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Emily Makowski China’s approval of the drug oligomannate earlier this month for treating mild to moderate Alzheimer’s disease has been met with surprise and skepticism from some members of the scientific community, who claim that the preclinical data raise questions about the underlying mechanism of the drug. One microbiome researcher has pointed out inconsistencies between the researchers’ data and their proposed mechanism for how oligomannate could treat Alzheimer’s. “The field is seeing this [research] with a large dose of skepticism,” Malú Tansey, a neuroimmunologist at the University of Florida College of Medicine, tells The Scientist. On November 2, Shanghai Green Valley Pharmaceuticals announced that oligomannate, an oligosaccharide mixture derived from brown algae, had been approved by the National Medical Product Administration (NMPA), China’s equivalent of the US Food and Drug Administration. The announcement followed the completion of a Phase 3 clinical trial in China that found the drug appeared to slow cognitive decline in Alzheimer’s patients. In addition, researchers led by Meiyu Geng at the Shanghai Institute of Materia Medica published a paper in Cell Research in September on oligomannate’s ability to remodel the gut microbiome in mice and reduce neuroinflammation. There is an emerging link between the gut microbiome and Alzheimer’s disease in humans. In the study, the researchers gave oligomannate to mice that are genetically engineered to show physical and behavioral symptoms similar to Alzheimer’s disease. The team collected mouse feces to study the microorganisms present in gut microbiota, drew blood to analyze the presence of immune cells, and also examined the levels of cytokines, which are inflammatory compounds, in the brain. © 1986–2019 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26821 - Posted: 11.16.2019

By Gary Stix Socrates famously railed against the evils of writing. The sage warned that it would “introduce forgetfulness into the soul of those who learn it: they will not practice using their memory because they will put their trust in writing.” He got a few things wrong. For one, people nurture Socrates’ memory because of all of the books written about him. But he also was off the mark in his musings about a forgetfulness of the soul. If anything, it appears that just the opposite holds: a study of hundreds of illiterate people living at the northern end of an island considered to be a world media capital roundly contradicts the father of Western philosophy. Evaluations of the elderly in the environs of Manhattan’s Washington Heights (the neighborhood immortalized by a Lin-Manuel Miranda musical) reveal that the very act of reading or writing—largely apart from any formal education—may help protect against the forgetfulness of dementia. “The people who were illiterate in the study developed dementia at an earlier age than people who were literate in the study,” says Jennifer J. Manly, senior author of the paper, which appeared on November 13in Neurology. Earlier studies trying to parse this topic had not been able to disentangle the role of reading and writing from schooling to determine whether literacy, by itself, could be a pivotal factor safeguarding people against dementia later in life. The researchers conducting the new study, who are mostly at Columbia University’s Vagelos College of Physicians and Surgeons, recruited 983 people with four years or less of schooling who were part of the renowned Washington Heights–Inwood Columbia Community Aging Project. Of that group, 238 were illiterate, which was determined by asking the participants point-blank, “Did you ever learn to read or write?”—followed by reading tests administered to a subsample. Even without much time in school, study subjects sometimes learned from other family members. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26819 - Posted: 11.14.2019

By Sara Manning Peskin, M.D. At 66, Bob Karger was losing language. It was not the tip-of-the-tongue feeling that melts when you recall a sought-after word. He had lost the connection between sounds and meaning — the way ba-na-na recalls a soft, yellow fruit or ea-gle calls to mind a large bird of prey. In a recent conversation, he had thought acorns grew on pine trees. Mr. Karger did not know how to use items around the house, either. When he picked up a can opener, he would not realize it could remove the top from a tin. If he held a hammer, he might grasp it by the head, turning it around in his palm, not knowing he could swing it into a nail. His world was filled with incomprehensible items. His wife, Sandy Karger, noticed other changes. When she told her husband about a family member who died, Mr. Karger laughed instead of comforting her. He tipped excessively, slipping $20 bills to strangers, because they reminded him of close friends. He fixated on obese people. “Look at that person, they’re really fat,” he would say loudly, in public. Overcome by impatience, he would push people ahead of him in line at the store. “Can’t you hurry up?” he’d yell. “Do you really need to buy that?” In other ways, Mr. Karger’s mind was as sharp as it had ever been. He could remember upcoming appointments and recent dinners. He didn’t repeat himself in conversation. His long-term memory was at times better than Ms. Karger’s. After two years of worsening symptoms, the Kargers found Dr. Murray Grossman at the University of Pennsylvania. Dr. Grossman is short and charismatic, a quick-witted Montreal native who has mentored me since I began training in neurology. For the past several decades, he has pioneered research on neurodegenerative diseases that change behavior and language. When he saw Mr. Karger in 2007, the diagnosis was clear within the hour: Mr. Karger had a type of frontotemporal dementia. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26799 - Posted: 11.07.2019

By Andrew Joseph, STAT Chinese regulators have granted conditional approval to an Alzheimer’s drug that is derived from seaweed, potentially shaking up the field after years of clinical failures involving experimental therapies from major drug companies. The announcement over the weekend has been met with caution as well as an eagerness from clinicians and others to see full data from the drug maker, Shanghai Green Valley Pharmaceuticals. The company said its drug, Oligomannate, improved cognitive function in patients with mild to moderate Alzheimer’s compared to placebo in a Phase 3 trial, with benefits seen in patients as early as week four and persisting throughout the 36 weeks of the trial. It has been almost two decades since any Alzheimer’s drug was approved. Oligomannate has received scant attention in the United States during its development. Advertisement Although full data on the drug have not yet been made available, the conditional approval by regulators means Oligomannate, also known as GV-971, will on the market in China by the end of the year, Green Valley said. The company will have to submit additional research on the mechanism of the drug and its long-term safety and effectiveness to the country’s National Medical Products Administration, Reuters reported. Green Valley also said it would launch a global Phase 3 trial next year in hopes of filing for approval in other countries as well. “It’s good to see that drug regulators in China are prioritizing emerging treatments for Alzheimer’s, but we do still need to see more evidence that this drug is safe and effective,” Carol Routledge, the director of research at Alzheimer’s Research UK, said in a statement. “For any potential drug to gain a stamp of approval by regulators in the UK, we’ll need to see larger trials in countries around the world to back up the evidence from China.” © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26795 - Posted: 11.06.2019

By Gretchen Reynolds Being physically fit may sharpen the memory and lower our risk of dementia, even if we do not start exercising until we are middle-aged or older, according to two stirring new studies of the interplay between exercise, aging, aerobic fitness and forgetting. But both studies, while underscoring the importance of activity for brain health, also suggest that some types of exercise may be better than others at safeguarding and even enhancing our memory. The scientific evidence linking exercise, fitness and brain health is already hefty and growing. Multiple studies have found that people with relatively high levels of endurance, whatever their age, tend to perform better on tests of thinking and memory than people who are out of shape. Other studies associate better fitness with less risk for developing Alzheimer’s disease. But many of these studies have been one-time snapshots of people’s lives and did not delve into whether and how changing fitness over time might alter people’s memory skills or dementia risk. They did not, in other words, tell us whether, by midlife or retirement age, it might be too late to improve our brain health with exercise. So, for the first of the new studies, which was published this month in The Lancet Public Health, researchers at the Norwegian University of Science and Technology in Trondheim, Norway, helpfully decided to look into that very issue, taking advantage of the reams of health data available on average Norwegians. They began by turning to records from a large-scale health study that had enrolled almost every adult resident in the region around Trondheim beginning in the 1980s. The participants completed health and medical testing twice, about 10 years apart, that included estimates of their aerobic fitness. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 26794 - Posted: 11.06.2019

By Pam Belluck The woman’s genetic profile showed she would develop Alzheimer’s by the time she turned 50. She, like thousands of her relatives, going back generations, was born with a gene mutation that causes people to begin having memory and thinking problems in their 40s and deteriorate rapidly toward death around age 60. But remarkably, she experienced no cognitive decline at all until her 70s, nearly three decades later than expected. How did that happen? New research provides an answer, one that experts say could change the scientific understanding of Alzheimer’s disease and inspire new ideas about how to prevent and treat it. In a study published Monday in the journal Nature Medicine, researchers say the woman, whose name they withheld to protect her privacy, has another mutation that has protected her from dementia even though her brain has developed a major neurological feature of Alzheimer’s disease. This ultra rare mutation appears to help stave off the disease by minimizing the binding of a particular sugar compound to an important gene. That finding suggests that treatments could be developed to give other people that same protective mechanism. “I’m very excited to see this new study come out — the impact is dramatic,” said Dr. Yadong Huang, a senior investigator at Gladstone Institutes, who was not involved in the research. “For both research and therapeutic development, this new finding is very important.” A drug or gene therapy would not be available any time soon because scientists first need to replicate the protective mechanism found in this one patient by testing it in laboratory animals and human brain cells. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26792 - Posted: 11.05.2019

By Derek Lowe So Amgen has exited the neuroscience area, with a good-sized round of layoffs at their research site Cambridge. The company has a migraine drug (Aimovig) that they’ll continue to support, and they’ll stick with their existing clinical programs, but it looks like all the early-stage stuff is gone. What does this mean? Not as much as you might think. Neuroscience is indeed hard, and Amgen’s not the only company to rethink its commitment to it (Eli Lilly did something similar last month with their neuro efforts in the UK). But there are still plenty of participants, large and small – it’s not that the field is being totally abandoned by pharma. It’s just being abandoned by Amgen, because they have other areas that look a lot more promising for them. And let’s face it, Amgen is a bit of an oddity, anyway – it’s not for nothing that they get referred to as a law firm with fume hoods. Enbrel is what pays a lot of the bills over there, and Enbrel is (and has long been) a patent-court story, not a research one. Inflammation, cardiovascular disease, and oncology are going to be the focus there, and given the company’s portfolio, that makes a lot of sense. It looks like the only neuro programs going on will be the ones that intersect with the larger inflammation area. One interesting thing that came out of the company’s statements was that management felt that a lot of the neuroscience landscape is focused on what their CFO David Meline called “orphan or niche diseases”, and that the company wants to work on things that will have a broader impact. Now, it’s not like there isn’t a neuroscience disease with a huge health impact, and it’s one that even has some inflammation and cardiovascular connections. So one of the things that Amgen is saying is “No Alzheimer’s research for us, thanks”. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26777 - Posted: 11.01.2019

By Meredith Wadman, Kelly Servick Biogen stunned investors and scientists alike today, announcing it will resurrect an Alzheimer’s drug it had declared a failure in March; the company plans in early 2020 to ask the U.S. Food and Drug Administration for marketing approval of aducanumab, an antibody designed to bind and eliminate the protein beta-amyloid in the brain. As STAT reports, Biogen says the about-face came after it assessed clinical trial data from a larger number of patients than it first analyzed. Whereas an initial “futility” analysis of data from two late-stage clinical trials found that the drug failed to meaningfully slow progression of early Alzheimer’s disease, the company now concludes that, due primarily to the responses of people on the higher of two doses of the antibody, the drug did significantly slow people’s cognitive decline and their functional decline, meaning their ability to cope with activities of daily living. Biogen’s first analysis used data from 1748 patients who had completed 18 months on a low dose or a high dose of the drug; the new analysis, whose underlying data are not yet publicly available nor described in a journal article, included 2066 such patients. Bart De Strooper, who directs the UK Dementia Research Institute at University College London, called the news “fantastic. … We currently have no effective treatments to slow or halt the progression of Alzheimer’s disease and I hope this signifies a turning point.” He also suggested the result could revive the once-dominant theory that the neurodegenerative condition is largely due to the brain’s accumulation of toxic amyloid. “We should now redouble our efforts to tackle this central problem in Alzheimer’s disease.” © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26743 - Posted: 10.23.2019

By Gina Kolata Biogen, the drug company, said on Tuesday that it would ask the Food and Drug Administration to approve an experimental drug, aducanumab, to treat people with mild cognitive impairment and the earliest signs of Alzheimer’s disease. About 10 million Americans might qualify for treatment if the drug were approved, according to Michel Vounatsos, the company’s chief executive. Even so, it is not quite time for these patients to celebrate. The company has not published the most recent analyses, and experts are mostly in the dark as to how well the drug works. It neither prevents nor cures Alzheimer’s; the company claims only that aducanumab may slow cognitive decline in some patients. In fact, Biogen announced in March that it was halting two large studies of aducanumab for treatment of Alzheimer’s disease because data showed the effort was likely to be futile. The company resurrected the drug after additional analyses suggested it might have some effect at higher doses. (“Just in time for Halloween, aducanumab has risen from the dead,” one drug industry analyst said in an email.) Here are some takeaways from Tuesday’s announcement. What is this drug? Drug companies have spent billions of dollars on failed trials for Alzheimer’s drugs. So frustrating have the findings been that some have decided to abandon the search altogether. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26742 - Posted: 10.23.2019

Ian Sample Science editor Doctors in the US have launched a clinical trial to see whether exposure to flickering lights and low frequency sounds can slow the progression of Alzheimer’s disease. A dozen patients enrolled in the trial will have daily one-hour sessions of the radical therapy which researchers hope will induce brain activity that protects against the disorder. Animal tests have shown that exposure to light and sound waves at 40Hz reinforces so-called gamma waves in the brain, with knock-on effects across the organ. In mice used to model the disease, the therapy appears to boost the activity of the brain’s immune cells, making them clear the aberrant proteins that build up in Alzheimer’s. Li-Huei Tsai, a neuroscientist who is leading the trial at MIT, told the Society for Neuroscience meeting in Chicago on Tuesday that the therapy improved the survival and health of the animals’ neurons, boosted their connectivity, and dilated blood vessels, all of which may benefit patients. “We would like to see if our approach slows Alzheimer’s disease,” Tsai told the Guardian. The patients enrolled on the trial will have cognitive tests every three months to assess their brain function and regular scans to measure their brain activity and the connectivity of neurons across the organ. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26741 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Wide swings in blood sugar can mess with sleep. Food’s relationship with sleep gets even more muddled when signs of Alzheimer’s disease are present, a study of mice suggests. The results, presented in a news briefing October 20 at the annual meeting of the Society for Neuroscience, show that Alzheimer’s disease is not confined to the brain. “Your head is attached to your body,” says neuroscientist Shannon Macauley of Wake Forest School of Medicine in Winston-Salem, N.C. Metabolism, sleep and brain health “don’t happen in isolation,” she says. Along with Caitlin Carroll, also of Wake Forest, Macauley and coauthors rigged up a way to simultaneously measure how much sugar the brain consumes, the rate of nerve cell activity and how much time mice spend asleep. Injections of glucose into the blood led to changes in the brain: a burst of metabolism, a bump in nerve cell activity and more time spent awake. “It’s like giving a kid a lollipop,” Macauley says. “They’re going to run around in a circle.” But a dip in blood sugar, caused by insulin injections, also led to more nerve cell action and more wakefulness. “You can have it go up high or go down low, and it was just really bad either way,” Macauley says. Researchers did similar analyses in mice genetically engineered to have one of two key signs of Alzheimer’s. Some of these mice had clumps of amyloid-beta protein between nerve cells, while others had tangles of a protein called tau inside nerve cells. © Society for Science & the Public 2000–2019.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 26740 - Posted: 10.23.2019

Jon Hamilton Brain scientists are offering a new reason to control blood sugar levels: It might help lower your risk of developing Alzheimer's disease. "There's many reasons to get [blood sugar] under control," says David Holtzman, chairman of neurology at Washington University in St. Louis. "But this is certainly one." Holtzman moderated a panel Sunday at the Society for Neuroscience meeting in Chicago that featured new research exploring the links between Alzheimer's and diabetes. "The risk for dementia is elevated about twofold in people who have diabetes or metabolic syndrome (a group of risk factors that often precedes diabetes)," Holtzman says. "But what's not been clear is, what's the connection?" One possibility involves the way the brain metabolizes sugar, says Liqin Zhao, an associate professor in the school of pharmacy at the University of Kansas. Zhao wanted to know why people whose bodies produce a protein called ApoE2 are less likely to get Alzheimer's. Previous research has shown that these people are less likely to develop the sticky plaques in the brain associated with the disease. But Zhao looked at how ApoE2 affects glycolysis, a part of the process that allows brain cells to turn sugar into energy. So she gave ApoE2 to mice that develop a form of Alzheimer's. And sure enough, Zhao says, the substance not only improved energy production in brain cells but made the cells healthier overall. "All of this together increased the brain's resilience against Alzheimer's disease," she says. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26728 - Posted: 10.22.2019

By Austin Frakt To ward off age-related cognitive decline, you may be tempted to turn to brain training apps. Last year, consumers spent nearly $2 billion on them, some of which claim to improve cognitive skills. Evidence suggests you’d be better off spending more time exercising and less time staring at your phone. This year the World Health Organization released evidence-based guidelines on reducing risks of cognitive decline and dementia. Although it pointed to some systematic reviews that reported positive cognitive effects of brain training, the W.H.O. judged the studies to be of low quality. Among the studies’ limitations is that they measure only short-term effects and in areas targeted by the training. There is no long-term evidence of general improvement in cognitive performance. Instead of mind games, moving your body is among the most helpful things you can do. At least 150 minutes of moderate physical activity per week, including strength training, yields not just physical benefits but cognitive ones as well. But to be most effective, you need to do it before cognitive decline starts, according to the W.H.O. Some evidence to support this recommendation comes from short-term studies. Several randomized studies of tai chi for older adults found it yielded cognitive benefits. Likewise, randomized studies of aerobic exercise for older adults found short-term improvements in cognitive performance. A systematic review published this year in PLOS One examined 36 randomized studies of exercise programs that were as short as four weeks and as long as a year. It found cognitive benefits of activities such as bicycling, walking, jogging, swimming and weight training. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26727 - Posted: 10.21.2019

By Nicholas Bakalar Your personality in high school may help predict your risk of dementia decades later. Researchers reached this conclusion using a 150-item personality inventory given to a national sample of teenagers in 1960. The survey assessed character traits — sociability, calmness, empathy, maturity, conscientiousness, self-confidence and others — using scores ranging from low to high. For their study, in JAMA Psychiatry, scientists linked the scores of 82,232 of the test-takers to Medicare data on diagnoses of dementia from 2011 to 2013. They found that high extroversion, an energetic disposition, calmness and maturity were associated with a lower risk of dementia an average of 54 years later, though the association did not hold for students with low socioeconomic status. Calmness and maturity have been linked to lower levels of stress, which may help explain the association. Lower socioeconomic status, which often increases chronic stress, may negate the apparent benefits of those personality traits. “The study was not set up to discern a causal link,” said the lead author, Benjamin P. Chapman, an associate professor of psychiatry at the University of Rochester. “Most likely these traits lead to all kinds of other things over 50 years that culminate in a diagnosis of dementia. We tried to rule out as many other factors as possible, but our findings are suggestive, and we don’t want to draw strong conclusions about causation.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26716 - Posted: 10.18.2019

National Institutes of Health scientists have developed an ultrasensitive new test to detect abnormal forms of the protein tau associated with uncommon types of neurodegenerative diseases called tauopathies. As they describe in Acta Neuropathologica, this advance gives them hope of using cerebrospinal fluid, or CSF—an accessible patient sample—to diagnose these and perhaps other, more common neurological diseases, such as Alzheimer’s disease. Scientists have linked the abnormal deposition of tau in the brain to at least 25 different neurodegenerative diseases. However, to accurately diagnose these diseases, brain tissue often must be analyzed after the patient has died. For their study, the researchers used the same test concept they developed when using post-mortem brain tissue samples to detect the abnormal tau types associated with Pick disease, Alzheimer’s disease and chronic traumatic encephalopathy (CTE). They adapted the test to use CSF for the detection of abnormal tau of progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and other less common tauopathies. They detected abnormal tau in CSF from both living and deceased patients. In one case, the test led to a corrected diagnosis in a patient who had died from CBD, but who was initially diagnosed with PSP. The new test is called 4R RT-QuIC—which stands for 4-repeat tau protein amplified in a real-time, quaking-induced conversion process.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26711 - Posted: 10.17.2019

Diana Kwon There are approximately 5.6 million people over the age of 65 living with Alzheimer’s disease in the United States. With the population aging, that number is projected to grow to 7.1 million by 2025. Researchers know that age, a family history of the disease, and carrying a genetic variant known as APOE4 are all associated with a higher chance of developing the condition. But the biological mechanisms leading to Alzheimer’s are still largely a mystery. Over the last decade, scientists have amassed evidence for a hypothesis that, prior to developing full-blown Alzheimer’s disease, patients experience a period of hyperactivity and hyperconnectivity in the brain. Several functional magnetic resonance imaging studies have reported that people with mild cognitive impairment (MCI), a condition that often precedes Alzheimer’s, appear to have higher brain activity levels than their age-matched counterparts. Researchers have also found signs of such changes in healthy people carrying the APOE4 allele, as well as in presymptomatic stages of Alzheimer’s in rodent models of the disease. Krishna Singh, a physicist and imaging neuroscientist at the Cardiff University Brain Research Imaging Center (CUBRIC) in the UK, and his colleagues wanted to investigate this theory further. Previous studies of brain activity in young APOE4 carriers were mostly conducted using small sample sizes, according to Singh. But by the mid-2010s, his team had access to neuroimaging data from close to 200 participants studied at CUBRIC as part of an effort to build a massive dataset of healthy brains. So the researchers decided to use the data to search for signs of unusual brain activity and connectivity in people with the APOE4 allele. © 1986–2019 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 26709 - Posted: 10.16.2019

Laura Sanders Alzheimer’s disease destroys command centers in the brain that keep people awake. That finding could explain why the disease often brings daytime drowsiness. Sleep problems can precede dementias, including Alzheimer’s, sometimes by decades. But the new result, described online August 12 in Alzheimer’s & Dementia, suggests that disordered sleeping isn’t just an early harbinger of Alzheimer’s. Instead, sleep trouble is “part of the disease,” says Lea Grinberg, a neuropathologist at the University of California, San Francisco. Grinberg and colleagues focused on the brain stem and a structure perched above it called the hypothalamus. Together, these parts of the nervous system oversee crucial jobs such as keeping people awake and paying attention. Though important, the brain stem and its neighbors have been largely overlooked in studies of dementia, Grinberg says. In particular, the researchers searched for evidence of tau, a protein that can form tangles inside nerve cells, in postmortem brains of people who died with Alzheimer’s disease. Three small regions of the hypothalamus and brain stem, all of which usually contain nerve cells that keep people awake during the day, were packed with tau, the team found. And two of the three areas had lost over 70 percent of their nerve cells, or neurons. These areas “are hit hard, and they are hit by tau,” Grinberg says. That destruction could be part of the reason people with Alzheimer’s disease often feel tired during the day, even if they slept the night before. |© Society for Science & the Public 2000 - 2019.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26509 - Posted: 08.17.2019

By John Williams The first, startling epigraph in Nicci Gerrard’s new book, “The Last Ocean,” comes from Emily Dickinson: “Abyss has no Biographer.” Gerrard sets out to tell the story of dementia, a disease that can appear to consume those it afflicts. After her father, John, died in 2014, the author — who writes best-selling thrillers with her husband under the name Nicci French — embarked on learning more about the disease as both a journalist and an activist. The result is a tender, inquisitive tour of a subject that can be raw and painful. Below, Gerrard talks about loss, art that punches you in the solar plexus and the experience of writing a book that doesn’t answer questions. When did you first get the idea to write this book? I first had the idea when my father, who’d been living with dementia for over 10 years, went into hospital in February 2014. After four weeks without anyone to see him — we were allowed in for very limited times and then not at all, because of a norovirus outbreak — I barely recognized him. I will, for the rest of my life, feel terribly that I didn’t get him out earlier. Then he lived at home for nine months. He had become skeletal, immobile, inarticulate, and in a way he felt utterly lost, like a ghost in our lives and in his own life. He would lay downstairs in a hospital bed, looking outside at the garden he used to love. There was this clear sense that he’d already lost everything he had, everything he was, all his capacity, there was nothing left — and yet somehow that he didn’t lose himself. In the book I say that if I were religious, I would call that self he retained his soul. Something very indelible remained. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26508 - Posted: 08.17.2019

By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 26504 - Posted: 08.15.2019

­­­In a nationwide study, researchers used magnetic resonance imaging (MRI) to scan the brains of hundreds of participants in the National Institutes of Health’s Systolic Blood Pressure Intervention Trial (SPRINT) and found that intensively controlling a person’s blood pressure was more effective at slowing the accumulation of white matter lesions than standard treatment of high blood pressure. The results complement a previous study published by the same research group which showed that intensive treatment significantly lowered the chances that participants developed mild cognitive impairment. “These initial results support a growing body of evidence suggesting that controlling blood pressure may not only reduce the risk of stroke and heart disease but also of age-related cognitive loss,” said Walter J. Koroshetz, M.D., director of the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “I strongly urge people to know your blood pressure and discuss with your doctors how to optimize control. It may be a key to your future brain health.” Brain white matter is made up of billions of thin nerve fibers, called axons, that connect the neurons with each other. The fibers are covered by myelin, a white fatty coating that protects axons from injury and speeds the flow of electrical signals. White matter lesions, which appear bright white on MRI scans, represent an increase in water content and reflect a variety of changes deep inside the brain, including the thinning of myelin, increased glial cell reactions to injury, leaky brain blood vessels, or multiple strokes. These changes are associated with high blood pressure, or “hypertension”.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26496 - Posted: 08.14.2019