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

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: 26069 - Posted: 03.23.2019

By Kelly Servick “Futile”—that’s the devastating label now attached to two highly anticipated clinical trials of a drug that targets β-amyloid, the neuron-killing protein fragment littering the brains of people with Alzheimer’s disease. Biogen in Cambridge, Massachusetts, and Eisai in Tokyo, the pharmaceutical partners developing the drug, called aducanumab, today announced their decision to halt a pair of ongoing phase III trials after seeing the results of a “futility analysis,” in which an independent committee found that the drug was unlikely to slow cognitive decline as intended. This latest blow to the β-amyloid approach has left researchers asking: Do any of the remaining antiamyloid drug trials have a better chance, or is it time to declare the whole approach, well, futile? “Amyloid definitely has something to do with Alzheimer’s—there’s far too much evidence to dismiss,” organic chemist Derek Lowe wrote today on his drug industry blog In the Pipeline. (The blog is hosted by Science Translational Medicine, which, like ScienceInsider, is published by AAAS.) “But the situation is clearly more complicated than people have hoped, because otherwise, all the attempts to address amyloid … would have yielded some tiny bit of clinical benefit.” There were reasons to think that aducanumab might succeed where antiamyloid drugs from Merck & Co., Eli Lilly and Company, and others had failed. The drug is an antibody designed to bind to and eliminate sticky β-amyloid plaques that build up around neurons, block their communication, and, ultimately, kill them. And it was clear from a smaller clinical trial that this drug was very effective at clearing plaques—“that’s one of the reasons we were sanguine about this trial,” says neurologist Dennis Selkoe of Brigham and Women’s Hospital in Boston, who treats patients who were enrolled in one of the trials. Studies also suggest aducanumab can attack the most noxious form of amyloid—so-called oligomers—that other drugs may have left untouched. © 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: 26061 - Posted: 03.22.2019

Jon Hamilton In the U.S., older people with dementia are usually told they have Alzheimer's disease. But a range of other brain diseases can also impair thinking, and memory and judgment, according to scientists attending a summit on dementias held Thursday and Friday at the National Institutes of Health. These include strokes, a form of Parkinson's disease, and a disease that damages brain areas that regulate emotion and behavior. "There's a host of things that can cause loss of cognitive function," says Dr. Julie Schneider, a professor at the Rush Alzheimer's Disease Center in Chicago and scientific chair of the NIH summit. And many patients have more than one disease affecting the brain, she says. Most of these diseases can't be stopped, Schneider says. But it's important that families get the right diagnosis in order to get the best care and plan for the future. The emphasis on non-Alzheimer's dementias reflects a change in doctors' understanding of what happens to aging brains. When Schneider was training to be a doctor in the 1980s and '90s, dementia was simple. "We were taught that almost all dementia is Alzheimer's disease," she says. But since then, studies have shown that 20 percent to 40 percent of the nation's 5.8 million dementia patients have some other disease. © 2019 npr

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: 26044 - Posted: 03.18.2019

By Pam Belluck Could people’s eyes and ears help fix the damage Alzheimer’s disease does to the brain? Just by looking at flashing light and listening to flickering sound? A new study led by a prominent M.I.T. neuroscientist offers tantalizing promise. It found that when mice engineered to exhibit Alzheimer’s-like qualities were exposed to strobe lights and clicking sounds, important brain functions improved and toxic levels of Alzheimer’s-related proteins diminished. What’s more, the rapid-fire soundtrack appeared to make mice better at cognitive and memory skills, like navigating mazes and recognizing objects. Of course, mice are not people. And many drugs that have helped Alzheimer’s-engineered mice haven’t done much for people with Alzheimer’s, which affects 44 million people worldwide, including 5.5 million Americans. Also, because the technique didn’t have long-lasting effects — results faded about a week after the sensory stimulation was stopped — any therapy developed from the research might have to be repeated regularly. Still, seeing that a noninvasive daily dose of light and sound could have such significant effects in mice give some experts reason for optimism. “It’s exciting, I think,” said Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease, who was not involved in the study. “Reading the paper made me quite enthusiastic about seeing this move forward into some well-crafted clinical trials.” The experiments were led by Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory. She and her colleagues showed that light and sound delivered to mice at a certain frequency — 40 hertz or 40 flashes or clicks per second — appears to synchronize the rhythm of the brain’s gamma waves, which is disrupted in patients with Alzheimer’s. Gamma waves are among several types of electrical brain waves believed to be involved in concentration, sleep, perception and movement. The experiment setup where flickering light and sound were delivered to Alzheimer’s-engineered mice in the tubs.CreditPicower Institute for Learning and Memory, M.I.T. © 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: 26040 - Posted: 03.15.2019

Eating mushrooms more than twice a week could prevent memory and language problems occurring in the over-60s, research from Singapore suggests. A unique antioxidant present in mushrooms could have a protective effect on the brain, the study found. The more mushrooms people ate, the better they performed in tests of thinking and processing. But researchers said it was not possible to prove a direct link between the fungi and brain function. The National University of Singapore study's findings were based on 663 Chinese adults, aged over 60, whose diet and lifestyle were tracked from 2011 to 2017. Over the six-year study the researchers found that eating more than two portions of mushrooms a week lowered the chances of mild cognitive impairment by 50%, compared with those who ate fewer than one portion. Mild cognitive impairment (MCI) can make people forgetful, affect their memory and cause problems with language, attention and locating objects in spaces - but the changes can be subtle. It is not serious enough to be defined as dementia. The participants in the study were asked how often they ate six different types of mushrooms: oyster, shiitake, white button, dried, golden and tinned. Mushroom eaters performed better in brain tests and were found to have faster processing speed - and this was particularly noticeable in those who ate more than two portions a week, or more than 300g (10.5oz). "This correlation is surprising and encouraging," said assistant professor Lei Feng, the lead study author, from the university's department of psychological medicine. Image copyright Getty Images "It seems that a commonly available single ingredient could have a dramatic effect on cognitive decline. © 2019 BBC

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: 26034 - Posted: 03.15.2019

GPs are urging women not to be alarmed by research linking long-term hormone replacement therapy (HRT) use with a small increased risk of Alzheimer's. They say HRT is an effective and safe treatment for most women with menopause symptoms and the risk is "extremely low". The BMJ research looked at data on 170,000 women in Finland over 14 years. It found a 9%-17% increased risk for Alzheimer's, particularly in women taking HRT for more than 10 years. This equates to between nine and 18 extra cases of the disease per year in every 10,000 women aged between 70 and 80, the researchers said. But the study was observational and, as a result, it cannot be said for certain that other factors had not affected the results. Other studies have found that HRT actually improves brain function. The Royal College of GPs said the research does not prove that HRT causes Alzheimer's disease, and women currently taking it should continue to do so. Prof Helen Stokes-Lampard, chairwoman of the College, said: "Hormone replacement therapy can be of greatest benefit to many women who are suffering from some of the unpleasant side-effects of the menopause, such as hot flushes and night sweats - and there is a large body of evidence that shows it is an effective and safe treatment for most women. "We would urge patients not to be alarmed by this research - as the researchers state, any risk is extremely low - and if they are currently taking HRT, to continue doing so as prescribed by their doctor. " However, she said there were risks with any medication and it was important that women were aware of them. "To minimise any risk, best practice for most women is to prescribe the lowest possible dose of hormones for the shortest possible time in order to achieve satisfactory relief of symptoms," Prof Stokes-Lampard said. © 2019 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26015 - Posted: 03.07.2019

By Karen Weintraub For decades researchers have focused their attacks against Alzheimer’s on two proteins, amyloid beta and tau. Their buildup in the brain often serves as a defining indicator of the disease. Get rid of the amyloid and tau, and patients should do better, the thinking goes. But drug trial after drug trial has failed to improve patients’ memory, agitation and anxiety. One trial of a drug that removes amyloid even seemed to make some patients worse. The failures suggest researchers were missing something. A series of observations and recently published research findings have hinted at a somewhat different path for progression of Alzheimer’s, offering new ways to attack a disease that robs memories and devastates the lives of 5.7 million Americans and their families. One clue hinting at the need to look further afield was a close inspection of the 1918 worldwide flu pandemic, which left survivors with a higher chance of later developing Alzheimer’s or Parkinson’s. A second inkling came from the discovery that the amyloid of Alzheimer’s and the alpha-synuclein protein that characterizes Parkinson’s are antimicrobials, which help the immune system fight off invaders. The third piece of evidence was the finding in recent years, as more genes involved in Alzheimer’s have been identified, that traces nearly all of them to the immune system. Finally, neuroscientists have paid attention to cells that had been seen as ancillary—“helper” or “nursemaid” cells. They have come to recognize these brain cells, called microglia and astrocytes, play a central role in brain function—and one intimately related to the immune system. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26007 - Posted: 03.05.2019

By Paula Span Donna Kaye Hill realized that her 80-year-old mother was faltering cognitively when her phone suddenly stopped working. When Ms. Hill called the phone company, “they told me she hadn’t paid her bill in three months.” Finding other alarming evidence of memory gaps, she took her mother, Katie, to a memory clinic. A geriatrician there diagnosed dementia and recommended two prescription drugs and a dietary supplement, a form of vitamin E. Katie Hill dutifully took vitamin E capsules, along with a host of other medications, until she died four years later. As she declined, her daughter didn’t think the vitamin, or the two prescription medications, was making much difference. “But if it doesn’t hurt, if there’s a chance it helps even a tiny bit, why not?” she reasoned. Ms. Hill, 62, a retired public employee in Danville, Va., takes fish oil capsules daily herself, hoping they’ll help ward off the disease that killed her mother. The elder Ms. Hill was unusual only in that a doctor had recommended the supplement; most older Americans are taking them without medical guidance. The Food and Drug Administration estimates that 80 percent of older adults rely on dietary supplements, many purporting to prevent or treat Alzheimer’s and other forms of dementia. Last month, the F.D.A. cracked down on this burgeoning market, sending warning letters or advisories to 17 companies selling about 60 supplements with names like Cogni-Flex and Mind Ignite. The warnings pointed out that the companies had touted these products as working like Alzheimer’s drugs, “but naturally and without side effects.” Or as “clinically shown to help diseases of the brain, such as Alzheimer’s.” The pills, oils and capsules were said to treat other diseases, too, from stroke to erectile dysfunction. © 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: 26002 - Posted: 03.02.2019

Analysis of genetic data from more than 94,000 individuals has revealed five new risk genes for Alzheimer’s disease, and confirmed 20 known others. An international team of researchers also reports for the first time that mutations in genes specific to tau, a hallmark protein of Alzheimer’s disease, may play an earlier role in the development of the disease than originally thought. These new findings support developing evidence that groups of genes associated with specific biological processes, such as cell trafficking, lipid transport, inflammation and the immune response, are “genetic hubs” that are an important part of the disease process. The study, which was funded in part by the National Institute on Aging (NIA) and other components of the National Institutes of Health, follows results from 2013. It will be published online February 28, 2019 in the journal Nature Genetics . “This continuing collaborative research into the genetic underpinnings of Alzheimer’s is allowing us to dig deeper into the complexities of this devastating disease,” said Richard J. Hodes, M.D., director of the NIA. “The size of this study provides additional clarity on the genes to prioritize as we continue to better understand and target ways to treat and prevent Alzheimer’s.” The researchers, members of the International Genomic Alzheimer’s Project (IGAP), analyzed both rare and common gene variants in 94,437 individuals with late onset Alzheimer’s disease, the most common form of dementia in older adults. IGAP is made up of four consortia in the United States and Europe that have been working together since 2011 on genome-wide association studies (GWAS) involving thousands of DNA samples and shared datasets. GWAS are aimed at detecting variations in the genome that are associated with Alzheimer’s. Understanding genetic variants is helping researchers define the molecular mechanisms that influence disease onset and progression.

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: 26001 - Posted: 03.02.2019

By Pallab Ghosh Science correspondent, BBC News, Washington DC New results suggest ageing brains can potentially be rejuvenated, at least in mice, according to researchers. Very early-stage experiments indicate that drugs can be developed to stop or even reverse mental decline. The results were presented at the 2019 meeting of the American Association for the Advancement of Science. The US and Canadian researchers took two new approaches to trying to prevent the loss of memory and cognitive decline that can come with old age. One team, from the University of California, Berkeley, showed MRI scans which indicated that mental decline may be caused by molecules leaking into the brain. Blood vessels in the brain are different from those in other parts of the body. They protect the organ by allowing only nutrients, oxygen and some drugs to flow through into the brain, but block larger, potentially damaging molecules. This is known as the blood-brain barrier. The scans revealed that this barrier becomes increasingly leaky as we get older. For example, 30-40% of people in their 40s have some disruption to their blood-brain barrier, compared with 60% of 60-year-olds. The scans also showed that the brain was inflamed in the leaky areas. Prof Daniela Kaufer, who leads the Berkeley group, said that young mice altered to have leaky blood-brain barriers showed many signs of aging. She discovered a chemical that stops the damage to the barrier from causing inflammation to the brain. Prof Kaufer told BBC News that not only did the chemical stop the genetically altered young mice from showing signs of aging, it reversed the signs of aging in older mice. © 2019 BBC

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: 25966 - Posted: 02.15.2019

Ian Sample Science editor An experimental drug that bolsters ailing brain cells has raised hopes of a treatment for memory loss, poor decision making and other mental impairments that often strike in old age. The drug could be taken as a daily pill by over-55s if clinical trials, which are expected to start within two years, show that the medicine is safe and effective at preventing memory lapses. Tests in the lab showed that old animals had far better memory skills half an hour after receiving the drug. After two months on the treatment, brain cells which had shrunk in the animals had grown back, scientists found. Etienne Sibille, at the Centre for Addiction and Mental Health in Toronto, said the treatment was aimed not only at the “normal” cognitive decline that leads to senior moments, but at memory loss and mental impairments that commonly afflict people with depression, schizophrenia and Alzheimer’s disease. If the drug did well in human trials, Sibille said it was possible that “anybody over the age of 55-60 who may be at risk of cognitive problems later on could benefit from this treatment”. “Our findings have direct implications for poor cognition in normal ageing,” he said, with the drug potentially improving learning, memory, decision making and essential life planning. “But we see this deficiency across disorders from depression to schizophrenia and Alzheimer’s.” © 2019 Guardian News & Media Limited

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: 25964 - Posted: 02.14.2019

By Nicholas Bakalar Chronic inflammation in middle age may lead to memory and thinking problems later in life. Unlike acute inflammation, which arises in response to injury, chronic inflammation persists over months or years. Autoimmune disease, lingering infection, exposure to polluted air, psychological stress and other conditions can all promote chronic inflammation. Researchers did blood tests on 12,336 men and women, average age 57, assigning them an “inflammation composite score” based on white blood cell count, clotting factors and other tests. They also assessed their cognition with standardized tests of memory, processing speed and verbal fluency. The study is in Neurology. After controlling for age, education, blood pressure, cholesterol, heart disease and many other factors, they found that the greater the number of inflammatory factors, the steeper the cognitive decline over 20 years of follow-up. Inflammation was most strongly associated with declines in memory. “We know that dementia starts earlier than the appearance of symptoms,” said the lead author, Keenan A. Walker, a postdoctoral researcher at Johns Hopkins, “and we’ve shown that levels of inflammation matter for dementia risk. Reducing chronic inflammation involves the same health behaviors that we already know are important for other reasons — regular exercise, healthy diet, avoiding excessive weight gain and so on.” © 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: 25962 - Posted: 02.14.2019

Catherine Offord Researchers in the UK and New Zealand have created the largest-ever database of protein expression changes associated with Alzheimer’s disease, according to a study published today (February 4) in Communications Biology. The data, which are freely available to researchers online, reveal new insights into the brain areas affected by Alzheimer’s, as well as the molecular pathways leading to the disease. “This database provides a huge opportunity for dementia researchers around the world to progress and to follow-up new areas of biology and develop new treatments,” study coauthor Richard Unwin of the University of Manchester says in a statement. “It’s very exciting to be able to make these data public so scientists can access and use this vital information.” The team analyzed the expression data of more than 5,500 proteins spanning six brain regions in postmortem tissue of nine healthy and nine Alzheimer’s-affected patients. The results provide a map of changes associated with the disease, identifying certain areas of the brain as more affected than others. Heavily affected areas include the hippocampus, the entorhinal cortex, and the cingulate gyrus, the analysis showed. The researchers also found that the cerebellum, an area of the brain thought to be less damaged by Alzheimer’s disease, showed substantial changes in protein expression, but that these changes qualitatively differed from those in other regions. © 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: 25934 - Posted: 02.06.2019

By Howard M. Fillit Alzheimer's disease is the sixth leading cause of death in the U.S., and unlike with cancer and heart disease, we lack the tools to effectively diagnose and treat it. In sharp contrast to other illnesses and despite many efforts, huge expense and hundreds of clinical trials, no new treatments have been approved in the past 16 years. The emphasis has been on drugs targeting beta-amyloid proteins, which clump into plaques in the brains of afflicted people. Unfortunately, these approaches have not yet yielded the results we hoped for. So now it is time to target novel pathways to tackle this incredibly complex disease. This has been a challenge because of the absence of affordable and noninvasive tests based on biomarkers that doctors can easily use in their offices. The alternatives have been expensive and invasive spinal taps or neuroimaging tests that can be performed only in a hospital or freestanding radiology office. New biomarkers are needed for specific molecular targets that can be used to subtype patients; for predicting the likelihood that they will acquire Alzheimer's; and possibly for providing a diagnosis even before symptoms are noticeable, enabling prevention. That is, they could do what currently available amyloid positron-emission tomography (PET) scans and cerebrospinal fluid tests do. Biomarkers can also be used to enroll patients in clinical trials directed to a specific target, such as beta-amyloid, and to measure how the body responds to a treatment—as was done most recently by Biogen with its anti-beta-amyloid monoclonal antibody. Ultimately biomarkers can determine which therapies would be most effective for an individual. © 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: 25927 - Posted: 02.02.2019

Laura Sanders Do you floss regularly? A study published January 23 in Science Advances — and the news stories that it inspired — might have scared you into better oral hygiene by claiming to find a link between gum bacteria and Alzheimer’s disease. Those experiments hinted that the gum disease–causing bacteria Porphyromonas gingivalis was present in the brains of a small number of people who died with the degenerative brain disease. Some headlines trumpeted that the cause of Alzheimer’s had finally been found. Enzymes made by P. gingivalis, called gingipains, interact with key Alzheimer’s proteins called amyloid-beta and tau in test tube experiments and in the brains of mice, the researchers found. Gingipains prod A-beta to accumulate and tau to behave abnormally, both signs of Alzheimer’s disease in people, the experiments suggest. And compounds that block gingipains seemed to reduce the amount of A-beta in the infected mice. The findings “offer evidence that P. gingivalis and gingipains in the brain play a central role” in the development of Alzheimer’s disease, the researchers write in their study. The research was paid for and conducted in part by employees of Cortexyme, Inc., a San Francisco–based biotech company that’s developing these compounds. The results fit with an idea that’s gaining traction among Alzheimer’s researchers — that bacteria, viruses and even fungi could spark the disease (SN: 7/21/18, p. 10). But the Science Advances study is far from conclusive, cautions Rudolph Tanzi, an Alzheimer’s researcher at Massachusetts General Hospital in Boston. Science News asked him what the study can, and can’t, answer about Alzheimer’s disease. His responses are edited for length and clarity. |© 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: 25920 - Posted: 02.01.2019

By Pam Belluck In dementia research, so many paths have led nowhere that any glimmer of optimism is noteworthy. So some experts are heralding the results of a large new study, which found that people with hypertension who received intensive treatment to lower their blood pressure were less likely than those receiving standard blood pressure treatment to develop minor memory and thinking problems that often progress to dementia. The study, published Monday in JAMA, is the first large, randomized clinical trial to find something that can help many older people reduce their risk of mild cognitive impairment — an early stage of faltering function and memory that is a frequent precursor to Alzheimer’s disease and other dementias. The results apply only to those age 50 or older who have elevated blood pressure and who do not have diabetes or a history of stroke. But that’s a condition affecting a lot of people — more than 75 percent of people over 65 have hypertension, the study said. So millions might eventually benefit by reducing not only their risk of heart problems but of cognitive decline, too. “It’s kind of remarkable that they found something,” said Dr. Kristine Yaffe, a professor of psychiatry and neurology at University of California San Francisco, who was not involved in the research. “I think it actually is very exciting because it tells us that by improving vascular health in a comprehensive way, we could actually have an effect on brain health.” © 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: 25913 - Posted: 01.29.2019

By Jocelyn Kaiser Poor oral health is a risk factor for Alzheimer’s disease. What’s not clear is whether gum disease causes the disorder or is merely a result—many patients with dementia can’t take care of their teeth, for example. Now, a privately sponsored study has confirmed that the bacteria that cause gum disease are present in the brains of people with Alzheimer’s, not just in their mouths. The study also finds that in mice, the bacteria trigger brain changes typical of the disease. The provocative findings are the latest in a wave of research suggesting microbial infections may play a role in Alzheimer’s disease. But even some scientists who champion that once-fringy notion aren’t convinced that Porphyromonas gingivalis, the species fingered in the new study, is behind the disorder. “I'm fully on board with the idea that this microbe could be a contributing factor. I'm much less convinced that [it] causes Alzheimer’s disease,” says neurobiologist Robert Moir of the Harvard University–affiliated Massachusetts General Hospital (MGH) in Boston, whose work suggests the β-amyloid protein that forms plaques in the brains of Alzheimer’s patients is a protective response to microbial invaders. The new study, published today in Science Advances, was sponsored by the biotech startup Cortexyme Inc. of South San Francisco, California. Co-founder Stephen Dominy is a psychiatrist who in the 1990s became intrigued by the idea that Alzheimer’s could have an infectious cause. At the time, he was treating people with HIV at the University of California, San Francisco. Some had HIV-related dementia that resolved after they got antiviral drugs. Dominy began a side project looking for P. gingivalis in brain tissue from deceased patients with Alzheimer’s, and—after his work found hints—started the company with entrepreneur Casey Lynch, who had studied Alzheimer’s as a graduate student. © 2018 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: 25899 - Posted: 01.24.2019

Jef Akst Levels of a protein called neurofilament light chain increase in the blood and spinal fluid of some Alzheimer’s patients 16 years before they develop symptoms, according to a study published today (January 21) in Nature Medicine. The results suggest that neurofilament light chain (NfL), which is part of the cytoskeleton of neurons and has previously been tied to brain damage in mice, could serve as a biomarker to noninvasively track the progression of the disease. “This is something that would be easy to incorporate into a screening test in a neurology clinic,” coauthor Brian Gordon, an assistant professor of radiology at Washington University, says in a press release. Gordon and his colleagues measured NfL in nearly 250 people carrying an Alzheimer’s-risk allele and more than 160 of their relatives who did not carry the variant. They found that those at risk of developing the disease had higher levels of the protein early on, and that NfL levels in both the blood and spinal fluid were on the rise well before the patients began to show signs of neurodegeneration, more than 16 years before disease onset. Examining a subset of the patients more closely, the team saw that the rate of increase in NfL correlated with the shrinkage of a brain region called the precuneus, and patients whose NfL levels were rising rapidly tested worse on cognitive tests. “It is not necessarily the absolute levels which tell you your neurodegeneration is ongoing, it is the rate of change,” coauthor Mathias Jucker, a professor of cellular neurology at the German Center for Neurodegenerative Diseases in Tübingen, tells The Guardian. © 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: 25894 - Posted: 01.24.2019

By John Horgan In my freshman humanities class, I make students ponder the pros and cons of knowledge. We talk about Plato’s parable, in which people imprisoned in a cave mistake shadows projected on a wall for reality. I ask, Assuming we’re in the cave, how many of you want to escape? Most students dutifully raise their hands, because of course truth is good and ignorance is bad. Then I ask, What if the cave is comfy and the outside world nasty? I bring up The Matrix, in which humans live in a computer simulation, called the Matrix, constructed by evil machines. A band of rebels who have escaped this digital cave is trying to liberate other humans. A rebel named Cypher gives Agent Smith, nasty sentient software created by the machines, information to help him capture the rebels. Agent Smith asks Cypher what he wants for betraying his comrades, and Cypher says he doesn't want to live in reality any more. It’s ugly and stressful, and he hates being bossed around by the rebel leader. Cypher asks for a happy simulated life in the Matrix. Here is an excerpt from his dialogue with Agent Smith, which takes place in a virtual restaurant: Cypher: You know, I know this steak doesn't exist. I know that when I put it in my mouth, the Matrix is telling my brain that it is juicy and delicious. After nine years, you know what I realize? Ignorance is bliss. Agent Smith: Then we have a deal? Cypher: I don't want to remember nothing. Nothing. You understand? And I want to be rich. You know, someone important, like an actor. Agent Smith: Whatever you want.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 25885 - Posted: 01.21.2019

Nicola Davis Moving more might help to keep people’s brains sharp as they age – even in the face of dementia, researchers have said. Scientists have found older adults fared better when it came to cognitive tasks if they clocked up higher levels of daily activity on a wrist-based tracker – something the researchers said picked up everything from exercising to mundane tasks like chopping onions. What’s more, the benefits of movement remained even when the team took into account the level of tell-tale signs of Alzheimer’s and other dementia-related diseases in the brain. Co-author of the Rush University study, Dr Aron Buchman, said the results showed that “even though we don’t have a treatment for Alzheimer’s disease pathology, and we know people are accumulating it, you can mitigate the deleterious effects … by having more activity.” But it’s not only moving more which is linked to better scores for traits like thinking, comprehension and and memory: the team found better motor abilities, as measured through tasks like the strength in gripping items or speed of turning on the spot, also seemed to offer protection when it comes to cognitive prowess. The team say previous work has shown that moving more is linked to a lower risk of dementia, and slows the decline in thinking and memory skills in older adults as they age – but the latest research goes further. © 2019 Guardian News and Media Limited

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: 25872 - Posted: 01.17.2019