under some colored cups on a lazy Susan, then gives the tray a whirl. When the spinning stops, a preschooler must find the hidden stickers. Most children remember where the stickers are, but a few have to check every single cup. The game tests working memory, which is among the set of mental skills known as executive function that can be impaired in children who faced trauma early in life. Adversity wreaks havoc, and from there, “you have a system that responds differently,” says Megan Gunnar, a developmental psychobiologist at the University of Minnesota in Minneapolis who has spent two decades studying the impact of early-life adversity in adopted children. The focus of this work is extreme adversity, such as being orphaned, rather than everyday challenges, which might teach beneficial resilience. A childhood characterized by hardship, negligence or abuse can also alter the neuroendocrine system that regulates how the body responds to stress. Problems in the stress response can set kids on a path toward behavior struggles along with increased risk for depression, diabetes and a host of other health problems. But recent studies offer hints that such a difficult future may not be inevitable. As Gunnar and others have shown, impaired stress responses can return to normal during puberty, raising the possibility that imbalances created by early trauma can be erased. The research is prompting a new view of puberty as an opportunity — a chance for people who had a shaky start to reset their physiological responses to stress. © Society for Science & the Public 2000–2020.

Keyword: Stress; Development of the Brain
Link ID: 27441 - Posted: 08.29.2020

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

Keyword: Autism; Emotions
Link ID: 27440 - Posted: 08.29.2020

by Nicholette Zeliadt An experimental drug prevents seizures and death in a mouse model of Dravet syndrome, a severe form of epilepsy that is related to autism, researchers reported 18 October 2019. The drug works by silencing a DNA segment called a ‘poison exon’ and is expected to enter clinical trials next year. If it works, it offers hope for treating not just Dravet, but other forms of autism as well: Another team has identified a poison exon in SYNGAP1, an autism gene that also causes epilepsy. Poison exons seem to impede the production of certain crucial proteins; blocking these segments would restore normal levels of the proteins. “The beauty of the technology,” says Gemma Carvill, assistant professor of neurology and pharmacology at Northwestern University in Chicago, Illinois, “is that “any gene that has a poison exon is potentially a target.” Several teams presented unpublished work on poison exons in a standing-room-only session at the 2019 American Society of Human Genetics meeting in Houston, Texas. People with Dravet often have autism, and most die in childhood2. The syndrome typically stems from mutations in a gene called SCN1A, which encodes an essential sodium channel in neurons. Only about 25 percent of mice with mutations in SCN1A live beyond 30 days of age. The new drug consists of short strands of ‘antisense’ RNA that restore normal levels of the channel, said Lori Isom of the University of Michigan, who presented the work. And all but 1 of 33 mice that received a single injection of the drug at 2 days of age remained alive 88 days later. © 2020 Simons Foundation

Keyword: Epilepsy; Autism
Link ID: 27437 - Posted: 08.29.2020

Although the number of people with dementia continues to increase, the rate of growth has declined by 13 percent in each of the past three decades. The brain disorder currently affects nearly 50 million people worldwide and nearly 6 million in the United States. The new finding, reported by Harvard researchers in the journal Neurology, suggests that the number of people developing dementia in coming years may be less than expected. Nonetheless, that number — known as the prevalence of dementia — is expected to triple in the next 30 years, growing to more than 150 million people worldwide, due in large part to increases in life expectancy and population size. Dementia, which involves deterioration in memory, thinking and behavior beyond what is considered a normal part of aging, includes but is not limited to Alzheimer’s disease, which accounts for 60 to 70 percent of dementia cases. The researchers cited a “somewhat stronger” decline in the rate of growth — referred to as the incidence rate — among men than women (24 percent vs. 8 percent). They projected that, if the trend continues, it is possible that up to 60 million fewer people than expected would develop dementia worldwide by 2040. The researchers did not determine underlying causes of the decline in incidence, but they did note that improvements in lifestyle overall — as well as better control of blood pressure and cardiovascular issues — may have contributed to the decline. Their research was based on data from seven long-term studies, involving 49,202 people 65 and older from six countries in Europe and North America, including the United States. But the database included only people of European ancestry, and other research has found stable or increasing rates of dementia diagnoses in other ethnic and geographic regions. — Linda Searing

Keyword: Alzheimers
Link ID: 27432 - Posted: 08.26.2020

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

Keyword: Autism; Development of the Brain
Link ID: 27430 - Posted: 08.22.2020

When it comes to brain cells, one size does not fit all. Neurons come in a wide variety of shapes, sizes, and contain different types of brain chemicals. But how did they get that way? A new study in Nature suggests that the identities of all the neurons in a worm are linked to unique members of a single gene family that control the process of converting DNA instructions into proteins, known as gene expression. The results of this study could provide a foundation for understanding how nervous systems have evolved in many other animals, including humans. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The central nervous systems of all animals, from worms to humans, are incredibly intricate and highly ordered. The generation and diversity of a plethora of neuronal cell types is driven by gene expression,” said Robert Riddle, Ph.D., program director at NINDS. “So, it is surprising and exciting to consider that the cell diversity we see in the entire nervous system could come from a just a single group of genes.” Researchers led by Oliver Hobert, Ph.D., professor of biochemistry and molecular biophysics at Columbia University in New York City and graduate student Molly B. Reilly, wanted to know how brain cells in the C. elegans worm got their various shapes and functions. For these experiments, the researchers used a genetically engineered worm in which individual neurons were color coded. In addition, coding sequences for green fluorescence protein were inserted into homeobox genes, a highly conserved set of genes known to play fundamental roles in development. Homeobox gene expression patterns were determined by examining the patterns of the glowing fluorescent marker.

Keyword: Development of the Brain; Brain imaging
Link ID: 27428 - Posted: 08.20.2020

By Simon Makin New research could let scientists co-opt biology's basic building block—the cell—to construct materials and structures within organisms. A study, published in March in Science and led by Stanford University psychiatrist and bioengineer Karl Deisseroth, shows how to make specific cells produce electricity-carrying (or blocking) polymers on their surfaces. The work could someday allow researchers to build large-scale structures within the body or improve brain interfaces for prosthetic limbs. In the medium term, the technique may be useful in bioelectric medicine, which involves delivering therapeutic electrical pulses. Researchers in this area have long been interested in incorporating polymers that conduct or inhibit electricity without damaging surrounding tissues. Stimulating specific cells—to intervene in a seizure, for instance—is much more precise than flooding the whole organism with drugs, which can cause broad side effects. But current bioelectric methods, such as those using electrodes, still affect large numbers of cells indiscriminately. The new technique uses a virus to deliver genes to desired cell types, instructing them to produce an enzyme (Apex2) on their surface. The enzyme sparks a chemical reaction between precursor molecules and hydrogen peroxide, infused in the space between cells; this reaction causes the precursors to fuse into a polymer on the targeted cells. “What's new here is the intertwining of various emerging fields in one application,” says University of Florida biomedical engineer Kevin Otto, who was not involved in the research but co-authored an accompanying commentary in Science. “The use of conductive polymers assembled [inside living tissue] through synthetic biology, to enable cell-specific interfacing, is very novel.” © 2020 Scientific American

Keyword: Development of the Brain; Epigenetics
Link ID: 27411 - Posted: 08.11.2020

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

Keyword: Autism; Genes & Behavior
Link ID: 27410 - Posted: 08.11.2020

By Gina Kolata Despite the lack of effective treatments or preventive strategies, the dementia epidemic is on the wane in the United States and Europe, scientists reported on Monday. The risk for a person to develop dementia over a lifetime is now 13 percent lower than it was in 2010. Incidence rates at every age have steadily declined over the past quarter-century. If the trend continues, the paper’s authors note, there will be 15 million fewer people in Europe and the United States with dementia than there are now. The study is the most definitive yet to document a decline in dementia rates. Its findings counter warnings from advocacy groups of a coming tsunami of Alzheimer’s disease, the most common form of dementia, said Dr. John Morris, director of the Center for Aging at Washington University in St. Louis. It is correct that there are now more people than ever with dementia, but that is because there are more and more older people in the population. The new incidence data are “hopeful,” Dr. Morris said. “It is such a strong study and such a powerful message. It suggests that the risk is modifiable.” Researchers at Harvard University in Cambridge, Mass., reviewed data from seven large studies with a total of 49,202 individuals. The studies followed men and women aged 65 and older for at least 15 years, and included in-person exams and, in many cases, genetic data, brain scans and information on participants’ risk factors for cardiovascular disease. The data also include a separate assessment of Alzheimer’s disease. Its incidence, too, has steadily fallen, at a rate of 16 percent per decade, the researchers found. Their study was published in the journal Neurology. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27404 - Posted: 08.06.2020

by Chloe Williams A new atlas lays bare how neuronal connections, or synapses, change from birth to old age in mice1. The ‘synaptome’ may help researchers investigate how mutations linked to autism affect these connections at different stages of life. Synapses are the junctions where information is transferred between cells, and they are integral to functions such as learning, behavior and movement. Autism is linked to several mutations that alter synaptic proteins. In 2018, researchers created the first synaptome of the mouse brain, mapping billions of synapses and sorting them into types based on their size, shape and composition2. The map revealed that synapse subtypes have distinct distributions in the brain, suggesting they have specific functions. This synaptome mapped the mouse brain only at one point in time, however. In the new work, the team charted five billion synapses in mice at 10 different ages, revealing how synapses change in number, structure and molecular makeup throughout life. “It’s the first time anybody’s ever done that in any species,” says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland, who led the research. To create the atlas, the team engineered mice to express fluorescent markers of different colors on two proteins — PSD95 and SAP102 — that frequently line the signal-receiving end of excitatory synapses, which make up the preponderance of synapses in the brain. Mutations in these proteins have been linked to autism, schizophrenia and intellectual disability. © 2020 Simons Foundation

Keyword: Development of the Brain
Link ID: 27402 - Posted: 08.06.2020

Nicola Davis Excessive drinking, exposure to air pollution and head injuries all increase dementia risk, experts say in a report revealing that up to 40% of dementia cases worldwide could be delayed or prevented by addressing 12 such lifestyle factors. Around 50 million people around the world live with dementia, including about 850,000 people in the UK. By 2040, it has been estimated there will be more than 1.2 million people living with dementia in England and Wales. There is currently no cure. However, while some risk factors for dementia cannot be changed, for example particular genes or ethnicity, many are down to lifestyle. “Dementia is potentially preventable – you can do things to reduce your risk of dementia, whatever stage of life you are at,” said Gill Livingston, professor of psychiatry of older people at University College London and a co-author of the report. She added such lifestyle changes could reduce the chances of developing dementia in both those with and without a high genetic risk for such conditions. The report from the Lancet Commission on dementia prevention, intervention and care builds on previous work revealing that about a third of dementia cases could be prevented by addressing nine lifestyle factors, including midlife hearing loss, depression, less childhood education and smoking. The research weighs up the latest evidence, largely from high-income countries, supporting the addition of a further three risk factors to the list. It suggests that 1% of dementia cases worldwide are attributable to excessive mid-life alcohol intake, 3% to mid-life head injuries and 2% a result of exposure to air pollution in older age – although they caution that the latter could be an underestimate. © 2020 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 27394 - Posted: 07.31.2020

By Nicholas Bakalar Severe gum disease and tooth loss may be linked to an increased risk for developing dementia, a new study has found. Researchers looked at 8,275 men and women whose average age was 63 at the start of the study. Over an average follow-up of more than 18 years, 19 percent of them developed Alzheimer’s disease or other forms of dementia. After controlling for various characteristics, including age, sex, education, cholesterol, high blood pressure, coronary heart disease, smoking and body mass index, they found that compared with people with healthy gums, those who had severe gingivitis with tooth loss had a 22 percent increased relative risk for dementia. Being toothless was associated with a 26 percent increased risk. The report is in the journal Neurology. Previous studies have shown that bacteria present in periodontal disease, particularly certain spirochetes, can travel along the trigeminal nerve that connects the mucous membranes of the mouth to the brain, potentially causing brain damage. The researchers also suggest that the connection could be more indirect, with the inflammation of gum disease leading to cardiovascular disease or diabetes, which are known risk factors for dementia. “We haven’t proven causation,” said the lead author, Ryan T. Demmer, an associate professor of epidemiology at the University of Minnesota. “But if it is causal, the population impact could be significant. Half the population has periodontal disease severe enough to put them at higher risk.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27392 - Posted: 07.31.2020

By Pam Belluck A newly developed blood test for Alzheimer’s has diagnosed the disease as accurately as methods that are far more expensive or invasive, scientists reported on Tuesday, a significant step toward a longtime goal for patients, doctors and dementia researchers. The test has the potential to make diagnosis simpler, more affordable and widely available. The test determined whether people with dementia had Alzheimer’s instead of another condition. And it identified signs of the degenerative, deadly disease 20 years before memory and thinking problems were expected in people with a genetic mutation that causes Alzheimer’s, according to research published in JAMA and presented at the Alzheimer’s Association International Conference. Such a test could be available for clinical use in as little as two to three years, the researchers and other experts estimated, providing a readily accessible way to diagnose whether people with cognitive issues were experiencing Alzheimer’s, rather than another type of dementia that might require different treatment or have a different prognosis. A blood test like this might also eventually be used to predict whether someone with no symptoms would develop Alzheimer’s. “This blood test very, very accurately predicts who’s got Alzheimer’s disease in their brain, including people who seem to be normal,” said Dr. Michael Weiner, an Alzheimer’s disease researcher at the University of California, San Francisco, who was not involved in the study. “It’s not a cure, it’s not a treatment, but you can’t treat the disease without being able to diagnose it. And accurate, low-cost diagnosis is really exciting, so it’s a breakthrough.” Nearly six million people in the United States and roughly 30 million worldwide have Alzheimer’s, and their ranks are expected to more than double by 2050 as the population ages. Blood tests for Alzheimer’s, which are being developed by several research teams, would provide some hope in a field that has experienced failure after failure in its search for ways to treat and prevent a devastating disease that robs people of their memories and ability to function independently. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27388 - Posted: 07.29.2020

Jon Hamilton This is the story of a fatal genetic disease, a tenacious scientist and a family that never lost hope. Conner Curran was 4 years old when he was diagnosed with Duchenne Muscular Dystrophy, a genetic disease that causes muscles to waste away. Conner's mother, Jessica Curran, remembers some advice she got from the doctor who made that 2015 diagnosis: "Take your son home, love him, take him on trips while he's walking, give him a good life and enjoy him because there are really not many options right now." Five years later, Conner is not just walking, but running faster than ever, thanks to an experimental gene therapy that took more than 30 years to develop. Conner was the first child to receive the treatment — a single infusion designed to fix the genetic mutation that was gradually causing his muscles cells to die. The treatment can't bring back the cells he's lost (he remains smaller and weaker than his twin brother, Kyle), but it has allowed the muscle cells he still has to function better. Since Conner's treatment, eight other boys with Duchenne have received two different doses of the gene therapy. Preliminary results on six of them, tested a year after treatment, showed they, too, had improved strength and endurance at an age when boys with Duchenne usually become weaker. © 2020 npr

Keyword: Muscles; Movement Disorders
Link ID: 27387 - Posted: 07.27.2020

Jon Hamilton For years, public health officials have been trying to dispel the myth that people who get a flu shot are more likely to get Alzheimer's disease. They are not. And now there is evidence that vaccines that protect against the flu and pneumonia may actually protect people from Alzheimer's, too. The evidence comes from two studies presented Monday at this year's Alzheimer's Association International Conference, which is being held as a virtual event. "We've always known that vaccines are very important to our overall health," says Maria Carrillo, chief science officer of the Alzheimer's Association. "And maybe they even contribute to protecting our memory, our cognition, our brain." The first study came from a team at the University of Texas that combed through millions of medical records in a national database. The goal was to find factors that affected a person's risk of getting certain diseases, including Alzheimer's. "And one of the things that came back was flu shots," says Albert Amran, a medical student of the McGovern Medical School at the University of Texas Health Science Center in Houston and an author of the study. That seemed odd. So Amran and a team of researchers took a closer look at the medical records of about 9,000 people who were at least 60 years old. Some had received a seasonal flu shot. Some hadn't. "We [tried] to make sure that both groups had an equal amount of, say, smoking status, obesity, diabetes, cardiovascular disease," Amran says. Those are known risk factors for Alzheimer's. The team also looked at factors like education and income, and indicators like the number of prescriptions a person had received, to make sure that people who got vaccines weren't just healthier overall. They weren't. © 2020 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 27385 - Posted: 07.27.2020

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

Keyword: Autism
Link ID: 27380 - Posted: 07.25.2020

A scientific analysis of more than 2,000 brain scans found evidence for highly reproducible sex differences in the volume of certain regions in the human brain. This pattern of sex-based differences in brain volume corresponds with patterns of sex-chromosome gene expression observed in postmortem samples from the brain’s cortex, suggesting that sex chromosomes may play a role in the development or maintenance of sex differences in brain anatomy. The study, led by researchers at the National Institute of Mental Health (NIMH), part of the National Institutes of Health, is published in Proceedings of the National Academy of Sciences. “Developing a clearer understanding of sex differences in human brain organization has great importance for how we think about well-established sex differences in cognition, behavior, and risk for psychiatric illness. We were inspired by new findings on sex differences in animal models and wanted to try to close the gap between these animal data and our models of sex differences in the human brain,” said Armin Raznahan, M.D., Ph.D., study co-author and chief of the NIMH Section on Developmental Neurogenomics. Researchers have long observed consistent sex-based differences in subcortical brain structures in mice. Some studies have suggested these anatomical differences are largely due to the effects of sex hormones, lending weight to a “gonad-centric” explanation for sex-based differences in brain development. However, more recent mouse studies have revealed consistent sex differences in cortical structures, as well, and gene-expression data suggest that sex chromosomes may play a role in shaping these anatomical sex differences. Although the mouse brain shares many similarities with the human brain, it is not clear whether these key findings in mice also apply to humans.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 27377 - Posted: 07.21.2020