Links for Keyword: Alzheimers

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By Erika Mailman In summer 2014, when he was 54, Sacramento artist David Wetzl was exhibiting the behaviors of an elderly man with Alzheimer’s. “I have a bad brain,” he told everyone repeatedly, using a simple phrase to explain his diagnosis to the world. Two years before that, his wife, Diana Daniels, had asked for an MRI because she was suspicious that things weren’t right and fearful when he couldn’t remember the word “shoelaces.” The scan showed with horrific clarity how sections of his brain had shriveled. “The devastation began on his left temporal lobe, working its greatest damage,” says Diana. “By the time of diagnosis, his right temporal lobe also had significant atrophy.” David was diagnosed with frontotemporal dementia, or FTD, part of a group of disorders caused by nerve cell damage to the brain. The disease comes with a dispiriting prognosis. There is no cure (although symptoms can be treated), and patients usually die within seven to 13 years from the onset of symptoms. As FTD progresses, behavior can become strange and antisocial, says Matt Ozga, communications manager at the Association for Frontotemporal Degeneration in King of Prussia, Pa. Patients lose their filter and can make embarrassing remarks. For the spouses who are caught off guard, thinking their mate’s worst setback for the next few decades will be graying hair and a paunch, it’s a shock. The couple may find themselves confronted  by different challenges than those who encounter dementia later in life.

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: 27150 - Posted: 03.30.2020

By Nicholas Bakalar There is good evidence that a daily baby aspirin reduces the risk for heart disease and stroke, and some have thought its inflammation-lowering effect might also help in delaying cognitive decline. But taking a daily low-dose aspirin did not appear to be effective in lowering the risk of Alzheimer’s disease or other forms of dementia, a new study reports. For the study, in Neurology, researchers set up a controlled trial with 19,114 men and women older than 70 who were free of cardiovascular disease and dementia at the start. Half were randomly assigned to take a daily 100-milligram aspirin, while the other half took a placebo. After an average follow-up of almost five years with annual examinations, the researchers found no difference between the groups in diagnoses of Alzheimer’s disease or mild cognitive impairment. They did find declining cognitive function over time, but the speed and degree of that decline was the same in both groups. The researchers found no effect in various subgroups either — people with hypertension or diabetes, smokers or people with high cholesterol, or those who were overweight or obese. A limitation of the study was that patients were followed for less than five years. “If you’re 70 or older and healthy, without evidence of cardiovascular disease, it’s very difficult to improve on your success. The relatively low risk of dementia in this study was not further lowered with aspirin,” said a co-author, Dr. Anne B. Newman, a professor of epidemiology at the University of Pittsburgh. © 2020 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: 27147 - Posted: 03.30.2020

By Julie Halpert As the coronavirus advances, it is taking a particularly harsh toll on the many who are caring for a loved one with dementia or Alzheimer’s, the most common form of dementia. According to a report by the Alzheimer’s Association, more than 16 million Americans are providing unpaid care for those with Alzheimer’s or other types of dementia. For them the virus is “really a double whammy,” said Lynn Friss Feinberg, a senior strategic policy adviser at AARP’s Public Policy Institute. “You’re worrying about your own health and that of your family member.” While the disease itself does not necessarily place patients at high risk for contracting the virus, they and their caregivers face a range of special challenges. Dementia patients are typically very sensitive to changes in routine and often require a great deal of hands-on care, both factors that are hard to manage now. Family members who usually rely on day care programs or visiting caregivers may be finding themselves with full-time responsibilities, while others whose loved ones are in facilities are unable to visit them now. Among the greatest challenges is how to minimize disruption in care that is intensely personal. “Care for dementia patients is ‘high touch,’” said Peter Lichtenberg, a professor of psychology and director of the Institute of Gerontology at Wayne State University. He recommends that caregivers take measures to avoid their own exposures by having provisions delivered, disinfecting surfaces and employing proper hand-washing techniques. K.C. Mehta has been caring for his wife, Sumi, since 2013, when she was given a diagnosis of Alzheimer’s at the age of 59. A former engineering executive at Chrysler, Mr. Mehta, who is 72 and lives in Rochester Hills, Mich., spends each day focused on maintaining his wife’s routine. Twice during the night, he changes her diaper. When she awakes, he bathes and dresses her. © 2020 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: 27146 - Posted: 03.27.2020

By Amanda McCracken Over 30 years ago, Tom Johnson identified a gene that extended the very short life of a tiny roundworm, propelling him to the forefront of research on aging and raising the tantalizing possibility that aging could someday be slowed down in people, too. His work transformed the mind-set of scientists, launching a new field in the science of aging when he demonstrated that identifying and manipulating genes could lengthen life span. Although Johnson’s research has led to drug development to slow the effects of age-related diseases, he has yet to find the secret to stop aging. Now the soft-spoken redheaded scientist is running out of time as he confronts his own mortality. Five years ago, at age 66, work got confusing for Johnson, a professor in the Institute for Behavioral Genetics at the University of Colorado at Boulder. He found it impossible to keep track of his many projects. He began wondering whether he had Alzheimer’s like his newly diagnosed sister. He spoke to his wife, Vicki Simpson, about the little dogs he frequently saw running around the house (even though he knew they weren’t real). Simpson, a retired anesthesiologist, later learned such hallucinations are a trademark sign of Lewy body dementia. At first, she praised his imagination and then after several months suggested they visit a memory clinic. There he was diagnosed with probable Lewy body — a fatal disease with inescapable dementia that can be diagnosed with certainty only at death. Right now, there is no cure, only ways to ease symptoms.

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: 27134 - Posted: 03.23.2020

By Adrienne Raphel Let me tell you a tale of two grandfathers, Irv and Murray. For decades, Irv, an introverted, quiet, retired bartender and former military engineer, had the same morning routine: coffee and cream; a roll; and the puzzle page of the Press of Atlantic City. He methodically and religiously worked his way through each one, from the crossword to the jumble to the cryptoquip, a substitution cipher that asks solvers to decode clues and figure out the pun. Extroverted and spontaneous Murray, a successful businessman and local politician, also had his morning routine: coffee with lots of sugar; oatmeal; and tinkering on one of his many writing projects, such as a loosely autobiographical musical about a traveling salesman. Murray swam a few times a week, devoured books and loved to travel. But he never did crosswords. Irv died at age 94, and he barely experienced any cognitive loss before the last six months of his life, when he exhibited rapid mental decline. Murray lived to be 91, but the last several years of his life were marked with severe dementia. When I was researching my book Thinking Inside the Box: Adventures with Crosswords and the Puzzling People Who Can’t Live Without Them, I was fascinated by my family’s case study. The evidence, it seemed, couldn’t be clearer: doing crosswords late in life prevents dementia. And at first, all the studies I found seemed to bear this hypothesis out. “Regular crosswords and number puzzles linked to sharper brain in later life,” a May 2019 Science Daily headline proclaims. According to a University of Exeter study, older adults who regularly did word and number puzzles had increased mental acuity. A 2011 experiment with members of the Bronx Aging Study found that a regular regimen of crosswords might delay the onset of cognitive decline. Belief in puzzle power has fueled multimillion-dollar industry of brain-training games like Lumosity or Dakim. © 2020 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: 27124 - Posted: 03.17.2020

By Linda Searing Alzheimer’s disease, the most common dementia among older adults, now affects about 5.8 million U.S. residents 65 and older — 10 percent of that age group, according to a new report from the Alzheimer’s Association. Age is considered the biggest risk factor for Alzheimer’s, with 3 percent of people 65 to 74, 17 percent of those 75 to 84 and 32 percent of people 85 and older — or nearly a third — having the disease. By 2050, the number of U.S. adults 65 and older with Alzheimer’s is expected to reach 13.8 million, with about half of them 85 or older. The association’s report attributes the growing number of Americans with Alzheimer’s to the projected aging of the U.S. population, with the West and Southeast regions of the country expected to experience the largest increases in the next five years. Sometimes, people under 65 develop what is called early-onset Alzheimer’s, but that is much less common. Although there is no known average age for the onset of Alzheimer’s, symptoms tend to be noticeable in the mid-60s, with memory issues typically one of the first signs. Alzheimer’s is an irreversible brain disorder that slowly destroys memory and thinking skills, can alter mood and personality and eventually disrupts the ability to carry out simple day-to-day tasks. Hallucinations, agitation and aggression are common symptoms as the condition advances. Although there is no cure for the disease — or even drugs to slow or stop progression — some medications can temporarily improve cognitive or behavioral symptoms. Non-medication therapies — exercise, music to stir recall or special lighting to ease sleep disorders — also can be helpful, but the report says that they also do not stop or slow the disease.

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: 27123 - Posted: 03.17.2020

Amelia Hill A low carbohydrate diet may prevent and even reverse age-related damage to the brain, research has found. By examining brain scans, researchers found that brain pathways begin to deteriorate in our late 40s – earlier than was believed. “Neurobiological changes associated with ageing can be seen at a much younger age than would be expected, in the late 40s,” said Lilianne R Mujica-Parodi, a professor in the department of biomedical engineering at Stony Brook University in New York. “However, the study also suggests that this process may be prevented or reversed based on dietary changes that involve minimising the consumption of simple carbohydrates,” added Mujica-Parodi. To better understand how diet influences brain ageing, researchers concentrated on young people whose brains showed no signs of ageing. This is the period during which prevention may be most effective. Using brain scans of nearly 1,000 individuals between the ages of 18 to 88, researchers found that the damage to neural pathways accelerated depending on where the brain was getting its energy from. Glucose, they found, decreased the stability of the brain’s networks while ketones – produced by the liver during periods of carbohydrate restrictive diets – made the networks more stable. “What we found with these experiments involves both bad and good news,” said Mujica-Parodi, “The bad news is that we see the first signs of brain ageing much earlier than was previously thought. “However, the good news is that we may be able to prevent or reverse these effects with diet … by exchanging glucose for ketones as fuel for neurons,” she added in the study, which is published in PNAS. © 2020 Guardian News & Media Limited

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: 27103 - Posted: 03.07.2020

By Nicholas Bakalar Moderate alcohol consumption is associated with reduced levels of beta amyloid, the protein that forms the brain plaques of Alzheimer’s disease, a new study suggests. Korean researchers studied 414 men and women, average age 71, who were free of dementia or alcohol-related disorders. All underwent physical exams, tests of mental acuity, and PET and M.R.I. scans. They were carefully interviewed about their drinking habits. The study, in PLOS Medicine, measured drinking in “standard drinks” — 12 ounces of beer, five ounces of wine, or one-and-a-half ounces of hard liquor. Compared with abstainers, those who drank one to 13 standard drinks a week had a 66 percent lower rate of beta amyloid deposits in their brains. The results applied only to those who drank moderately for decades, and not to those who recently began drinking moderately or drank more than 13 drinks a week. The study controlled for age, sex, education, socioeconomic status, body mass index, vascular health and many other factors. Dr. Dong Young Lee, the senior author and a professor of psychiatry at Seoul National University College of Medicine, cautioned that this was an observational study that looked at people at one point in time, and does not prove cause and effect. Still, he said, “In people without dementia and without alcohol abuse or dependency, moderate drinking appears to be helpful as far as brain health is concerned.” © 2020 The New York Times Company

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: 27096 - Posted: 03.06.2020

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.

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: 27094 - Posted: 03.05.2020

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.

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: 27064 - Posted: 02.24.2020

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

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: 27056 - 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

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: 27038 - Posted: 02.13.2020

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

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: 27023 - Posted: 02.07.2020

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

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: 27015 - Posted: 02.04.2020

By Laura Sanders A cruel twist of genetic fate brought Alzheimer’s disease to a sprawling Colombian family. But thanks to a second twist, one member of the clan, a woman, managed to evade the symptoms for decades. Her escape may hold the key to halting, or even preventing, Alzheimer’s. The inherited version of Alzheimer’s disease erodes people’s memories early, starting around age 40. In this family and others, a mutation in a gene called presenilin 1 eventually leaves its carriers profoundly confused and unable to care for themselves. Locals around the Colombian city of Medellín have a name for the condition: la bobera, or “the foolishness.” The woman in the afflicted family who somehow fended off the disease carried the same mutation that usually guarantees dementia. And her brain was filled with plaques formed by a sticky protein called amyloid. Many scientists view that accumulation as one of the earliest signs of the disease. Yet she stayed sharp until her 70s. Researchers were stumped, until they discovered that the woman also carried another, extremely rare genetic mutation that seemed to be protecting her from the effects of the first one. This second mutation, in a different Alzheimer’s-related gene called APOE, seemed to slow the disease down by decades, says Joseph Arboleda-Velasquez, a cell biologist at Harvard Medical School. “There was this idea of inevitability,” he says. But the woman’s circumstances bring “a different perspective” — one in which amyloid buildup no longer guarantees problems. Arboleda-Velasquez and colleagues reported the details of the woman’s exceptional case November 4 in Nature Medicine, omitting the woman’s name and precise age to protect her privacy. © Society for Science & the Public 2000–2020

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: 26999 - Posted: 01.27.2020

Katarina Zimmer Around 30 years ago, researchers in the UK discovered DNA strands of herpes simplex virus 1 in postmortem brain samples of Alzheimer’s patients at much higher levels than in healthy brains, hinting that viral infection could be somehow involved in the disease. Since then, a string of studies has bolstered the association between Alzheimer’s disease and HSV1, as well as other pathogens, particularly the herpesviruses HHV6A and HHV6B, yet proving causality has remained elusive. Now, in an extensive screen of hundreds of diseased brains from three separate cohorts, a collaboration of US-based researchers reports no evidence for increased RNA or DNA levels of HHV6A or HHV6B in tissue from people with Alzheimer’s disease relative to that from healthy individuals, contradicting the results of some previous results. The scientists also failed to find an association between transcripts of other viruses that have been linked to Alzheimer’s, such as Epstein-Barr virus and cytomegalovirus, and Alzheimer’s, they report today (January 23) in Neuron. “I’m very surprised,” Ruth Itzhaki, an Alzheimer’s disease researcher currently at the University of Oxford who was among those who first associated HSV1, and later HHV6, with the disease, writes to The Scientist in an email. “If their findings are correct, absence of HHV6 would make any involvement in Alzheimer’s disease unlikely,” although not impossible, she notes. Several groups have reported the presence of HHV6 viruses in the brains of Alzheimer’s patients, most notably in a 2018 Neuron study. In that investigation, researchers had found higher levels of HHV6A in patients than in healthy controls, largely based on RNA and DNA sequencing data. © 1986–2020 The Scientist

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: 26989 - Posted: 01.24.2020

Edward Bullmore Unlikely as it may seem, #inflammation has become a hashtag. It seems to be everywhere suddenly, up to all sorts of tricks. Rather than simply being on our side, fighting infections and healing wounds, it turns out to have a dark side as well: the role it plays in causing us harm. It’s now clear that inflammation is part of the problem in many, if not all, diseases of the body. And targeting immune or inflammatory causes of disease has led to a series of breakthroughs, from new treatments for rheumatoid arthritis and other auto-immune diseases in the 1990s, through to the advent of immunotherapy for some cancers in the 2010s. Even more pervasively, low-grade inflammation, detectable only by blood tests, is increasingly considered to be part of the reason why common life experiences such as poverty, stress, obesity or ageing are bad for public health. Advertisement The brain is rapidly emerging as one of the new frontiers for inflammation. Doctors like myself, who went to medical school in the 20th century, were taught to think that there was an impermeable barrier between the brain and the immune system. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time. Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders. Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems. The reasonably well-informed hope – and I emphasise those words at this stage – is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS. Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. © 2020 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26975 - Posted: 01.21.2020

By Karen Weintraub Alzheimer's disease has long been characterized by the buildup of two distinct proteins in the brain: first beta-amyloid, which accumulates in clumps, or plaques, and then tau, which forms toxic tangles that lead to cell death. But how beta-amyloid leads to the devastation of tau has never been precisely clear. Now a new study at the University of Alabama at Birmingham appears to describe that missing mechanism. The study details a cascade of events. Buildup of beta-amyloid activates a receptor that responds to a brain chemical called norepinephrine, which is commonly known for mobilizing the brain and body for action. Activation of this receptor by both beta-amyloid and norepinephrine boosts the activity of an enzyme that activates tau and increases the vulnerability of brain cells to it, according to the study, published in Science Translational Medicine. Essentially, beta-amyloid hijacks the norepinephrine pathway to trigger a toxic buildup of tau, says Qin Wang, the study’s senior author and a professor of neuropharmacology in the department of cell, developmental and integrative biology at the University of Alabama at Birmingham. “We really show that this norepinephrine is a missing piece of this whole Alzheimer’s disease puzzle,” she says. This cascade explains why so many previous Alzheimer’s treatments have failed, Wang says. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloid. But the new research suggests that norepinephrine amplifies the damage wrought by that protein. © 2020 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: 26967 - Posted: 01.17.2020

There are differences in the way English and Italian speakers are affected by dementia-related language problems, a small study suggests. While English speakers had trouble pronouncing words, Italian speakers came out with shorter, simpler sentences. The findings could help ensure accurate diagnoses for people from different cultures, the researchers said. Diagnostic criteria are often based on English-speaking patients. In the University of California study of 20 English-speaking patients and 18 Italian-speaking patients, all had primary progressive aphasia - a neuro-degenerative disease which affects areas of the brain linked to language. It is a feature of Alzheimer's disease and other dementia disorders. Brain scans and tests showed similar levels of cognitive function in people in both language groups. But when the researchers asked participants to complete a number of linguistic tests, they picked up obvious differences between the two groups in the challenges they faced. 'Easier to pronounce' "We think this is specifically because the consonant clusters that are so common in English pose a challenge for a degenerating speech-planning system," said study author Maria Luisa Gorno-Tempini, professor of neurology and psychiatry. "In contrast, Italian is easier to pronounce, but has much more complex grammar, and this is how Italian speakers with [primary progressive aphasia] tend to run into trouble." As a result, the English speakers tended to speak less while the Italian speakers had fewer pronunciation problems, but simplified what they did say. English is a Germanic language while Italian is a Romance language, derived from Latin along with French, Spanish and Portuguese. The researchers, writing in Neurology, are concerned that many non-native English speakers may not be getting the right diagnosis "because their symptoms don't match what is described in clinical manuals based on studies of native English speakers". The San Francisco research team says it now wants to repeat the research in larger groups of patients, and look for differences between speakers of other languages, such as Chinese and Arabic. © 2020 BBC

Related chapters from BN8e: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Brain Asymmetry, Spatial Cognition, and Language; Chapter 13: Memory, Learning, and Development
Link ID: 26954 - Posted: 01.13.2020

Jerold Chun, M.D., Ph.D. Alzheimer’s disease (AD) is the most common cause of dementia, currently affecting an estimated 5.8 million Americans. It has been over a century since AD was first described, but it is still not sufficiently well understood to enable development of drugs to treat it. As lifespan continues to rise and for myriad other reasons, the number of AD cases per state in the US is predicted to increase 12 to 43 percent over the next five years. The lack of disease-modifying treatments may reflect a feature of AD pathology that was first noted in its initial description: the vast heterogeneity of the hallmark “senile plaques” that are found in all AD brains. When Alois Alzheimer and Oskar Fischer described the first cases of AD, they noted plaque accumulations of a protein called amyloid that builds up in between brain cells and interrupts cell-to-cell communication; amyloid plaques vary in size, shape, abundance, and location within the brain. “Among the plaques in the cerebral cortex many were of an extraordinary size, such as I have never seen,” Alois Alzheimer stated. “Some evidently arose from the fusion of smaller ones since they contained several central cores, but others had one exceptionally big central core and uncommonly large halo.” Disease heterogeneity extends to behavior and includes varying age of onset, symptoms, and disease progression. Some variability may be explained by genetic heterogeneity, since more than 33 AD risk factor genes have been identified via a technique called “genome wide association studies” (GWAS), which broadly samples DNA from cells outside of the brain to identify mutations that are present in every cell of the body. None of these genes, however, are considered to cause AD. © 2020 The Dana Foundation

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: 26931 - Posted: 01.04.2020