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

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By Alice Klein Four genes have been identified that are linked to obsessive compulsive disorder (OCD). The genes all play a role in the same brain circuit, and may help explain why people are more likely to have OCD if they have a relative with the condition. People with OCD have intrusive thoughts and feel driven to repeat rituals, such as handwashing, to relieve their anxiety. To investigate if OCD has a genetic basis, Hyun Ji Noh at the Broad Institute of MIT and Harvard and her colleagues compared more than 600 genes across 592 people with OCD, and 560 people who don’t have it. They chose these candidate genes from several lines of evidence. Of these genes, 222 had been linked to compulsive grooming in mice, and 196 had been linked to autism in people – a condition that can involve repetitive behaviours. The team also looked at 56 genes that they had identified in a study of dogs with canine compulsive disorder, a condition in which dogs repeatedly chase their tails, pace back and forth, groom themselves or sucks things, sometimes for hours at a time. Brain safety circuit The analysis identified four genes that are different in people who have OCD. All four of these are active in a brain circuit that links the striatum, thalamus and cortex regions. © Copyright New Scientist Ltd.

Keyword: OCD - Obsessive Compulsive Disorder; Genes & Behavior
Link ID: 24210 - Posted: 10.18.2017

Jon Hamilton Brain imaging studies have a diversity problem. That's what researchers concluded after they re-analyzed data from a large study that used MRI to measure brain development in children from 3 to 18. Like most brain imaging studies of children, this one included a disproportionate number of kids who have highly educated parents with relatively high household incomes, the team reported Thursday in the journal Nature Communications. For example, parents of study participants were three times more likely than typical U.S. parents to hold an advanced degree. And participants' family incomes were much more likely to exceed $100,000 a year. So the researchers decided to see whether the results would be different if the sample represented the U.S. population, says Kaja LeWinn, an assistant professor at the University of California, San Francisco School of Medicine. "We were able to weight that data so it looked more like the U.S." in terms of race, income, education and other variables, she says. And when the researchers did that, the picture of "normal" brain development changed dramatically. For instance, when the sample reflected the U.S. population, children's brains reached several development milestones much earlier. © 2017 npr

Keyword: Brain imaging; Development of the Brain
Link ID: 24204 - Posted: 10.17.2017

By Rhianna Schmunk, CBC News Researchers from the University of British Columbia are retracting their scientific paper linking aluminum in vaccines to autism in mice, because one of the co-authors claims figures published in the study were deliberately altered before publication — an issue he says he realized after allegations of data manipulation surfaced online. The professor also told CBC News there's no way to know "why" or "how" the figures were allegedly contorted, as he claims original data cited in the study is inaccessible, which would be a contravention of the university's policy around scientific research. The paper looked at the effects of aluminum components in vaccines on immune response in a mouse's brain. It was published in the Journal of Inorganic Biochemistry on Sept. 5. Co-authored by Dr. Chris Shaw and Lucija Tomljenovic, it reported aluminum-triggered responses "consistent with those in autism." Shaw said he and Tomljenovic drew their conclusions from data that was "compiled" and "analyzed" for the paper, rather than raw data. However, subsequent scrutiny has raised questions about the validity of the data, with one doctor calling the paper "anti-vaccine pseudoscience." By the middle of September, commenters on PubPeer — a database where users can examine and comment on published scientific papers — pointed out that figures in the study appeared to have been altered, and in one case lifted directly from a 2014 study also authored by Shaw and Tomljenovic. ©2017 CBC/Radio-Canada.

Keyword: Autism
Link ID: 24199 - Posted: 10.16.2017

by Sari Harrar, AARP Bulletin, At 99 years old Brenda Milner continues to explore the mind and its relationship to people’'s behavior. You'’re a preeminent neuroscientist, and a professor at Canada's prestigious McGill University. At age 99, what motivates you to keep up your research at the Montreal Neurological Institute and Hospital? I am very curious. Human quirks attract my interest. If you’'re a theoretical person, you can sit and dream up beautiful theories, but my approach is, “What would happen if …”or, “Why is this person doing [that] …”and then, “How can I measure it?” I wouldn't still be working if I didn't find it exciting. AARP Membership: Join or Renew for Just $16 a Year Are you curious in real life, too? Yes. I'm a good "noticer—" of behavior as much as the kind of furniture people have! In the 1950s, you made a revolutionary discovery— that memories are formed in a brain area called the hippocampus, which is now getting lots of attention for its role in memory loss and dementia. Has brain research gotten easier? Nowadays, everyone has functional magnetic resonance imaging. Anybody with access to a medical school can get a good look at the patients' brain while they're alive and young, but it wasn't like that [then]. Psychologists were studying patients who were much older and beginning to show memory impairment. Then they had to wait for their patients to die.

Keyword: Learning & Memory
Link ID: 24196 - Posted: 10.16.2017

By Emily Underwood If you’ve ever found yourself in an MRI machine, you know keeping still isn’t easy. For newborns, it’s nearly impossible. Now, a portable, ultrasonic brain probe about the size of a domino could do similar work, detecting seizures and other abnormal brain activity in real time, according to a new study. It could also monitor growing babies for brain damage that can lead to diseases like cerebral palsy. “This is a window of time we haven’t had access to, and techniques like this are really going to open that up,” says Moriah Thomason, a neuroscientist at Wayne State University in Detroit, Michigan, who wasn’t involved in the new study. Researchers have long been able to take still pictures of the newborn brain and study brain tissue after death. But brain function during the first few weeks of life, which is “utterly essential to future human health,” has always been something of a black box, Thomason says. Two techniques used in adults—functional magnetic resonance imaging (fMRI), which can measure blood flow; and electroencephalography (EEG), which measures electrical activity in the outer layers of the brain—have their drawbacks. FMRI doesn’t work well with squirmy tots, is expensive, and is too big to haul to a delicate baby’s bedside. EEG—which only requires attaching a few wires to someone’s head—can’t penetrate deeper brain structures or show where a seizure begins, critical information for doctors weighing treatment options, says Olivier Baud, a developmental neuroscientist at the Robert Debré University Hospital in Paris. © 2017 American Association for the Advancement of Science.

Keyword: Brain imaging; Development of the Brain
Link ID: 24183 - Posted: 10.12.2017

By Esther Landhuis Among hundreds of genes that might nudge your risk of Alzheimer's up or down, Apolipoprotein E (APOE) has the strongest effect. Scientists discovered a quarter century ago that people with the APOE ε4 version of this gene are four to 15 times more likely to develop Alzheimer’s, a deadly brain disorder that afflicts more than five million Americans. Yet how APOE actually sets off dementia has been somewhat of a mystery—and efforts to use it as a drug target have floundered. The field’s attention has focused on another “A” word—amyloid beta (Aβ). This protein can unwittingly accrue in the brain for years, disrupting nerve connections essential for thinking and memory. APOE has been thought of as a co-conspirator in this process, but finding ways to undermine its collusion have proved challenging. Anti-amyloid drugs have consumed the labors of pharmaceutical companies. If a drug could break those insidious clumps of protein or keep them from forming, drug developers reasoned, it could in theory halt the progression of the disease. But billions of dollars have poured into large-scale clinical trials of amyloid-lowering therapies that so far have failed. Advertisement APOE has hovered on the periphery as far as drug development, but this could soon change. Connections have emerged between the functioning of APOE and Aβ. In 2012 Boston scientists studying autopsy tissue from Alzheimer’s patients found APOE ε4 individuals had unusually high levels of brain Aβ. And they noticed Aβ clumped more readily in test tubes if mixed with ApoE proteins, especially ApoE4. Mouse data from teams at Washington University in Saint Louis and the University of California, San Francisco—suggested a similar relationship. Each lab worked with existing Alzheimer’s mouse models and further modified their genomes to make different types and amounts of ApoE proteins. In both studies animals with less ApoE had fewer Aβ plaques in their brains. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 24176 - Posted: 10.12.2017

By NICHOLAS BAKALAR Women with high blood pressure in their 40s are at increased risk for dementia in later years, researchers report. But the finding does not hold for men. Beginning in 1964, investigators collected health and lifestyle information on 5,646 men and women when they were 30 to 35 years old, and again when they were in their 40s. From 1996 to 2015, 532 of them were found to have Alzheimer’s or other forms of dementia. The study is in Neurology. Hypertension in women in their 30s was not associated with dementia. But women who were hypertensive at an average age of 44 had a 68 percent higher risk for dementia than those who had normal blood pressure at that age, even after adjusting for B.M.I., smoking and other risk factors. High blood pressure in men in their 30s or 40s was not associated with later dementia, but the study’s senior author, Rachel A. Whitmer, said that studies have tied hypertension in men in their 50s to later dementia. Dr. Whitmer, a senior research scientist at Kaiser Permanente in Oakland, Calif., added that hypertension is more common in men, and the hypertensive men in the study tended to die at a younger age than the women. “The big picture here is that brain health is a lifelong issue,” she said. “What you do in young adulthood matters for your brain in old age.” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 24175 - Posted: 10.12.2017

By BENOIT DENIZET-LEWIS The disintegration of Jake’s life took him by surprise. It happened early in his junior year of high school, while he was taking three Advanced Placement classes, running on his school’s cross-country team and traveling to Model United Nations conferences. It was a lot to handle, but Jake — the likable, hard-working oldest sibling in a suburban North Carolina family — was the kind of teenager who handled things. Though he was not prone to boastfulness, the fact was he had never really failed at anything. Not coincidentally, failure was one of Jake’s biggest fears. He worried about it privately; maybe he couldn’t keep up with his peers, maybe he wouldn’t succeed in life. The relentless drive to avoid such a fate seemed to come from deep inside him. He considered it a strength. Jake’s parents knew he could be high-strung; in middle school, they sent him to a therapist when he was too scared to sleep in his own room. But nothing prepared them for the day two years ago when Jake, then 17, seemingly “ran 150 miles per hour into a brick wall,” his mother said. He refused to go to school and curled up in the fetal position on the floor. “I just can’t take it!” he screamed. “You just don’t understand!” Jake was right — his parents didn’t understand. Jake didn’t really understand, either. But he also wasn’t good at verbalizing what he thought he knew: that going to school suddenly felt impossible, that people were undoubtedly judging him, that nothing he did felt good enough. “All of a sudden I couldn’t do anything,” he said. “I was so afraid.” His tall, lanky frame succumbed, too. His stomach hurt. He had migraines. “You know how a normal person might have their stomach lurch if they walk into a classroom and there’s a pop quiz?” he told me. “Well, I basically started having that feeling all the time.” © 2017 The New York Times Company

Keyword: Development of the Brain; Stress
Link ID: 24174 - Posted: 10.11.2017

By Shawna Williams THE PAPER P. Réu et al., “The lifespan and turnover of microglia in the human brain,” Cell Rep, 20:779-84, 2017. A RENEWABLE RESOURCE? Evidence has emerged that some of the brain’s cells can be renewed in adulthood, but it is difficult to study the turnover of cells in the human brain. When it comes to microglia, immune cells that ward off infection in the central nervous system, it’s been unclear how “the maintenance of their numbers is controlled and to what extent they are exchanged,” says stem cell researcher Jonas Frisén of the Karolinska Institute in Sweden. NUCLEAR SIGNATURE Frisén and colleagues used brain tissue from autopsies, together with the known changes in concentrations of carbon-14 in the atmosphere over time, to estimate how frequently microglia are renewed. They also analyzed microglia from the donated brains of two patients who had received a labeled nucleoside as part of a cancer treatment trial in the 1990s. SLOW CHURN Microglia, which populate the brain as blood cell progenitors during fetal development, were replaced at a median rate of 28 percent per year; on average, the cells were 4.2 years old. For Marie-Ève Tremblay, a neuroscientist at the Université Laval in Québec City who was not involved in the study, what stands out is the range of microglia ages found—from brand-new to more than 20 years old. “That’s quite striking!” she writes in an email to The Scientist. © 1986-2017 The Scientist

Keyword: Glia; Development of the Brain
Link ID: 24159 - Posted: 10.07.2017

By GINA KOLATA For the first time, doctors have used gene therapy to stave off a fatal degenerative brain disease, an achievement that some experts had thought impossible. The key to making the therapy work? One of medicine’s greatest villains: HIV. The patients were children who had inherited a mutated gene causing a rare disorder, adrenoleukodystrophy, or ALD. Nerve cells in the brain die, and in a few short years, children lose the ability to walk or talk. They become unable to eat without a feeding tube, to see, hear or think. They usually die within five years of diagnosis. The disease strikes about one in 20,000 boys; symptoms first occur at an average age of 7. The only treatment is a bone-marrow transplant — if a compatible donor can be found — or a transplant with cord blood, if it was saved at birth. But such transplants are an onerous and dangerous therapy, with a mortality rate as high as 20 percent. Some who survive are left with lifelong disabilities. Now a new study, published online in the New England Journal of Medicine, indicates that gene therapy can hold off ALD without side effects, but only if it is begun when the only signs of deterioration are changes in brain scans. The study involved 17 boys (the disease strikes males almost exclusively), ages 4 to 13. All got gene therapy. Two years later, 15 were functioning normally without obvious symptoms. “To me, it seems to be working,” said Dr. Jim Wilson, director of the gene therapy program at the University of Pennsylvania’s Perelman School of Medicine, who was not involved in the new study. © 2017 The New York Times Company

Keyword: Genes & Behavior; Development of the Brain
Link ID: 24157 - Posted: 10.06.2017

By Clare Wilson OUR braininess may have evolved thanks to gene changes that made our brain cells less sticky. The cortex is the thin, highly folded outer layer of our brains and it is home to some of our most sophisticated mental abilities, such as planning, language and complex thoughts. Around three millimetres thick, this layer is folded into an intricate pattern of ridges and valleys, which allows the cortex to be large, but still fit into a relatively small space. Many larger mammals, such as primates, dolphins and horses, have various patterns of folds in their cortex, but folds are rarer in smaller animals like mice. So far, we have only identified a few genetic mutations that contributed to the evolution of the human brain, including ones that boosted the number of cells in the cortex. One theory about how the cortex came to be folded is that it buckled as the layer of cells expanded. Daniel del Toro at the Max Planck Institute of Neurobiology in Munich, Germany, and colleagues wondered if some of the genetic changes in our brain’s evolution might have been about more than just an increasing number of cells. They investigated the genes for two molecules – FLRT1 and FLRT3 – which make developing brain cells stick to each other more. Human brain cells produce only a small amount of these compounds, while mice brain cells make lots. Del Toro’s team created mice embryos that lacked functioning FLRT1 and FLRT3 genes, which meant their cortex cells were only loosely attached to each other, like those of humans. © Copyright New Scientist Ltd.

Keyword: Development of the Brain; Learning & Memory
Link ID: 24153 - Posted: 10.05.2017

Anna Gorman Kerri De Nies received the news this spring from her son's pediatrician: Her chubby-cheeked toddler has a rare brain disorder. She'd never heard of the disease — adrenoleukodystrophy, or ALD — but soon felt devastated and overwhelmed. "I probably read everything you could possibly read online — every single website," De Nies says as she cradles her son, Gregory Mac Phee. "It's definitely hard to think about what could potentially happen. You think about the worst-case scenario." ALD is a genetic brain disorder depicted in the 1992 movie Lorenzo's Oil, which portrayed a couple whose son became debilitated by the disease. The most serious form of the illness typically strikes boys between the ages of 4 and 10. Most are diagnosed too late for treatment to be successful, and they often die before their 10th birthday. The more De Nies learned about ALD, the more she realized how fortunate the family was to have discovered Gregory's condition so early. Her son's blood was tested when he was about 10 months old. Dr. Florian Eichler, a neurologist at Massachusetts General Hospital, says newborn screening is a game changer for children with the ALD, because it allows doctors to keep a close eye on kids who test positive for an ALD mutation from the beginning. © 2017 npr

Keyword: Development of the Brain
Link ID: 24147 - Posted: 10.05.2017

Jon Hamilton Fresh evidence that the body's immune system interacts directly with the brain could lead to a new understanding of diseases from multiple sclerosis to Alzheimer's. A study of human and monkey brains found lymphatic vessels — a key part of the body's immune system — in a membrane that surrounds the brain and nervous system, a team reported Tuesday in the online journal eLife. Lymphatic vessels are a part of the lymphatic system, which extends throughout the body much like our network of veins and arteries. Instead of carrying blood, though, these vessels carry a clear fluid called lymph, which contains both immune cells and waste products. The new finding bolsters recent evidence in rodents that the brain interacts with the body's lymphatic system to help fend off diseases and remove waste. Until a few years ago, scientists believed that the brain's immune and waste removal systems operated independently. The discovery of lymphatic vessels near the surface of the brain could lead to a better understanding of multiple sclerosis, which seems to be triggered by a glitch in the immune system, says Dr. Daniel Reich, an author of the study and a senior investigator at the National Institute of Neurological Disorders and Stroke. © 2017 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 24146 - Posted: 10.04.2017

By GRETCHEN REYNOLDS Because we can never have enough reasons to keep exercising, a new study with mice finds that physical activity not only increases the number of new neurons in the brain, it also subtly changes the shape and workings of these cells in ways that might have implications for memory and even delaying the onset of dementia. As most of us have heard, our brains are not composed of static, unchanging tissue. Instead, in most animals, including people, the brain is a dynamic, active organ in which new neurons and neural connections are created throughout life, especially in areas of the brain related to memory and thinking. This process of creating new neurons, called neurogenesis, can be altered by lifestyle, including physical activity. Many past studies have shown that in laboratory rodents, exercise doubles or even triples the number of new cells produced in adult animals’ brains compared to the brains of animals that are sedentary. But it has not been clear whether the new brain cells in active animals are somehow different from comparable new neurons in inactive animals or if they are just more numerous. That question has long interested scientists at the Laboratory of Neurosciences at the National Institute on Aging, who have been examining how running alters the brains and behavior of lab animals. Last year, in an important study published in NeuroImage, the researchers found for the first time that young brain cells in adult mice that spent a month with running wheels in their cages did seem to be different from those in animals that did not run. For the experiment, the scientists injected a modified rabies vaccine into the animals, where it entered the nervous system and brain. They then tracked and labeled connections between brain cells and learned that compared to the sedentary animals’ brain cells, the runners’ newborn neurons had more and longer dendrites, the snaky tendrils that help to connect the cells into the neural communications network. They also found that more of these connections led to portions of the brain that are important for spatial memory, which is our internal map of where we have been and how we got there. © 2017 The New York Times Company

Keyword: Neurogenesis; Development of the Brain
Link ID: 24145 - Posted: 10.04.2017

By NICHOLAS BAKALAR A poor sense of smell may indicate an increased risk for dementia, a new study has found. Researchers recruited 2,906 men and women ages 57 to 85, testing their ability to identify five odors — orange, leather, peppermint, rose and fish. Five years later, 4.1 percent of them had dementia. Of all the factors the researchers measured — age, sex, race, ethnicity, education, other diseases the subjects may have had — only cognitive ability at the start of the study and poorer performance on the “smell test” were associated with an increased risk for dementia. The study is in the Journal of the American Geriatrics Society. The risk went up steadily with the number of odors they failed to recognize, and over all, compared with those with no olfactory impairment, those with smelling difficulties had more than twice the likelihood of developing dementia. Even among those who initially tested within the normal range for mental ability, a poor sense of smell more than doubled the risk for dementia five years later. “This is not a simple, single-variable test for the risk of dementia,” said the lead author, Dr. Jayant M. Pinto, a specialist in sinus and nasal diseases at the University of Chicago. “But sensory function is an indicator of brain function. When sensory function declines, it can be a signal to have a more detailed examination to see if everything’s O.K.” © 2017 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Alzheimers
Link ID: 24137 - Posted: 10.03.2017

By PERRI KLASS, M.D. More than 30 years ago, my toddler stood up in his stroller, evading the various belts and restraints, and took a dramatic header down onto the pavement. He cried right away — a good thing, because it meant he didn’t lose consciousness, and by the time we got home, he seemed to be consoled, though he was already developing a major goose egg. I was a fourth-year medical student at the time and called the pediatric practice at University Health Services, and explained, somewhat frantically, that I was due to get on a flight to California with him in a couple of hours; I was going out for my all-important residency interviews. No problem, said the sympathetic doctor on call, all those years ago. You’re a medical student, you must have a penlight. Just take it along on the plane, and make sure you wake your son up every two hours and check that his pupils are equal, round and reactive to light. And he wished me good luck at my interviews. I hung up, much comforted. It was not until we were sitting on the airplane, me with my penlight in my pocket, that it occurred to me to wonder what I was supposed to do if somewhere over the Midwest, his pupils were not equal, round and reactive. We’ve gotten better, I hope, at some of the advice we give, but for pediatricians and for parents, head trauma in children is still an occasion for difficult decision making. Unlike broken limbs, usually detected because of pain and clearly diagnosed with X-rays, head injuries are tricky to diagnose and manage. In many cases where the concern is concussion, there is no medication or surgery that can make a difference — the primary treatment is rest. Public awareness over the ties between concussions and later problems for children, and publicity about chronic traumatic encephalopathy in athletes may be making parents even more anxious about treating head injuries. But with increasing concern in recent years about the radiation risk to children of CT scans, doing a head CT just to reassure a worried parent — or even a worried doctor — is generally seen as bad medicine; if you’re giving a child a significant dose of possibly dangerous radiation, you need to have some evidence that you may actually be doing something necessary for that child’s safety. © 2017 The New York Times Company

Keyword: Brain Injury/Concussion; Brain imaging
Link ID: 24135 - Posted: 10.02.2017

Juli Fraga Becoming a mother is often portrayed as a magical and glorious life event. But many women don't feel joyful after giving birth. In fact, according to the American Psychological Association, almost 15 percent of moms suffer from a postpartum mood disorder like anxiety or depression, making maternal mental health concerns the most common complication of childbirth in the U.S. And even though these mental illnesses affect millions of women each year, new research shows 20 percent of mothers don't disclose their symptoms to healthcare providers. "Many women feel hesitant discussing their emotional difficulties, especially when they're experiencing symptoms of postpartum depression and anxiety," says Sarah Checcone, founder and director of The Postpartum Society of Florida. The Sarasota-based non-profit organization is testing out a new way to support struggling mothers and their families by offering a mother-to-mother mentorship program known as SISTER (Self-Image Support Team and Emotional Resource). Volunteers are mothers who've recovered from a maternal mental illness, as well as those impacted by a friend or family member's postpartum challenges. Sister moms seek to build community, creating a safe space. And that just might help women to open up about their difficulties. "Many women falsely believe that admitting they're anxious or depressed is the same as admitting weakness. They may even fear that speaking about their feelings may make them more real. We need to do a better job explaining to patients that anxiety and depression have nothing to do with being a 'bad mom,' " says Dr. Alexandra Sacks, a psychiatrist in New York City, specializing in maternal mental health and reproductive psychiatry. © 2017 npr

Keyword: Depression; Sexual Behavior
Link ID: 24126 - Posted: 09.30.2017

A tiny change—just one mutation—appears to have boosted the modern Zika virus’s ability to attack fetal brain cells, fueling the wave of birth defects involving microcephaly (small head size) that recently swept across the Americas. The findings are reported Thursday in Science. Researchers in China found that a single swap of amino acids—from serine to asparagine—on a structural protein of the Zika virus occurred a few months before the pathogen first took off in French Polynesia in 2013. The team’s results may begin to answer an outstanding question from the Zika epidemic: Why have Zika-related microcephaly and other brain abnormalities been seen in areas hard-hit by outbreaks in the past few years but not in the decades following the virus’s discovery in 1947? One theory is that the Zika–microcephaly connection previously flew under the radar because there were too few cases to see the link. Another leading theory is that something about the modern virus has changed, allowing it to infect brain cells more efficiently than its ancestors could. The new work suggests the latter is true. “This is a very good study and it gives a plausible explanation that is scientifically based,” says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the U.S. National Institutes of Health. He adds that the results will be further strengthened if other groups replicate them. © 2017 Scientific American,

Keyword: Development of the Brain
Link ID: 24121 - Posted: 09.29.2017

Greta Jochem Concussions have gotten a lot of attention in recent years, especially as professional football players' brains have shown signs of degenerative brain disease linked with repeated blows to the head. Now, a new analysis confirms what many doctors fear — that concussions start showing up at a high rate in teens who are active in contact sports. About 20 percent of teens said they have been diagnosed with at least one concussion. And nearly 6 percent said they've been diagnosed with more than one, according to a research letter published Tuesday in the Journal of the American Medical Association. The Centers for Disease Control and Prevention says concussions can result in headaches, nausea and irritability. While most people do not suffer from long-term impacts from a concussion, between 10 percent and 20 percent may experience symptoms like depression, headaches or difficulty concentrating. Some people experience sleep problems, and multiple concussions are one way to cause chronic traumatic encephalopathy, a degenerative brain disease notably found in some NFL players. The letter's authors looked at 13,000 questionnaire responses from the 2016 version of Monitoring the Future. Each year since 1975, the study, run by the University of Michigan Survey Research Center, has surveyed high school students all over the country about their behaviors and attitudes. According to Philip Veliz, an author of the JAMA letter and an assistant research professor at the University of Michigan's Institute for Research on Women & Gender, in 2016, the survey added a question asking whether students had ever had a concussion. © 2017 npr

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 24117 - Posted: 09.28.2017

By JANE E. BRODY Now and then I hear someone (myself included) proclaim “my brain is on overload.” This is not surprising given the myriad complex tasks the brain performs, among them enabling you to learn, plan, remember, communicate, see, hear and smell. Perhaps also not surprising, a growing number of studies have linked compromised sensory functions like poor vision and hearing to a decline in cognitive abilities. The brain, it seems, can do only so much, and when it must struggle to make sense of the world – from reading the words on a page to understanding the spoken word – it may be less able to perform other important tasks. While a cause-and-effect relationship has yet to be established, evidence is gradually increasing to suggest that uncorrected deficits in vision and hearing can accelerate cognitive decline. National statistics demonstrate the importance of this relationship. The number of Americans with poor vision, often undetected among older adults, is expected to double by 2050; hearing loss – mostly untreated or undertreated – afflicts nearly two-thirds of adults over 70; both vision and hearing impairment occur in one person in nine age 80 and older (fewer than one in five have neither), and the prevalence of dementia is now doubling every 20 years. The latest study, published in August in JAMA Ophthalmology, found that among a representative sample of nearly 3,000 older Americans and a second sample of 30,000 Medicare beneficiaries, poor vision was associated with poor cognition. The two data sets used different measurements of cognitive abilities like memory, orientation and planning, and the consistency of their findings suggests that the association between vision impairment and compromised brain function is real, the researchers concluded. © 2017 The New York Times Company

Keyword: Vision; Hearing
Link ID: 24114 - Posted: 09.26.2017