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

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By David H. Freedman Two levels below ground, under a small, drab building at the University of Bonn, is a wall of cages containing mice that, according to standard tests, are extraordinarily average. They learn and remember how to run mazes no better nor worse than other mice. It takes them a typical amount of time to figure out how to extricate themselves from a tank of water with hidden exit steps. There’s nothing out of line about how they interact with other mice, nor their willingness to explore open spaces. And yet these mice are the center of attention at the lab of Andreas Zimmer. That’s because their boringly average minds may well hold the key to beating Alzheimer’s and elderly dementia. Many of the mice are 18 months old, roughly equivalent to a 70-year-old human. Mice normally start to show mental decline at around a year old, and by 18 months, struggle with mazes and other mental tasks, as well as with socializing. But not these rodent seniors. “You can’t tell the difference between them and two-month-old mice,” says Zimmer. Even more surprising is what Zimmer has done to get these elderly mice remembering and behaving like younger ones. It’s not special genes, a particular training regimen, nor an unusual diet. They don’t get any approved memory drug, nor a new investigational procedure. Basically, Zimmer keeps them very slightly stoned. A longtime U.S. National Institutes of Health (NIH) researcher who is now one of Germany’s most respected neuroscientists, Zimmer has been on a long journey to answer a question that few researchers had thought to ask: Is it possible that weed, long seen as the stuff of slackers, might actually contain the secret to sharpening the aging brain? © 2020 Kalmbach Media Co.

Keyword: Alzheimers; Drug Abuse
Link ID: 27094 - Posted: 03.05.2020

By Simon Makin Neuroscientists understand much about how the human brain is organized into systems specialized for recognizing faces or scenes or for other specific cognitive functions. The questions that remain relate to how such capabilities arise. Are these networks—and the regions comprising them—already specialized at birth? Or do they develop these sensitivities over time? And how might structure influence the development of function? “This is an age-old philosophical question of how knowledge is organized,” says psychologist Daniel Dilks of Emory University. “And where does it come from? What are we born with, and what requires experience?” Dilks and his colleagues addressed these questions in an investigation of neural connectivity in the youngest humans studied in this context to date: 30 infants ranging from six to 57 days old (with an average age of 27 days). Their findings suggest that circuit wiring precedes, and thus may guide, regional specialization, shedding light on how knowledge systems emerge in the brain. Further work along these lines may provide insight into neurodevelopmental disorders such as autism. In the study, published Monday in Proceedings of the National Academy of Sciences USA, the researchers looked at two of the best-studied brain networks dedicated to a particular visual function—one that underlies face recognition and another that processes scenes. The occipital face area and fusiform face area selectively respond to faces and are highly connected in adults, suggesting they constitute a face-recognition network. The same description applies to the parahippocampal place area and retrosplenial complex but for scenes. All four of these areas are in the inferior temporal cortex, which is behind the ear in humans. © 2020 Scientific American,

Keyword: Development of the Brain; Vision
Link ID: 27088 - Posted: 03.03.2020

By Jillian Kramer One of the strongest predictors of becoming an alcoholic is family history: the offspring of people with the disorder are four times more likely than others to develop it, according to the National Institute on Alcohol Abuse and Alcoholism (NIAAA). But new research shows a family history of alcoholism (FHA) affects more than your desire to drink. It also changes how your brain transitions from one task to the next—going, say, from cooking breakfast to thinking about a work deadline. A whole line of research has found that having an alcoholic in the family can affect one’s mental processes. But these studies have not fully explored what is called executive function—planning, restraint and other behaviors that are impaired with FHA. To delve further, Enrico Amico, now at the Swiss Federal Institute of Technology in Lausanne, and his colleagues decided to focus on how the brain processes competing cognitive demands—the switching of neural activity from one brain network to another, which is critical to executive functioning. Prior studies acquired “snapshots” of network activity when subjects were either performing a task or resting quietly. But this approach does not provide a continuous record of what is happening in the brain to capture the dynamic transitions from active to resting states that occur constantly throughout the day. So Amico, then at Purdue University, and a team of researchers at Purdue and Indiana University set out to answer how the brain makes these transitions. © 2020 Scientific American

Keyword: Drug Abuse; Genes & Behavior
Link ID: 27086 - Posted: 03.03.2020

By Sarah Witman Nicole Dodds first noticed her son, Rowan, was having trouble using the right side of his body when he was about 6 months old. Babies typically use both hands to pick up toys and lift their chest off the floor at that age, but Rowan was mostly using his left arm and hand, keeping his right hand balled in a fist. That started a string of doctor visits. Around Rowan’s first birthday, doctors did an MRI and diagnosed his one-sided weakness as hemiplegia, probably caused by a stroke he sustained in utero. This surprised Dodds, since as far as she knew she’d had a totally normal pregnancy and birth Perinatal stroke — when an infant loses blood supply to the brain in late pregnancy, during birth or in the first month of life — is one of the most common causes of hemiplegia in infants, affecting anywhere from 1 in 2,500 to 1 in 4,000 live births in the United States every year. Like adult stroke, perinatal stroke is usually caused by a blood clot that jams brain arteries, or else by bleeding in or around the infant’s brain. Babies with heart disease, clotting disorders such as hemophilia, and bacterial infection among other factors have a higher risk of perinatal stroke, but the exact cause is often unknown. As in the case with Rowan, there are often no outward signs for up to a year that something is amiss, resulting in delayed or inconclusive diagnosis. It’s nearly impossible to detect a stroke in utero, or even in the first few weeks after birth, since the symptoms can seem within the norm for infants: favoring one side, extreme sleepiness, mild seizures that seem like shivering or sudden stiffening. More obvious behaviors such as trouble walking and talking don’t usually become apparent until the child turns 2, and are associated with other childhood problems.

Keyword: Stroke; Development of the Brain
Link ID: 27069 - Posted: 02.25.2020

By Jane Wakefield Technology reporter An ambitious project to develop a wearable device to detect early signs of Alzheimer's disease has been launched. The Early Detection of Neurodegenerative diseases (Edon) is being spearheaded by charity Alzheimer's Research UK. It will initially analyse data from continuing studies into the disease, using artificial intelligence. And this data will be used to design a prototype device within three years. Wearables collect a variety of data including gait, heart rate and sleep patterns and the hope is by analysing this data, researchers can begin to map signs of the disease years before symptoms develop. The global initiative has already won funding from tech founder turned philanthropist Bill Gates. But it also forms part of the UK government's wider ambition to use artificial intelligence and data to help better understand and prevent chronic diseases. Initially, EDoN will work with the UK's national institute for data science and artificial intelligence, The Alan Turing Institute, to trawl through data from continuing studies into Alzheimer's disease. Prof Chris Holmes, health programme director at the institute, said: "Artificial intelligence has the potential to transform the learning opportunities from large-scale data studies such as Edon by integrating information from multiple sources. "We will use AI to deliver new insights into the early signals of disease by combining digital data measurements with traditional sources such as brain imaging and memory tests." There are currently 850,000 people living with dementia in the UK, according to Alzheimer's Research UK. © 2020 BBC.

Keyword: Alzheimers
Link ID: 27064 - Posted: 02.24.2020

By Viviane Callier In 1688 Irish philosopher William Molyneux wrote to his colleague John Locke with a puzzle that continues to draw the interest of philosophers and scientists to this day. The idea was simple: Would a person born blind, who has learned to distinguish objects by touch, be able to recognize them purely by sight if he or she regained the ability to see? The question, known as Molyneux’s problem, probes whether the human mind has a built-in concept of shapes that is so innate that such a blind person could immediately recognize an object with restored vision. The alternative is that the concepts of shapes are not innate but have to be learned by exploring an object through sight, touch and other senses, a process that could take a long time when starting from scratch. An attempt was made to resolve this puzzle a few years ago by testing Molyneux's problem in children who were congenitally blind but then regained their sight, thanks to cataract surgery. Although the children were not immediately able to recognize objects, they quickly learned to do so. The results were equivocal. Some learning was needed to identify an object, but it appeared that the study participants were not starting completely from scratch. Lars Chittka of Queen Mary University of London and his colleagues have taken another stab at finding an answer, this time using another species. To test whether bumblebees can form an internal representation of objects, Chittka and his team first trained the insects to discriminate spheres and cubes using a sugar reward. The bees were trained in the light, where they could see but not touch the objects that were isolated inside a closed petri dish. Then they were tested in the dark, where they could touch but not see the spheres or cubes. The researchers found that the invertebrates spent more time in contact with the shape they had been trained to associate with the sugar reward, even though they had to rely on touch rather than sight to discriminate the objects. © 2020 Scientific American

Keyword: Development of the Brain; Vision
Link ID: 27061 - Posted: 02.21.2020

By Kim Tingley Hearing loss has long been considered a normal, and thus acceptable, part of aging. It is common: Estimates suggest that it affects two out of three adults age 70 and older. It is also rarely treated. In the U.S., only about 14 percent of adults who have hearing loss wear hearing aids. An emerging body of research, however, suggests that diminished hearing may be a significant risk factor for Alzheimer’s disease and other forms of dementia — and that the association between hearing loss and cognitive decline potentially begins at very low levels of impairment. In November, a study published in the journal JAMA Otolaryngology — Head and Neck Surgery examined data on hearing and cognitive performance from more than 6,400 people 50 and older. Traditionally, doctors diagnose impairment when someone experiences a loss in hearing of at least 25 decibels, a somewhat arbitrary threshold. But for the JAMA study, researchers included hearing loss down to around zero decibels in their analysis and found that they still predicted correspondingly lower scores on cognitive tests. “It seemed like the relationship starts the moment you have imperfect hearing,” says Justin Golub, the study’s lead author and an ear, nose and throat doctor at the Columbia University Medical Center and NewYork-Presbyterian. Now, he says, the question is: Does hearing loss actually cause the cognitive problems it has been associated with and if so, how? Preliminary evidence linking dementia and hearing loss was published in 1989 by doctors at the University of Washington, Seattle, who compared 100 patients with Alzheimer’s-like dementia with 100 demographically similar people without it and found that those who had dementia were more likely to have hearing loss, and that the extent of that loss seemed to correspond with the degree of cognitive impairment. But that possible connection wasn’t rigorously investigated until 2011, when Frank Lin, an ear, nose and throat doctor at Johns Hopkins School of Medicine, and colleagues published the results of a longitudinal study that tested the hearing of 639 older adults who were dementia-free and then tracked them for an average of nearly 12 years, during which time 58 had developed Alzheimer’s or another cognitive impairment. They discovered that a subject’s likelihood of developing dementia increased in direct proportion to the severity of his or her hearing loss at the time of the initial test. The relationship seems to be “very, very linear,” Lin says, meaning that the greater the hearing deficit, the greater the risk a person will develop the condition. © 2020 The New York Times Company

Keyword: Hearing; Alzheimers
Link ID: 27057 - Posted: 02.20.2020

By Judith Graham, Kaiser Health News Do I know I’m at risk for developing dementia? You bet. My father died of Alzheimer’s disease at age 72; my sister was felled by frontotemporal dementia at 58. And that’s not all: Two maternal uncles had Alzheimer’s, and my maternal grandfather may have had vascular dementia. (In his generation, it was called senility.) So what happens when I misplace a pair of eyeglasses or can’t remember the name of a movie I saw a week ago? “Now comes my turn with dementia,” I think. Then I talk myself down from that emotional cliff. Am I alone in this? Hardly. Many people, like me, who’ve watched this cruel illness destroy a family member, dread the prospect that they, too, might become demented. The lack of a cure or effective treatments only adds to the anxiety. It seems a common refrain, the news that another treatment to stop Alzheimer’s has failed. How do we cope as we face our fears and peer into our future? Andrea Kline, whose mother, as well as her aunt and uncle, had Alzheimer’s disease, just turned 71 and lives in Boynton Beach, Fla. She’s a retired registered nurse who teaches yoga to seniors at community centers and assisted-living facilities. “I worry about dementia incessantly: Every little thing that goes wrong, I’m convinced it’s the beginning,” she told me. Because Ms. Kline has had multiple family members with Alzheimer’s, she’s more likely to have a genetic vulnerability than someone with a single occurrence in their family. But that doesn’t mean this condition lies in her future. A risk is just that: It’s not a guarantee. The age of onset is also important. People with close relatives struck by dementia early — before age 65 — are more likely to be susceptible genetically. Ms. Kline was the primary caregiver for her mother, Charlotte Kline, who received an Alzheimer’s diagnosis in 1999 and passed away in 2007 at age 80. “I try to eat very healthy. I exercise. I have an advance directive, and I’ve discussed what I want” in the way of care “with my son,” she said. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27056 - Posted: 02.20.2020

Maternal obesity may increase a child’s risk for attention-deficit hyperactivity disorder (ADHD), according to an analysis by researchers from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), part of the National Institutes of Health. The researchers found that mothers — but not fathers — who were overweight or obese before pregnancy were more likely to report that their children had been diagnosed with attention-deficit hyperactivity disorder (ADHD) or to have symptoms of hyperactivity, inattentiveness or impulsiveness at ages 7 to 8 years old. Their study appears in The Journal of Pediatrics. The study team analyzed the NICHD Upstate KIDS Study, which recruited mothers of young infants and followed the children through age 8 years. In this analysis of nearly 2,000 children, the study team found that women who were obese before pregnancy were approximately twice as likely to report that their child had ADHD or symptoms of hyperactivity, inattention or impulsiveness, compared to children of women of normal weight before pregnancy. The authors suggest that, if their findings are confirmed by additional studies, healthcare providers may want to screen children of obese mothers for ADHD so that they could be offered earlier interventions. The authors also note that healthcare providers could use evidence-based strategies to counsel women considering pregnancy on diet and lifestyle. Resources for plus-size pregnant women and their healthcare providers are available as part of NICHD’s Pregnancy for Every Body initiative.

Keyword: ADHD; Development of the Brain
Link ID: 27055 - Posted: 02.20.2020

By Gina Kolata The study aimed to show that Alzheimer’s disease could be stopped if treatment began before symptoms emerged. The participants were the best candidates that scientists could find: still healthy, but with a rare genetic mutation that guaranteed they would develop dementia. For five years, on average, the volunteers received monthly infusions or injections of one of two experimental drugs, along with annual blood tests, brain scans, spinal taps and cognitive tests. Now, the verdict is in: The drugs did nothing to slow or stop cognitive decline in these subjects, dashing the hopes of scientists. Dr. Randall Bateman, a neurologist at Washington University in St. Louis and principal investigator of the study, said he was “shocked” when he first saw the data: “It was really crushing.” The results are a deep disappointment, scientists said — but not a knockout punch. The drugs did not work, but the problems may be fixable: perhaps the doses were too low, or they should have been given to patients much younger. Few experts want to give up on the hypothesis that amyloid plaques in the brain are intimately involved in Alzheimer’s disease. The data from this international study, called DIAN-TU, are still being analyzed and are to be presented on April 2 at scientific conferences in Vienna in April and in Amsterdam in July. The trial was sponsored by Washington University in St. Louis, two drug companies that supplied the drugs — Eli Lilly and Roche, with a subsidiary, Genentech — the National Institutes of Health and philanthropies, including the Alzheimer’s Association. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27038 - Posted: 02.13.2020

By Perri Klass, M.D. Whenever I write about attention deficit hyperactivity disorder — whether I’m writing generally about the struggles facing these children and their families or dealing more specifically with medications — I know that some readers will write in to say that A.D.H.D. is not a real disorder. They say that the rising numbers of children taking stimulant medication to treat attentional problems are all victims, sometimes of modern society and its unfair expectations, sometimes of doctors, and most often of the rapacious pharmaceutical industry. I do believe that A.D.H.D. is a valid diagnosis, though a diagnosis that has to be made with care, and I believe that some children struggle with it mightily. Although medication should be neither the first nor the only treatment used, some children find that the stimulants significantly change their educational experiences, and their lives, for the better. Dr. Mark Bertin, a developmental pediatrician in Pleasantville, N.Y., who is the author of “Mindful Parenting for A.D.H.D.,” said, “On a practical level, we know that correctly diagnosed A.D.H.D. is real, and we know that when they’re used properly, medications can be both safe and effective.” The choice to use medications can be a difficult one for families, he said, and is made even more difficult by “the public perception that they’re not safe, or that they fundamentally change kids.” He worries, he says, that marketing is really effective, and wants to keep it “at arm’s length,” far away from his own clinical decisions, not allowing drug reps in the office, not accepting gifts — but acknowledging, all the same, that it’s probably not possible to avoid the effects of marketing entirely. Still, he said, when it comes to stimulants, “the idea that we’re only using them because of the pharmaceutical industry is totally off base,” and can make it much harder to talk with parents about the potential benefits — and the potential problems — of treating a particular child with a particular medication. “When it comes to A.D.H.D. in particular, it’s a hard enough thing for families to be dealing with without all the fear and judgment added on.” © 2020 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 27030 - Posted: 02.10.2020

By Chris Woolston Sometimes it takes multitudes to reveal scientific truth. Researchers followed more than 7,000 subjects to show that a Mediterranean diet can lower the risk of heart disease. And the Women’s Health Initiative enlisted more than 160,000 women to show, among other findings, that postmenopausal hormone therapy put women at risk of breast cancer and stroke. But meaningful, scientifically valid insights don’t always have to come from studies of large groups. A growing number of researchers around the world are taking a singular approach to pain, nutrition, psychology and other highly personal health issues. Instead of looking for trends in many people, they’re designing studies for one person at a time. A study of one person — also called an N of 1 trial — can uncover subtle, important results that would be lost in a large-scale study, says geneticist Nicholas Schork of the Translational Genomics Research Institute in Phoenix. The results, he says, can be combined to provide insights for the population at large. But with N of 1 studies, the individual matters above all. “People differ at fundamental levels,” says Schork, who discussed the potential of N of 1 studies in a 2017 issue of the Annual Review of Nutrition. And the only way to understand individuals is to study them. Case studies of individuals in odd circumstances have a long history in medical literature. But the concept of a clinical medicine N of 1 study gathering the same level of information as a large study goes back to an article published in the New England Journal of Medicine in 1986. Hundreds of N of 1 studies have been published since then, and the approach is gaining momentum, says Suzanne McDonald, N of 1 research coordinator at the University of Queensland in Brisbane, Australia.

Keyword: Genes & Behavior; Schizophrenia
Link ID: 27027 - Posted: 02.10.2020

Abby Olena Researchers have shown previously that excessive proliferation of the cells of the brain, which can cause macrocephaly, or large head size, is associated with autism. Now, the authors of a study published in Cell Stem Cell last week (January 30) have connected that overgrowth with replication stress, subsequent DNA damage, and dysfunction in neural progenitor cells derived from induced pluripotent stem cells from patients with autism spectrum disorder. “It is striking,” Bjoern Schwer, a molecular biologist at the University of California, San Francisco, who studies DNA repair and genomic stability in neural cells and did not participate in the study, writes in an email to The Scientist. “These are fascinating findings with many implications for autism spectrum disorder—and potentially for other neurodevelopmental disorders too.” In 2016, a group led by Schwer and Frederick Alt of Boston Children’s Hospital showed that mice have clusters of double-strand DNA breaks in the genomes of their neural progenitor cells. These hotspots are concentrated in neural-specific genes, which tend to be longer than genes expressed in other cell types and have also been associated with neurological diseases. Rusty Gage, a neuroscientist at the Salk institute, Meiyan Wang, a graduate student in the Gage lab, and their colleagues collaborated with Alt to explore whether or not these same damaged clusters would show up in the genomes of human neural progenitor cells. Wang went to the Alt lab to learn how to map genome-wide double-strand breaks. Then, she used the technique on several neural progenitor cell lines that had been previously derived in the Gage lab: three from patients with macrocephalic autism spectrum disorder and three from neurotypical controls. © 1986–2020 The Scientist

Keyword: Autism; Genes & Behavior
Link ID: 27025 - Posted: 02.07.2020

Sarah O’Meara Xiaoming Zhou is a neurobiologist at East China Normal University in Shanghai. Here he speaks to Nature about his research into age-related hearing loss, and explains why he hopes that brain training could help to lessen declines in sensory perception generally, and so ward off neurodegenerative diseases. What is your current research focus? We want to better understand the neural basis for why a person’s hearing function declines as they grow older. For example, we have performed research to see whether we can reverse age-related changes to the auditory systems of rodents. We gave the animals a set of tasks, such as learning to discriminate between sounds of different frequencies or intensities. These exercises caused the rodents’ hearing to improve, and also promoted changes to the hippocampus, a part of the brain structure closely associated with learning and memory. The relationship with the hippocampus suggests that new kinds of brain training might help to attenuate our declines in perception and other brain functions, such as learning and memory, as we grow older — and so have the potential to stave off neurodegenerative diseases. How is ageing-related science developing in China? As has happened in the rest of the world, a rapidly ageing population has brought significant concern to policymakers. However, as far as I know, only a few neuroscience laboratories in China are specifically focused on learning more about the underlying mechanisms that cause changes in brain function as we age. This is despite the fact that such research could have a considerable impact on the welfare of older people in the future. © 2020 Springer Nature Limited

Keyword: Alzheimers
Link ID: 27023 - Posted: 02.07.2020

Jon Hamilton Scientists have found a clue to how autism spectrum disorder disrupts the brain's information highways. The problem involves cells that help keep the traffic of signals moving smoothly through brain circuits, a team reported Monday in the journal Nature Neuroscience. The team found that in both mouse and human brains affected by autism, there's an abnormality in cells that produce a substance called myelin. That's a problem because myelin provides the "insulation" for brain circuits, allowing them to quickly and reliably carry electrical signals from one area to another. And having either too little or too much of this myelin coating can result in a wide range of neurological problems. For example, multiple sclerosis occurs when the myelin around nerve fibers is damaged. The results, which vary from person to person, can affect not only the signals that control muscles, but also the ones involved in learning and thinking. The finding could help explain why autism spectrum disorders include such a wide range of social and behavioral features, says Brady Maher, a lead investigator at the Lieber Institute for Brain Development and an associate professor in the psychiatry department at Johns Hopkins School of Medicine. "Myelination could be a problem that ties all of these autism spectrum disorders together," Maher says. And if that's true, he says, it might be possible to prevent or even reverse the symptoms using drugs that affect myelination. © 2020 npr

Keyword: Autism; Glia
Link ID: 27019 - Posted: 02.04.2020

Alison Abbott Researchers studying the biological basis of mental illness have conducted the first genomic analysis of schizophrenia in an African population, and have identified multiple rare mutations that occur more frequently in people with the condition. The mutations are mainly in genes that are important for brain development and the brain’s synapses, tiny structures that coordinate communication between neurons. The genes match those identified in other similar studies of schizophrenia — but nearly all previous research has been conducted in European or Asian populations. The latest work was published1 in Science on 31 January. This research is particularly important because Africa has represented a big gap in the populations that geneticists have studied, says psychiatric geneticist Andreas Meyer-Lindenberg, director of the Central Institute of Mental Health in Mannheim, Germany. He says that the work lends support to current hypotheses about the biological origins of schizophrenia, which can cause a range of symptoms including hallucinations, delusions and disordered thinking. Researchers think that each mutation might contribute a small amount to the overall risk of developing the condition, and that disruption to synapses could be crucial to the disease’s development. Over the past decade, as studies that use genome sequencing to identify the genetic basis of diseases have flourished, geneticists have come under increasing fire for failing to sample diverse populations, largely neglecting African people. Around 80% of participants in genetic studies are of European descent, and less than 3% are of African descent. © 2020 Springer Nature Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27016 - Posted: 02.04.2020

By Nicholas Bakalar Flavonols, a large class of compounds found in most fruits and vegetables, may be associated with a reduced risk for Alzheimer’s disease. Flavonols are known to have antioxidant and anti-inflammatory effects, and animal studies have suggested they may improve memory and learning. A study in Neurology involved 921 men and women, average age 81 and free of dementia, who reported their diet using well-validated food questionnaires. During an average follow-up of six years, 220 developed Alzheimer’s disease. People with the highest levels of flavonol intake tended to have higher levels of education and were more physically active. But after controlling for these factors plus age, sex, the Apo E4 gene (which increases the risk for dementia) and late-life cognitive activity, the scientists found that compared with those in the lowest one-fifth for flavonol intake, those in the highest one-fifth had a 48 percent reduced risk for Alzheimer’s disease. The study covered four types of flavonols: kaempferol, quercetin, isorhamnetin and myricetin. All except quercetin showed a strong association with Alzheimer’s risk reduction. These flavonols are available as supplements, but the lead author, Dr. Thomas M. Holland, a professor of medicine at Rush Medical College in Chicago, said that foods are a better source. “You get a broader intake of vitamins, minerals and bioactives in food than in the supplements,” he said. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27015 - Posted: 02.04.2020

Timothy Bella The headaches had become so splitting for Gerardo Moctezuma that the pain caused him to vomit violently. The drowsiness that came with it had intensified for months. But it wasn’t until Moctezuma, 40, fainted without explanation at a soccer match in Central Texas last year that he decided to figure out what was going on. When Jordan Amadio looked down at his MRI results, the neurosurgeon recognized — but almost couldn’t believe — what looked to be lodged in Moctezuma’s brain. As he opened up Moctezuma’s skull during an emergency surgery in May 2019, he was able to confirm what it was that had uncomfortably set up shop next to the man’s brain stem: a tapeworm measuring about an inch-and-a-half. “It’s very intense, very strong, because it made me sweat too, sweat from the pain,” Moctezuma said to KXAN. The clear and white parasite came from tapeworm larva that Amadio believes Moctezuma, who moved from Mexico to the U.S. 14 years before his diagnosis, might have had in his brain for more than a decade undetected. His neurological symptoms had intensified due to his neurocysticercosis, which was the direct result of the tapeworm living in his brain. The cyst would trigger hydrocephalus, an accumulation of cerebrospinal fluid that increased pressure to the skull to the point that the blockage and pain had become life-threatening. “It’s a remarkable case where a patient came in and, if he had not been treated urgently, he would have died from tremendous pressure in the brain,” Amadio, attending neurosurgeon at the Ascension Seton Brain and Spine Institute in Austin, told The Washington Post on Thursday night.

Keyword: Development of the Brain
Link ID: 27013 - Posted: 02.01.2020

Madeline Andrews, Aparna Bhaduri, Arnold Kriegstein What was going on with our brain organoids? As neuroscientists, we use these three-dimensional clusters of cells grown in petri dishes to learn more about how the human brain works. Researchers culture various kinds of organoids from stem cells – cells that have the potential to become one of many different cell types found throughout the body. We use chemical signals to direct stem cells to produce brain-like cells that together resemble certain structural aspects of a real brain. While they are not “brains in a dish” – organoids cannot function or think independently – the idea is that organoid models let scientists see developmental processes that may yield insights into how the human brain works. If researchers better understand normal development, we may be able to understand when and how things go wrong in diseases. When we recently compared our lab’s organoid cells to normal brain cells, we were surprised to find that they didn’t look as similar as we’d expected. Our brain organoids, each the size of a few millimeters, were stressed out. Our investigation into why has important implications for this popular new method since many labs are using it to study brain function and neurological disease. Without accurate models of the brain, scientists will not be able to work toward disease treatments. Our lab is particularly interested in the human cerebral cortex – the brain’s bumpy exterior – because it is so different in human beings than it is in any other species. The human cortex is proportionally bigger than in our closest living relatives, the great apes, containing more and different types of cells. It’s the source of many unique human abilities, including our cognitive capacity. © 2010–2020, The Conversation US, Inc.

Keyword: Development of the Brain
Link ID: 27011 - Posted: 01.31.2020

By Leah Shaffer Football’s concussion crisis has been part of the NFL for almost two decades. But the pros aren’t the only ones reevaluating their relationship with the game. Now, studies are finding that parents of younger children are increasingly concerned about the long-term impacts of playing football. A national survey from 2015 found that 25 percent of parents do not let their kids play contact sports due to fear of concussions, while an Aspen Institute report recently found that participation in tackle football declined by 12 percent among children ages 6 to 12 between 2016 and 2017. The research into the risks of youth football is still coming into shape, and there’s disagreement about just how universal and severe the risks are. Some researchers think football is dangerous for everybody; others are finding evidence that some kids might be more predisposed to health consequences than others. In the last two years, some researchers have shown that head hits in youth sports increase the risk of developing chronic traumatic encephalopathy, or CTE, an untreatable degenerative brain disease with symptoms ranging from memory loss to progressive dementia. Other studies have shown that the longer a person plays football, the higher the risk they have for developing symptoms associated with CTE. So, case closed, right? No — football is not the only risk factor in developing symptoms of CTE. The same study that found an association between repetitive head impact and dementia in CTE also found that cardiovascular disease and dementia in CTE were correlated. And a separate study of some 10,000 people found no association between participation in contact sports and later cognitive decline or increase in symptoms of depression. © 2020 ABC News Internet Ventures

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 27010 - Posted: 01.31.2020