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

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Jessica Wright Sequencing can identify mutations linked to autism even before a child’s birth—especially in cases where doctors suspect problems, two new studies suggest. In the studies, scientists sequenced fetal DNA only when ultrasounds revealed atypical development of limbs or other organs, and they gave families only the results that seemed to explain those problems But there is a real risk that others might use the technique to test for mutations in any fetus—and to relay all the results to parents—without proper oversight, says Ronald Wapner, professor of obstetrics and gynecology at the Columbia Institute for Genomic Medicine, who led one of the studies. “Not everybody should be doing this; it should be in the hands of people that have expertise,” he says. Other types of analyses already detect mutations in a fetus: Some detect large DNA segments that are swapped between chromosomes, and others can pick up on missing or duplicated copies of DNA fragments. The new studies are among the first to scan for mutations across the fetal exome—essentially, the collection of genes in a genome. The field is fraught with ethical questions, including whether parents might choose to terminate a pregnancy based on the results. But the researchers note that most of the mutations they found pose serious health risks, which could be treated at birth or in utero. © 1986 - 2019 The Scientist

Keyword: Autism; Genes & Behavior
Link ID: 26168 - Posted: 04.24.2019

By Perri Klass, M.D. Every pediatrician knows that it’s important to diagnose autism when a child is as young as possible, because when younger children get help and intensive therapy, their developmental outcomes improve, as measured in everything from improved language, cognition and social skills to normalized brain activity. “The signs and symptoms for most children are there between 12 and 24 months,” said Dr. Paul S. Carbone, an associate professor of pediatrics at the University of Utah and a co-author of “Autism Spectrum Disorder: What Every Parent Needs to Know,” published by the American Academy of Pediatrics. “If we can get them in for evaluation by then, the therapies are available as young as those ages, you can easily start by 2,” he said. “We’d like to give kids the benefit of getting started early.” That means taking parents seriously when they bring up concerns about what they regard as strange behaviors and interactions on the part of babies and toddlers, and it also means that we try to screen all our patients, often with a checklist for parents to complete, like the Modified Checklist for Autism in Toddlers, or M-CHAT. Children whose scores indicate a concern are then supposed to be referred on for a full developmental assessment. The Centers for Disease Control and Prevention’s website lists developmental milestones to look for; missing them may be an early sign of autism. So we all know this is important. We also know that we are not, collectively, doing a very good job of screening all children, that the questionnaires often over-identify children who don’t actually need full assessments, and that the referral process can be plagued with long waits (and when a young child has to wait months for the assessment, that works against the benefit of early diagnosis). Children in minority groups are diagnosed at an older average age than white children, and therefore get therapy later, contributing to increased disparities. © 2019 The New York Times Company

Keyword: Autism
Link ID: 26160 - Posted: 04.22.2019

By Gina Kolata The study subjects had been thin all their lives, and not because they had unusual metabolisms. They just did not care much about food. They never ate enormous amounts, never obsessed on the next meal. Now, a group of researchers in Britain may have found the reason. The people carry a genetic alteration that mutes appetite. It also greatly reduces their chances of getting diabetes or heart disease. The scientists’ study, published on Thursday in the journal Cell, relied on data from the U.K. Biobank, which includes a half million people aged 40 to 69. Participants have provided DNA samples and medical records, and have allowed researchers to track their health over years. A second study in the same journal also used data from this population to develop a genetic risk score for obesity. It can help predict, as early as childhood, who is at high risk for a lifetime of obesity and who is not. Together, the studies confirm a truth that researchers wish more people understood. There are biological reasons that some struggle mightily with their weight and others do not, and the biological impacts often are seen on appetite, not metabolism. People who gain too much weight or fight to stay thin feel hungrier than naturally thin people. The study of the appetite-dulling mutation was led by Dr. Sadaf Farooqi, professor of metabolism and medicine at the University of Cambridge, and Nick Wareham, an epidemiologist at the university. The study drew on Dr. Farooqi’s research into a gene, MC4R. She has probed it for 20 years, but for the opposite reason: to understand why some people are overweight, not why some are thin. © 2019 The New York Times Company

Keyword: Obesity; Genes & Behavior
Link ID: 26156 - Posted: 04.19.2019

Tina Hesman Saey There’s a new way to predict whether a baby will grow into an obese adult. Combining the effect of more than 2.1 million genetic variants, researchers have created a genetic predisposition score that they say predicts severe obesity. People with scores in the highest 10 percent weighed, on average, 13 kilograms (about 29 pounds) more than those with the lowest 10 percent of scores, the team reports April 18 in Cell. The finding may better quantify genes’ roles in obesity than previous prediction scores, but still fails to account for lifestyle, which may be more important in determining body weight, other researchers say. Still, the study shows that “your genetics really start to take hold very early in life,” says coauthor Amit Khera, a cardiologist at Massachusetts General Hospital and the Broad Institute of MIT and Harvard. Weight differences showed up as early as age 3, and by age 18, those with the highest scores weighed 12.3 kilograms more on average than those with the lowest scores, Khera and his colleagues found. Some people with high genetic scores had normal body weights, but those people may have to work harder to maintain a healthy weight than others, he says. People with the highest scores were 25 times more likely to have severe obesity — a body mass index (BMI) greater than 40 — than those with the lowest scores. BMI is a measurement of body fat based on height and weight. A BMI of 18.5 (calculated as kilograms per meters squared of height) to 24.9 is considered healthy. BMIs 30 and above are considered obese. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity; Genes & Behavior
Link ID: 26155 - Posted: 04.19.2019

By Susan Gubar After the births of my babies in the ’70s, the umbilical cord connecting them to me was cut and trashed. But these days the blood inside can be preserved in a bank. It contains stem cells with the potential to save the lives of patients with leukemia, lymphoma or sickle cell disease. Stem cell treatments have been in the news lately because some companies are accused of selling unproven treatments that may actually harm patients. Earlier this month, the New York attorney general filed suit against one such company, claiming it knowingly performed rogue procedures on patients with a wide range of medical conditions. But there are legitimate lifesaving uses of cord blood that should not be tainted by these sham companies. Liars and thieves must not be allowed to detract from meticulous scientific research that has made umbilical cord blood mystic in its regenerative powers. A reader who is pregnant and whose first child had undergone successful leukemia treatments asked me about cord blood banking recently. Her obstetrician had suggested she bank her new baby’s cord blood as an insurance policy in case her first child suffered a recurrence. Cord blood transplants can be used to reconstitute a patient’s immune system. Blood from a sibling stands a good chance of being a suitable match for a transplant. Two impediments may influence parents against the risk-free practice of banking cord blood. First, some obstetricians believe that a brief wait before the clamping of an umbilical cord can enhance a child’s well-being, but delayed clamping compromises the volume and quality of collected cord blood cells. © 2019 The New York Times Company

Keyword: Stem Cells
Link ID: 26150 - Posted: 04.18.2019

Tina Hesman Saey ORLANDO — Being exposed to a chemical early in life can be a bit like a choose-your-own-adventure book: Some things that happen early on may hurt you later, but only if you make certain choices, an unpublished study in mice suggests. Mouse pups were exposed to the chemical bisphenol A (BPA) for only five days after birth, a crucial time during which mice’s livers develop. BPA, once common in plastics, has been linked to a host of health problems in people, from diabetes to heart disease (SN: 10/11/08, p. 14). But depending on diet as adults, the mice either grew up to be healthy or to have enlarged livers and high cholesterol. As long as the BPA-exposed mice ate mouse chow for the rest of their lives, the rodents remained healthy, molecular biologist Cheryl Walker of Baylor College of Medicine in Houston reported April 7 at the 2019 Experimental Biology meeting. But researchers switched some BPA-exposed mice to a high-fat diet as adults. Those mice had larger livers, higher cholesterol and more metabolic problems than mice who ate a high-fat diet but were not exposed to BPA as pups, Walker said. BPA exposure immediately altered epigenetic marks at more than 5,400 genes, including 3,000 involved in aging. Epigenetic marks are chemical tags on DNA or on histones — protein around which DNA winds in a cell — that don’t change information in genes themselves, but affect gene activity. |© Society for Science & the Public 2000 - 2019

Keyword: Neurotoxins; Development of the Brain
Link ID: 26134 - Posted: 04.13.2019

By Kelly Servick At age 16, Danielle Bassett spent most of her day at the piano, trying to train her fingers and ignoring a throbbing pain in her forearms. She hoped to pursue a career in music and had been assigning herself relentless practice sessions. But the more she rehearsed Johannes Brahms's feverish Rhapsody in B Minor on her family's Steinway, the clearer it became that something was wrong. Finally, a surgeon confirmed it: Stress fractures would force her to give up the instrument for a year. "What was left in my life was rather bleak," Bassett says. Her home-schooled upbringing in rural central Pennsylvania had instilled a love of math, science, and the arts. But by 17, discouraged by her parents from attending college and disheartened at her loss of skill while away from the keys, she expected that responsibilities as a housewife and mother would soon eclipse any hopes of a career. "I wasn't happy with that plan," she says. Instead, Bassett catapulted herself into a life of research in a largely uncharted scientific field now known as network neuroscience. A Ph.D. physicist and a MacArthur fellow by age 32, she has pioneered the use of concepts from physics and math to describe the dynamic connections in the human brain. "She's now the doyenne of network science," says theoretical neuroscientist Karl Friston of University College London. "She came from a formal physics background but was … confronted with some of the deepest questions in neuroscience." © 2019 American Association for the Advancement of Science.

Keyword: Brain imaging; Development of the Brain
Link ID: 26133 - Posted: 04.12.2019

By Gina Kolata Allan Gallup, a retired lawyer and businessman, grew increasingly forgetful in his last few years. Eventually, he could no longer remember how to use a computer or the television. Although he needed a catheter, he kept forgetting and pulling it out. It was Alzheimer’s disease, the doctors said. So after Mr. Gallup died in 2017 at age 87, his brain was sent to Washington University in St. Louis to be examined as part of a national study of the disease. But it wasn’t just Alzheimer’s disease, the researchers found. Although Mr. Gallup’s brain had all the hallmarks — plaques made of one abnormal protein and tangled strings of another — the tissue also contained clumps of proteins called Lewy bodies, as well as signs of silent strokes. Each of these, too, is a cause of dementia. Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities. For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame. Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia. These questions strike at the very definition of Alzheimer’s disease. And if you can’t define the condition, how can you find a treatment? © 2019 The New York Times Company

Keyword: Alzheimers; Brain imaging
Link ID: 26125 - Posted: 04.09.2019

/ By Jed Gottlieb In 1983, The New York Times published a bombshell report about President Ronald Reagan: Starkey Laboratories had fitted the President, then 72, with a hearing aid. The news was welcomed by health professionals who reckoned it could help to reduce the stigma associated with hearing loss. At the time, one in three people over the age of 60 was thought to have hearing problems, though only around 20 percent who needed hearing aids used them. “The way I do the math, a third of all adults have unaddressed hearing issues. That’s lot of people.” Indeed, Reagan’s handlers knew too well that the revelation risked making the president look like a feeble old man — and worse, someone ill-equipped to run the most powerful nation on earth. “Among Presidential advisers,” The New York Times noted, “Mr. Reagan’s use of a hearing aid revived speculation on whether his age would be an issue if he seeks re-election next year.” Reagan won re-election, of course, but nearly 40 years later, negative perceptions persist — and health advocates are more concerned than ever. Hearing loss, they say, is not just a functional disability affecting a subset of aging adults. With population growth and a boom in the global elderly population, the World Health Organization (WHO) now estimates that by 2050, more than 900 million people will have disabling hearing loss. A 2018 study of 3,316 children aged nine to 11 meanwhile, found that 14 percent already had signs of hearing loss themselves. While not conclusive, the study linked the loss to the rise of portable music players. Copyright 2019 Undark

Keyword: Hearing
Link ID: 26124 - Posted: 04.09.2019

By Benedict Carey Anyone above a certain age who has drawn a blank on the name of a favorite uncle, a friend’s phone number or the location of a house key understands how fragile memory is. Its speed and accuracy begin to slip in one’s 20s and keep slipping. This is particularly true for working memory, the mental sketch pad that holds numbers, names and other facts temporarily in mind, allowing decisions to be made throughout the day. On Monday, scientists reported that brief sessions of specialized brain stimulation could reverse this steady decline in working memory, at least temporarily. The stimulation targeted key regions in the brain and synchronized neural circuits in those areas, effectively tuning them to one another, as an orchestra conductor might tune the wind section to the strings. The findings, reported in the journal Nature Neuroscience, provide the strongest support yet for a method called transcranial alternating current stimulation, or tACS, as a potential therapy for memory deficits, whether from age-related decline, brain injury or, perhaps, creeping dementia. In recent years, neuroscientists have shown that memory calls on a widely distributed network in the brain, and it coordinates those interactions through slow-frequency, thrumming rhythms called theta waves, akin to the pulsing songs shared among humpback whales. The tACS technology is thought to enable clearer communication by tuning distant circuits to one another. The tACS approach is appealing for several reasons, perhaps most of all because it is noninvasive; unlike other forms of memory support, it involves no implant, which requires brain surgery. The stimulation passes through the skull with little sensation. Still, a widely available therapy is likely years away, as the risks and benefits are not fully understood, experts said. © 2019 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26123 - Posted: 04.09.2019

By Nicholas Wade Sydney Brenner, a South African-born biologist who helped determine the nature of the genetic code and shared a Nobel Prize in 2002 for developing a tiny transparent worm into a test bed for biological discoveries, died on Friday in Singapore. He was 92. He had lived and worked in Singapore in recent years, affiliated with the government-sponsored Agency for Science, Technology and Research, which confirmed his death. A witty, wide-ranging scientist, Dr. Brenner was a central player in the golden age of molecular biology, which extended from the discovery of the structure of DNA in 1953 to the mid-1960s. He then showed, in experiments with a roundworm known as C. elegans, how it might be possible to decode the human genome. That work laid the basis for the genomic phase of biology. Later, in a project still coming to fruition, he focused on understanding the functioning of the brain. “I think my real skills are in getting things started,” he said in his autobiography, “My Life in Science” (2001). “In fact, that’s what I enjoy most, the opening game. And I’m afraid that once it gets past that point, I get rather bored and want to do other things.” As a young South African studying at Oxford University, he was one of the first people to view the model of DNA that had been constructed in Cambridge, England, by Francis H. C. Crick and James D. Watson. He was 22 at the time and would call it the most exciting day of his life. “The double helix was a revelatory experience; for me everything fell into place, and my future scientific life was decided there and then,” Dr. Brenner wrote. Impressed by Dr. Brenner’s insights and ready humor, Dr. Crick recruited him to Cambridge a few years later. Dr. Crick, a theoretical biologist, liked to have with him someone he could bounce ideas off. Dr. Watson had played this role in the discovery of DNA, and Dr. Brenner became his successor, sharing an office with Dr. Crick for 20 years at the Medical Research Council Laboratory of Molecular Biology at Cambridge. © 2019 The New York Times Company

Keyword: Development of the Brain; Genes & Behavior
Link ID: 26116 - Posted: 04.06.2019

By Carl Zimmer In 2011, Dr. Dena Dubal was hired by the University of California, San Francisco, as an assistant professor of neurology. She set up a new lab with one chief goal: to understand a mysterious hormone called Klotho. Dr. Dubal wondered if it might be the key to finding effective treatments for dementia and other disorders of the aging brain. At the time, scientists only knew enough about Klotho to be fascinated by it. Mice bred to make extra Klotho lived 30 percent longer, for instance. But scientists also had found Klotho in the brain, and so Dr. Dubal launched experiments to see whether it had any effect on how mice learn and remember. The results were startling. In one study, she and her colleagues found that extra Klotho protects mice with symptoms of Alzheimer’s disease from cognitive decline. “Their thinking, in every way that we could measure them, was preserved,” said Dr. Dubal. She and her colleagues also bred healthy mice to make extra Klotho. They did better than their fellow rodents on learning mazes and other cognitive tests. Klotho didn’t just protect their brains, the researchers concluded — it enhanced them. Experiments on more mice turned up similar results. “I just couldn’t believe it — was it true, or was it just a false positive?” Dr. Dubal recalled. “But here it is. It enhances of cognition even in a young mouse. It makes them smarter.” Five years have passed since Dr. Dubal and her colleagues began publishing these extraordinary results. Other researchers have discovered tantalizing findings of their own, suggesting that Klotho may protect against other neurological disorders, including multiple sclerosis and Parkinson’s disease. © 2019 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26105 - Posted: 04.02.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 26101 - Posted: 04.01.2019

By Ilana Marcus Grit alone got Linda Greene through her husband’s muscular dystrophy, her daughter’s traumatic brain injury, and her own mysterious illness that lasted for three years and left her vomiting daily before doctors identified the cause. But eventually, after too many days sitting at her desk at work crying, she went to see her doctor for help. He prescribed an antidepressant and referred her to a psychiatrist. When the first medication didn’t help, the psychiatrist tried another — and another and another — hoping to find one that made her feel better. Instead, Greene felt like a zombie and sometimes she hallucinated and couldn’t sleep. In the worst moment, she found herself contemplating suicide. “It was horrible,” she said. She never had suicidal thoughts before and was terrified. She went back her primary care doctor. In the past, when Jeremy Bruce, Greene’s physician in Cincinnati, treated patients for depression, he followed the same steps for almost everyone: start the patient on one antidepressant and switch to another until something helped. Sometimes, before they found the right treatment, the patient would leave his practice to find a new doctor. “They would usually be very angry,” Bruce said. But about three years ago, Bruce tried a new approach. Linda Greene and her husband. She tried many antidepressants before her doctor suggested genetic testing to find a medicine that worked for her. Doctors increasingly use information about genes to evaluate potential risk for some diseases and to determine the best drug treatment. But using pharmacogenetics to help treat depression remains controversial. (Family Photo) © 1996-2019 The Washington Post

Keyword: Depression; Genes & Behavior
Link ID: 26099 - Posted: 04.01.2019

By Simon Makin Neurodegenerative diseases all involve the accumulation of toxic versions of naturally produced proteins in the brain. Multiple proteins are often abnormal in a patient, and the same aberrant protein can be involved in several different conditions. One common culprit is tau, which is abnormal in various conditions: chronic traumatic encephalopathy, a neurodegenerative disorder caused by repeated head trauma; a group of conditions known collectively as frontotemporal dementia; and, most famously, Alzheimer’s disease (AD). Normally, tau stabilizes structures inside neural connections, called microtubules, which facilitate chemical communication between cells. In disease states, tau is chemically altered, becoming misshapen and breaking away from microtubules. These toxic versions accumulate into structures called “neurofibrillary tangles,” which disrupt cells’ ability to communicate and may trigger other forms of damage, such as inflammation. Tau is involved in AD, but abnormalities in a different protein, amyloid-beta, are thought to be the initial trigger for a chain of biological events (including tau pathology) that underlies neurodegeneration. This is why most AD drugs developed to date have targeted amyloid, although tau has received increasing attention as multiple drugs intended to remove amyloid have failed. A new study, published Wednesday in Science Translational Medicine, suggests that an existing drug, lonafarnib, could be repurposed to treat neurodegenerative diseases that involve tau. A team of researchers, led by neuroscientist Kenneth Kosik of the University of California, Santa Barbara, found the drug had beneficial effects on tau-related pathology in mice, if administered early over an extended period. They also found evidence suggesting it works via a previously unknown biological mechanism. “This opens up a previously completely unsuspected pathway for tau degradation,” says Kosik, a longtime tau researcher. “We don’t have all the molecular details, but as a place to look, this is full of new opportunities.” © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26093 - Posted: 03.29.2019

By Nicholas Bakalar Urban air pollution is associated with an increased risk for psychotic experiences in teenagers, researchers report. A study published in JAMA Psychiatry included 2,063 British teenagers whose health had been followed from birth through age 18. Almost a third of them said they had at least one psychotic experience, ranging from a mild feeling of paranoia to a severe psychotic symptom, since age 12. Researchers linked air pollution data to locations where they spent most of their time — at home, school or work. Compared with teenagers who lived where pollution was lowest, those in the most polluted areas were 27 percent to 72 percent more likely to have psychotic experiences, depending on the type of pollutant; exposure to two pollutants, nitrogen dioxide and nitrogen oxides, accounted for 60 percent of the association. The study controlled for family psychiatric history, maternal psychosis, substance use, socioeconomic status, neighborhood social characteristics and other factors, but it is an observational study that does not prove causation. “From this one study, we can’t say that air pollution causes psychosis,” said the lead author, Helen L. Fisher, a research psychologist at King’s College London. “The study only says that these things commonly occur together.” © 2019 The New York Times Company

Keyword: Schizophrenia; Neurotoxins
Link ID: 26085 - Posted: 03.28.2019

By Karen Weintraub If the memory center of the human brain can grow new cells, it might help people recover from depression and post-traumatic stress disorder (PTSD), delay the onset of Alzheimer’s, deepen our understanding of epilepsy and offer new insights into memory and learning. If not, well then, it’s just one other way people are different from rodents and birds. For decades, scientists have debated whether the birth of new neurons—called neurogenesis—was possible in an area of the brain that is responsible for learning, memory and mood regulation. A growing body of research suggested they could, but then a Nature paper last year raised doubts. Now, a new study published today in another of the Nature family of journals—Nature Medicine—tips the balance back toward “yes.” In light of the new study, “I would say that there is an overwhelming case for the neurogenesis throughout life in humans,” Jonas Frisén, a professor at the Karolinska Institute in Sweden, said in an e-mail. Frisén, who was not involved in the new research, wrote a News and Views about the study in the current issue of Nature Medicine. Not everyone was convinced. Arturo Alvarez-Buylla was the senior author on last year’s Nature paper, which questioned the existence of neurogenesis. Alvarez-Buylla, a professor of neurological surgery at the University of California, San Francisco, says he still doubts that new neurons develop in the brain’s hippocampus after toddlerhood. © 2019 Scientific American

Keyword: Neurogenesis
Link ID: 26082 - Posted: 03.26.2019

By Emily Underwood One of the thorniest debates in neuroscience is whether people can make new neurons after their brains stop developing in adolescence—a process known as neurogenesis. Now, a new study finds that even people long past middle age can make fresh brain cells, and that past studies that failed to spot these newcomers may have used flawed methods. The work “provides clear, definitive evidence that neurogenesis persists throughout life,” says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto, Canada. “For me, this puts the issue to bed.” Researchers have long hoped that neurogenesis could help treat brain disorders like depression and Alzheimer’s disease. But last year, a study in Nature reported that the process peters out by adolescence, contradicting previous work that had found newborn neurons in older people using a variety of methods. The finding was deflating for neuroscientists like Frankland, who studies adult neurogenesis in the rodent hippocampus, a brain region involved in learning and memory. It “raised questions about the relevance of our work,” he says. But there may have been problems with some of this earlier research. Last year’s Nature study, for example, looked for new neurons in 59 samples of human brain tissue, some of which came from brain banks where samples are often immersed in the fixative paraformaldehyde for months or even years. Over time, paraformaldehyde forms bonds between the components that make up neurons, turning the cells into a gel, says neuroscientist María Llorens-Martín of the Severo Ochoa Molecular Biology Center in Madrid. This makes it difficult for fluorescent antibodies to bind to the doublecortin (DCX) protein, which many scientists consider the “gold standard” marker of immature neurons, she says. © 2019 American Association for the Advancement of Science

Keyword: Neurogenesis
Link ID: 26081 - Posted: 03.26.2019

By Jennifer Couzin-Franke Earlier this week, the Lieber Institute for Brain Development, a nonprofit housed at Johns Hopkins University School of Medicine in Baltimore, Maryland, announced a new neuroscience research initiative that aims to tackle a gaping hole in medicine: the interplay between brain diseases and their genomic drivers among African-Americans. The goal is to better understand how brain diseases play out in this population, which has been profoundly underrepresented in neuroscience research. To build trust among African-Americans in Baltimore and eventually beyond, the venture includes a partnership with the African-American Clergy Medical Research Initiative, a group of clergy leaders in the city. African-American scientists at Lieber are already involved, but project leaders hope to engage those at other institutions as the work expands. The effort builds on Lieber’s rapidly growing brain bank, which now stands at about 3000 brains, with more than 400 new brains collected each year, all donated by next of kin. Many are from young and middle-aged people who die suddenly of suicide, drug overdose, or other causes. Although most of the brains are from people of European ancestry, more than 700 are from African-Americans. Despite growing recognition that African-Americans are underrepresented in medical research—and face discrimination and other hardships that can heighten health risks—study of brain diseases in this population have lagged behind, says Daniel Weinberger, the institute’s director. ScienceInsider spoke with Weinberger, a psychiatrist and schizophrenia researcher who came to the Lieber Institute in 2011 from the National Institute of Mental Health. The conversation has been edited for brevity and clarity. © 2019 American Association for the Advancement of Science

Keyword: Alzheimers; Genes & Behavior
Link ID: 26069 - Posted: 03.23.2019

Katarina Zimmer It’s well established that exercise is good for the mammalian brain. As early as 1999, researchers discovered considerably more newborn neurons in the hippocampi of mice that had access to a running wheel than in animals that didn’t. But 20 years later, scientists are still trying to understand why. A team of Australian and German researchers has uncovered one mechanism that explains how exercise boosts neurogenesis in mice: the activity causes platelets circulating in the blood to release factors that boost the growth of neural precursor cells in the hippocampus, the researchers report today (March 21) in Stem Cell Reports. “We all know about the positive effect of exercise on the brain and other organ systems, but what the actual mechanism is to promote new neuron production is still a bit of a mystery,” remarks Vince Tropepe, who studies neurogenesis at the University of Toronto and who was not involved in the study. “This paper is quite interesting in that they’ve identified a player—these platelets and platelet-derived factors that are circulating in the blood after exercise—that might be a mediator of this effect.” The researchers came to this conclusion through a series of experiments comparing mice that had access to a running wheel for four days with control mice that didn’t. Lab mice voluntarily run up to 10 kilometers per night, “equivalent to us running more than a marathon a day,” explains coauthor Tara Walker, a senior research associate at the Queensland Brain Institute. © 1986 - 2019 The Scientist

Keyword: Neurogenesis; Development of the Brain
Link ID: 26066 - Posted: 03.23.2019