Chapter 7. Life-Span Development of the Brain and Behavior
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By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company
By CATHERINE SAINT LOUIS During her pregnancy, she never drank alcohol or had a cigarette. But nearly every day, Stacey, then 24, smoked marijuana. With her fiancé’s blessing, she began taking a few puffs in her first trimester to quell morning sickness before going to work at a sandwich shop. When sciatica made it unbearable to stand during her 12-hour shifts, she discreetly vaped marijuana oil on her lunch break. “I wouldn’t necessarily say, ‘Go smoke a pound of pot when you’re pregnant,’” said Stacey, now a stay-at-home mother in Deltona, Fla., who asked that her full name be withheld because street-bought marijuana is illegal in Florida. “In moderation, it’s O.K.” Many pregnant women, particularly younger ones, seem to agree, a recent federal survey shows. As states legalize marijuana or its medical use, expectant mothers are taking it up in increasing numbers — another example of the many ways in which acceptance of marijuana has outstripped scientific understanding of its effects on human health. Often pregnant women presume that cannabis has no consequences for developing infants. But preliminary research suggests otherwise: Marijuana’s main psychoactive ingredient — tetrahydrocannabinol, or THC — can cross the placenta to reach the fetus, experts say, potentially harming brain development, cognition and birth weight. THC can also be present in breast milk. “There is an increased perception of the safety of cannabis use, even in pregnancy, without data to say it’s actually safe,” said Dr. Torri Metz, an obstetrician at Denver Health Medical Center who specializes in high-risk pregnancies. Ten percent of her patients acknowledge recent marijuana use. © 2017 The New York Times Company
By Emma Hiolski Imagine cells that can move through your brain, hunting down cancer and destroying it before they themselves disappear without a trace. Scientists have just achieved that in mice, creating personalized tumor-homing cells from adult skin cells that can shrink brain tumors to 2% to 5% of their original size. Although the strategy has yet to be fully tested in people, the new method could one day give doctors a quick way to develop a custom treatment for aggressive cancers like glioblastoma, which kills most human patients in 12–15 months. It only took 4 days to create the tumor-homing cells for the mice. Glioblastomas are nasty: They spread roots and tendrils of cancerous cells through the brain, making them impossible to remove surgically. They, and other cancers, also exude a chemical signal that attracts stem cells—specialized cells that can produce multiple cell types in the body. Scientists think stem cells might detect tumors as a wound that needs healing and migrate to help fix the damage. But that gives scientists a secret weapon—if they can harness stem cells’ natural ability to “home” toward tumor cells, the stem cells could be manipulated to deliver cancer-killing drugs precisely where they are needed. Other research has already exploited this method using neural stem cells—which give rise to neurons and other brain cells—to hunt down brain cancer in mice and deliver tumor-eradicating drugs. But few have tried this in people, in part because getting those neural stem cells is hard, says Shawn Hingtgen, a stem cell biologist at the University of North Carolina in Chapel Hill. © 2017 American Association for the Advancement of Science.
New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”
James Gorman What fly is famous on TV? Think corpses and detectives wanting to know how long that body has been in a storage locker or suitcase. It’s the blowfly, of course. Its larvae, a.k.a. maggots, feed on rotting flesh, which could be that spouse or business partner who got in the way. Or, in a good police procedural, both the spouse and the business partner, sent to the great beyond together for their transgressions. By seeing whether the eggs have hatched and how big the larvae are, forensic scientists can get an idea of how much time has passed since the victims met their end and began the final chapter in the way of all flesh. By the way, if you have a problem with a spouse or business partner, it’s worth keeping in mind that the flies can indeed get into a suitcase. They stick their ovipositor through the gaps in the zipper. Or the newly hatched larvae themselves can sneak through. But there are aspects of the maggot’s life that have remained somewhat obscure. Martin Hall, a forensic entomologist at the Natural History Museum in London, thought that one part of the fly’s development in particular needed further study. The maggots are a bit like caterpillars in that at a certain point in their development they wrap themselves up in a case and go through one of the most astonishing events in the natural world: metamorphosis. In 10 days, the maggot, which has no legs or eyes and is something like “an animated sock,” Dr. Hall said, turns into the extraordinarily complex blowfly. No doubt blowflies are not as appealing as butterflies to most people, but chalk that up to a human bias for pretty fluttery things that land on flowers. It’s certainly not the fly’s fault. Any close-up image of its multifaceted, jewel-like eye shows that it is marvelous in its own way, even if it does feed on the dead. Science Times © 2017 The New York Times Company
Keyword: Development of the Brain
Link ID: 23169 - Posted: 01.31.2017
By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.
By Meredith Wadman Many children with congenital heart disease (CHD)—the most common major birth defect in the United States—sustain brain damage that often leads to problems with behavior, thinking, and learning. Now, for the first time, researchers have described how the lack of brain oxygen that results from heart malformations might stunt the brains of newborns, opening avenues to potential therapies that could be used even before babies are born. The results are “incredibly exciting,” says Caitlin Rollins, a child neurologist at Boston Children’s Hospital. “This kind of study allows us to start understanding the cellular mechanisms” behind the brain damage, she says. In the future, she adds, “we might be able to alter the course of brain development” with drugs targeted at the cellular anomalies and delivered during pregnancy. CHD reduces oxygen delivery to the brain at a time when the fetus most needs it. This lack of oxygen is thought to be a primary cause of the brain aberrations, which first become visible on MRI scans in the third trimester of pregnancy. (The heart anomalies themselves are commonly identified in the second trimester, on routine ultrasound scans.) Yet until now, scientists have been unclear about the underlying cellular process causing the brain problems. So a research team led by scientists at Children’s National Health System in Washington, D.C., delivered subpar levels of oxygen to newborn piglets, whose course of brain development and whose highly evolved brain structure mirrors in many respects those of humans. © 2017 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 23150 - Posted: 01.26.2017
By Andy Coghlan NEW drug will finally cure Alzheimer’s! Sound familiar? Seemingly every other week, the results of one preliminary trial or another promise that a game-changing drug for Alzheimer’s disease is just around the corner. Check back a few months later, though, and all mention of the drug has vanished, save perhaps for a terse story about a failed trial. Almost all clinical trials of new drugs to combat Alzheimer’s fail. No drug has bucked the trend in 20 years, but you wouldn’t know it from the constant promises of a breakthrough. Last November, after the failure of a particularly high-profile trial, for some the jig was up. “There are no treatments that can slow or reverse this devastating condition,” says Bryce Vissel at the University of Technology in Sydney, Australia. “There is no question that we have to look at Alzheimer’s in a different way.” So are we heading in the right direction, or do we need to rip up all the textbooks and start over? Alzheimer’s is the most common cause of dementia, and by some metrics its prevalence is rising. Alzheimer’s Disease International estimates that in 2015, 46.8 million people worldwide had dementia, a number that is set to double every 20 years, mostly because of an increasing number of older people in developing countries like India and China, leading to a global healthcare crisis. © Copyright Reed Business Information Ltd.
Link ID: 23149 - Posted: 01.26.2017
Sarah DeVos Targeting tangles of tau protein in mice with Alzheimer’s-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer’s disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer’s have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. “Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial,” says Tim Miller of Washington University in St Louis, Missouri. Now Miller’s team has purged tau tangles from the brains of Alzheimer’s-like mice for the first time. They used fragments of RNA called antisense oligonucleotides to sabotage the gene that makes tau, preventing it from being fully translated into protein. Once a day for four weeks, the team injected the antisense treatment, named Tau-ASO12, into the fluid at the base of each mouse’s spine. The mice had been genetically engineered to make a rogue form of tau similar to what is seen in people with Alzheimer’s, predisposing the mice to developing tau-related brain problems. The drug successfully spread throughout the brain, and was linked to a reduction in levels of tau that was made. It also seemed to destroy existing tau tangles, and prevent tau from spreading around the brain in older mice. © Copyright Reed Business Information Ltd.
Link ID: 23148 - Posted: 01.26.2017
By GRETCHEN REYNOLDS Being nearsighted is far more common than it once was. The prevalence of myopia, the condition’s medical name, in Americans has soared by 66 percent since the early 1970s, according to a 2009 study by the National Eye Institute; in China and other East Asian countries, as many as 90 percent of recent high school graduates are thought to be nearsighted. Myopia results when eyeballs are longer than normal, changing the angle at which light enters the eye and therefore the ability to focus on distant objects. The disorder involves a complex interplay of genetics and environment and usually begins before adolescence, when the eye is growing, but it can worsen in early adulthood. Some experts connect the elevated rates of myopia to the many hours young people stare at computers and other screens. But a recent study published in JAMA Ophthalmology suggests that a greater factor may be a side effect of all that screen-watching — it’s keeping children inside. This new study joins a growing body of research indicating that a lack of direct sunlight may reshape the human eye and impair vision. Researchers at King’s College London, the London School of Hygiene and Tropical Medicine and other institutions gave vision exams to more than 3,100 older European men and women and interviewed them at length about their education, careers and how often they remembered being outside during various stages of their lives. This biographical information was then cross-referenced with historical data about sunlight, originally compiled for research on skin cancer and other conditions. © 2017 The New York Times Company
About 11 per cent of Canadians aged 15 to 24 experienced depression at some point in their lives, and fewer than half of them sought professional help for a mental health condition over the previous year, according to Statistics Canada. The information was released Wednesday in the agency's Health Reports, and is based on data from the 2012 Canadian Community Health Survey Mental Health. The report was based on 4,031 respondents aged 15 to 24, which when extrapolated represents more than 4.4 million young people. Canadians 15 to 24 years old had a higher rate of depression than any other age group. Suicide is the second leading cause of death (after accidents), accounting for nearly a quarter of deaths in the 15-24 category, Statistics Canada said. An estimated 14 per cent of respondents reported having had suicidal thoughts at some point in their lives. The figure includes six per cent having that thought in the past 12 months. As well, 3.5 per cent had attempted suicide, according to the data. Report author Leanne Findlay said the findings confirm people with depression or suicidal thoughts are increasingly likely to seek professional help. Young people in the study were more likely to turn to friends or family, and when they did, generally felt they received a lot or some help. Factors such as perceived ability to deal with stress and "negative social interactions" — for instance, feeling others were angry with you — were related to depression and suicidal thoughts. Symptoms of depression include feeling sad or having trouble sleeping that last two weeks or more, Findlay said. "Knowledge of these risk and protective factors may facilitate early intervention," Findlay concluded. ©2017 CBC/Radio-Canada.
By Helen Briggs BBC News Babies build knowledge about the language they hear even in the first few months of life, research shows. If you move countries and forget your birth language, you retain this hidden ability, according to a study. Dutch-speaking adults adopted from South Korea exceeded expectations at Korean pronunciation when retrained after losing their birth language. Scientists say parents should talk to babies as much as possible in early life. Dr Jiyoun Choi of Hanyang University in Seoul led the research. The study is the first to show that the early experience of adopted children in their birth language gives them an advantage decades later even if they think it is forgotten, she said. ''This finding indicates that useful language knowledge is laid down in [the] very early months of life, which can be retained without further input of the language and revealed via re-learning,'' she told BBC News. In the study, adults aged about 30 who had been adopted as babies by Dutch-speaking families were asked to pronounce Korean consonants after a short training course. Korean consonants are unlike those spoken in Dutch. The participants were compared with a group of adults who had not been exposed to the Korean language as children and then rated by native Korean speakers. Both groups performed to the same level before training, but after training the international adoptees exceeded expectations. There was no difference between children who were adopted under six months of age - before they could speak - and those who were adopted after 17 months, when they had learned to talk. This suggests that the language knowledge retained is abstract in nature, rather than dependent on the amount of experience. © 2017 BBC
By Kevin Pelphrey, In September, the Florida State University football team made a visit to a Tallahassee middle school that would become famous. At lunchtime, student-athlete Travis Rudolph noticed sixth grader Bo Paske eating alone, so he joined Bo for the meal. Bo, who has autism, often sat by himself in the lunchroom. The world took note of the athlete’s gesture after his mother’s Facebook post about it went viral. “This is one day I didn’t have to worry if my sweet boy ate lunch alone, because he sat across from someone who is a hero in many eyes,” she wrote. This story touched people because it calls to mind something universal: the sting of social exclusion. We have all known children who often eat, or play, alone. And all of us have felt left out at one time or another. But although this experience may be universal, a new generation of children is experiencing a wave of inclusiveness. Technology of various types, often thought of as an isolating influence, can actually abet people’s good intentions or help those with autism learn to fit in. One new app called Sit With Us, invented by 16-year-old Natalie Hampton, helps vulnerable children who have difficulty finding a welcoming group in the lunchroom. Its motto is inspiring: “The first step to a warmer, more inclusive community can begin with LUNCH.” Sit With Us allows students to designate themselves as ‘ambassadors’ and to signal to anyone seeking company that they’re invited to join the ambassador’s table. © 2017 Scientific American
By JANE E. BRODY Insomnia is like a thief in the night, robbing millions — especially those older than 60 — of much-needed restorative sleep. As the king laments in Shakespeare’s “Henry IV, Part 2”: O sleep, O gentle sleep, Nature’s soft nurse, how have I frightened thee. That thou no more will weigh my eyelids down, And steep my senses in forgetfulness? The causes of insomnia are many, and they increase in number and severity as people age. Yet the problem is often overlooked during routine checkups, which not only diminishes the quality of an older person’s life but may also cause or aggravate physical and emotional disorders, including symptoms of cognitive loss. Most everyone experiences episodic insomnia, a night during which the body seems to have forgotten how to sleep a requisite number of hours, if at all. As distressing as that may seem at the time, it pales in comparison to the effects on people for whom insomnia — difficulty falling asleep, staying asleep or awakening much too early — is a nightly affair. A survey done in 1995 by researchers at the National Institute on Aging among more than 9,000 people aged 65 and older living in three communities revealed that 28 percent had problems falling asleep and 42 percent reported difficulty with both falling asleep and staying asleep. The numbers affected are likely to be much larger now that millions spend their pre-sleep hours looking at electronic screens that can disrupt the body’s biological rhythms. Insomnia, Dr. Alon Y. Avidan says, “is a symptom, not a diagnosis” that can be a clue to an underlying and often treatable health problem and, when it persists, should be taken seriously. Dr. Avidan is director of the sleep clinic at the University of California, Los Angeles, David Geffen School of Medicine. © 2017 The New York Times Company
By Ashley P. Taylor Neurodegenerative diseases are often associated with aging. To learn what happens within the aging brain and potentially gain information relevant to human health, researchers examined gene-expression patterns in postmortem brain samples. Overall, the researchers found, gene expression of glial cells changed more with age than did that of neurons. These gene-expression changes were most significant in the hippocampus and substantia nigra, regions damaged in Alzheimer’s and Parkinson’s diseases, respectively, according to the study published today (January 10) in Cell Reports. “Typically we have concentrated on neurons for studies of dementia, as they are the cells involved in brain processing and memories. [This] study demonstrates that glia are likely to be equally important,” study coauthors Jernej Ule and Rickie Patani of the Francis Crick Institute and University College London wrote in an email to The Scientist. “The authors’ effort in this comprehensive work is a ‘genomic tour de force,’ showing that, overall, non-neuronal cells undergo gene expression changes at a larger scale than previously thought in aging,” Andras Lakatos, a neuroscientist at the University of Cambridge, U.K., who was not involved in the study, wrote in an email. “This finding puts glial cells again at the center stage of functional importance in neurodegenerative conditions in which aging carries a proven risk.” © 1986-2017 The Scientist
By Andy Coghlan Can tiny brains grown in a dish reveal the secrets of sociability? Balls of brain tissue generated from stem cells are enabling us to understand the underlying differences between people who struggle to be sociable and those who have difficulty reining themselves in. Alysson Muotri at the University of California, San Diego, and his team created the mini-brains by exposing stem cells taken from the pulp of children’s milk teeth to cocktails of growth factors that help them mature. Eventually, they can develop as many as six layers of cerebral cortex – the outer surface of the brain. This region is much more sophisticated in humans than in other animals, and houses important circuitry governing our most complex thoughts and behaviours, including socialising with others. Each mini-brain is approximately 5 millimetres across. “Though they’re not as well defined as they are in a real brain, they resemble what you find in an embryonic fetus,” says Muotri. To understand how brain development affects sociability, the team used donated cells from children with autism and Rett syndrome, both of which are associated with impaired communication skills. They also used cells from children with Williams syndrome, a condition characterised by a hyper-sociable nature. People with Williams syndrome can be unable to restrain themselves from talking to complete strangers. © Copyright Reed Business Information Ltd.
Dima Amso, The early years of parenthood involve so many rewarding firsts—when your infant cracks a toothless grin, when he crawls and later walks, and, of course, when he utters a real, nonbabble word. A mother once told me she found it sad that if she were to pass away suddenly, her toddler wouldn't remember her or these exciting years. It is true that most of us don't remember much, if anything, from our infancy. So at what point do children start making long-term memories? I must first explain the different types of memory we possess. As I type this, I am using procedural memory—a form of motor memory in which my fingers just know how to type. In contrast, declarative memories represent two types of long-term recall—semantic and episodic. Semantic memory allows us to remember general facts—for example, that Alfred Hitchcock directed the film Vertigo; episodic memory encompasses our ability to recall personal experiences or facts—that Vertigo is my favorite film. Episodic memories are most relevant for understanding our childhood recollections. Making an episodic memory requires binding together different details of an event—when it happened and where, how we felt and who was there—and retrieving that information later. The processes involve the medial temporal lobes, most notably the hippocampus, and portions of the parietal and prefrontal cortices, which are very important in memory retrieval. Imaging studies often show that the same regions that encode an episode—for example, the visual cortex for vivid visual experiences—are active when we recall that memory, allowing for a kind of “mental time travel” or replay of the event. © 2017 Scientific American
By Greg Miller Babies born prematurely are prone to problems later in life—they’re more likely to develop autism or attention deficit hyperactivity disorder, and more likely to struggle in school. A new study that’s among the first to investigate brain activity in human fetuses suggests that the underlying neurological issues may begin in the womb. The findings provide the first direct evidence of altered brain function in fetuses that go on to be born prematurely, and they might ultimately point to ways to remediate or even prevent such early injuries. In the new study, published 9 January in Scientific Reports, developmental neuroscientist Moriah Thomason of Wayne State University School of Medicine in Detroit, Michigan, and colleagues report a difference in how certain brain regions communicate with each other in fetuses that were later born prematurely compared with fetuses that were carried to term. Although the findings are preliminary because the study was small, Thomason and other researchers say the work illustrates the potential (and the challenges) of the emerging field of fetal neuroimaging. “Harnessing the power of these advanced tools is offering us for the very first time the opportunity to explore the onset of neurologic insults that are happening in utero,” says Catherine Limperopoulos, a pediatric neuroscientist at Children’s National Medical Center in Washington, D.C. Thomason and colleagues used functional magnetic resonance imaging (fMRI) to investigate brain activity in 32 fetuses. The pregnant mothers were participants in a larger, long-term study of brain development led by Thomason. “The majority have just normal pregnancies, but they’re drawn from a low-resource population that’s at greater risk of early delivery and developmental problems,” she says. In the end, 14 of the fetuses were born prematurely. © 2017 American Association for the Advancement of Science.
By Meredith Wadman In athletes who suffered a concussion, a protein in their blood may be able to predict when they can return to action. A new study finds that those who took longer to return to play had higher levels of a protein known as tau in their blood in the 6 hours following the trauma than players who were cleared to return to the field sooner. Tau blood testing isn’t ready for prime time, but experts say that if it pans out it would become an invaluable tool for coaches and physicians alike. Trainers, sports physicians, and neurologists deal with some 3.8 million sports-related concussions in the United States each year. But they still lack an objective medical test to establish whether someone has sustained the injury, and at what point they have recovered enough from one to resume playing. Instead, they are forced to rely on often-nebulous physical signs, and on players’ self-reporting of symptoms. And it’s known that players, keen to get back on the field, often minimize these. “We don’t want a biomarker that just says somebody had a concussion,” says study leader Jessica Gill, a neuroscientist at the National Institute of Nursing Research in Bethesda, Maryland. “We want a biomarker that says who needs to be out of play to recover.” Gill, with concussion physician Jeffrey Bazarian of the University of Rochester School of Medicine and Dentistry in New York, and colleagues took preseason blood samples from more than 600 male and female University of Rochester athletes who participate in contact sports: football, basketball, hockey, and lacrosse. In it, they measured levels of tau, a protein linked to traumatic brain injury and Alzheimer’s disease, which has been found to be elevated in the blood of Olympic boxers and concussed ice hockey players. © 2017 American Association for the Advancement of Science.
By Joshua A. Krisch At the core of Alzheimer’s disease are amyloid-beta (Aβ) peptides, which self-assemble into protein fibrils that form telltale plaques in the brain. Now, the results of a study published today (January 4) in Nature suggest that certain fibril formations are more likely to appear in cases of rapidly progressive Alzheimer’s disease, as opposed to less-severe subtypes. The findings increase scientists’ understanding of the structure of these fibrils, and may eventually contribute to new tests and treatments for Alzheimer’s disease. “It is generally believed that some form of the aggregated Aβ peptide leads to Alzheimer’s disease, and it’s conceivable that different fibril structures could lead to neurodegeneration with different degrees of aggressiveness,” said coauthor Robert Tycko, a principal investigator at the National Institute of Diabetes and Digestive Kidney Disease. “But the mechanism by which this happens is uncertain. Some structures may be more inert and benign. Others may be more inherently toxic or prone to spread throughout the brain tissue.” Prior research has demonstrated that Aβ fibrils with various molecular structures exhibit different levels of toxicity in neuronal cell cultures, a finding confirmed in subsequent mouse trials. One study even demonstrated that Aβ fibrils cultured from patients with rapidly progressive Alzheimer’s disease are different in size and resistance to chemical denaturation than those isolated from patients with more slowly progressing disease. Building on these observations, Tycko and colleagues set out to better characterize the structures of these fibrils and get a better handle on the potential correlations between structure and disease subtype. © 1986-2017 The Scientist
Link ID: 23066 - Posted: 01.07.2017