Links for Keyword: Alzheimers

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Lauren Gravitz When Kate Sieloff's husband, Karl, began acting strange, she didn't know where to turn. Her hard-working, affectionate spouse was suddenly having fits of anger and aggression. He stopped paying the bills. Karl, 56 at the time, was an engineer at General Motors, where he'd worked for more than 40 years. But some days he didn't even show up for work, finding it too hard to get out of bed. Because the problems were sporadic, most people in her life couldn't see what was going on. They told Kate, of Romeo, Mich., that she was imagining things. Doctors suggested that Karl was depressed and tried him on a variety of medications. When he began depleting their savings on impulsive purchases, and grew even more aggressive and violent, her son—a neurologist at the University of Michigan's medical center in Ann Arbor—insisted she bring Karl to his hospital for evaluation. Doctors there quickly diagnosed him with frontotemporal dementia. For Kate, the diagnosis was a relief, but she still felt overwhelmed and needed help coping with her husband's illness. Getting his diabetes medications under control, and starting him on a mood stabilizer and a new antidepressant helped control his mood swings while restoring some of his loving personality. © 2018 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: 25456 - Posted: 09.17.2018

Bret Stetka Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer's disease, the most common form of dementia worldwide, caused by a germ? By "germ" he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer's is infectious. It's an idea that just a few years ago would've seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer's research for years, but until very recently not much of it went toward investigating infection in causing dementia. But this "germ theory" of Alzheimer's, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis. If the germ theory gets traction, even in some Alzheimer's patients, it could trigger a seismic shift in how doctors understand and treat the disease. For instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it's worth looking into. © 2018 npr

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: 25435 - Posted: 09.11.2018

By Nicholas Bakalar Yet another reason to stop smoking: It may reduce your risk for dementia. Korean researchers studied 46,140 men, 60 and older, following them for an average of eight years with periodic health examinations. Over the course of the study, 1,644 people were given a diagnosis of Alzheimer’s disease or another form of dementia. After controlling for age, body mass index, blood pressure, physical activity and other health and behavioral characteristics, they found that the less time men smoked, the less likely they were to have dementia. Compared with continual smokers, men who had quit for up to four years had a 13 percent lower risk, those who had quit for four years or more a 14 percent lower risk, and never-smokers a 19 percent lower risk. The study is in the Annals of Clinical and Translational Neurology. The authors acknowledge that they had no data on education level, which is a risk factor for dementia, and that the eight-year follow-up may not have been long enough to pick up all cases of dementia, a disease that develops slowly. “Smoking has not been well known as a risk factor for dementia,” said the lead author, Dr. Daein Choi, a researcher at the Seoul University College of Medicine. “Our findings suggest that smoking cessation, or reduced smoking, might be helpful in reducing the risk.” © 2018 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: 25427 - Posted: 09.10.2018

By Kelly Servick Stay active; age gracefully. Behind this truism, there’s a pile of unanswered scientific questions. Researchers are still sorting out what it is about physical activity that seems to lower the risk of dementia later in life. Even more uncertain is whether the effects of exercise can alter the course of diseases that cause dementia—chief among them, Alzheimer’s disease—once they’ve already taken root. A study published today in Science offers some new clues. In mice that mimic a severe, genetic form of Alzheimer’s disease, a combination of treatments that prompt the growth of new brain cells and protect them from damage can mimic the beneficial effects of exercise in preventing memory decline. So could we someday bottle the effects of exercise to treat Alzheimer’s? And if so, what exactly would we need to bottle? Here’s a rundown of what we know, and what’s still controversial. What’s the link between exercise and brain aging? Many large studies suggest staying active and fit throughout life lowers the risk of memory problems later on. For example, a recent project tracked more than 1000 Swedish women over 4 decades and found that for those judged to have “high” cardiovascular fitness on entering the study—as measured by the maximum workload they could handle on a stationary cycle machine before exhaustion—the onset of dementia was delayed, on average, by 9.5 years compared to those with “medium” fitness. But such studies can’t rule out all other confounding factors that might influence dementia risk—from genes to other aspects of a healthy lifestyle common in regular exercisers. And they don’t explain what exercise actually does to the brain. Does exercise fight the effects of Alzheimer’s disease once someone has it? © 2018 American Association for the Advancement of Scienc

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: 25423 - Posted: 09.07.2018

By Rebecca Nebel Growing older may be inevitable, but getting Alzheimer’s disease is not. Although we can’t stop the aging process, which is the biggest risk factor for Alzheimer’s, there are many other factors that can be modified to lower the risk of dementia. Yet our ability to reduce Alzheimer’s risk and devise new strategies for prevention and treatment is impeded by a lack of knowledge about how and why the disease differs between women and men. There are tantalizing hints in the literature about factors that act differently between the sexes, including hormones and specific genes, and these differences could be important avenues of research. Unfortunately, in my experience, most studies of Alzheimer’s risk combine data for women and men. For that reason, researchers at the Society for Women’s Health Research Interdisciplinary Network on Alzheimer’s Disease recently published a review paper in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association that calls for greater analysis of research data by sex to stimulate new approaches that will improve prevention, diagnosis and treatment of Alzheimer’s. We have some evidence, for example, that sex hormones such as estrogen influence the course of the disease, but we do not understand enough about why and how. Ovaries are the primary source of estrogen for premenopausal women, and surgical removal of a woman’s ovaries before menopause is associated with a higher risk of dementia. But using estrogen therapy after surgery until age 50 negates that risk. This fact suggests that estrogen may be protective in premenopausal women. © 2018 Scientific American

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: 25418 - Posted: 09.05.2018

By Jocelyn Kaiser When molecular biologist Darren Baker was winding up his postdoc studying cancer and aging a few years ago at the Mayo Clinic in Rochester, Minnesota, he faced dispiritingly low odds of winning a National Cancer Institute grant to launch his own lab. A seemingly unlikely area, however, beckoned: Alzheimer's disease. The U.S. government had begun to ramp up research spending on the neurodegenerative condition, which is the sixth-leading cause of death in the United States and will afflict an estimated 14 million people in this country by 2050. "There was an incentive to do some exploratory work," Baker recalls. Baker's postdoc studies had focused on cellular senescence, the cellular version of aging, which had not yet been linked to Alzheimer's. But when he gave a drug that kills senescent cells to mice genetically engineered to develop an Alzheimer's-like illness, the animals suffered less memory loss and fewer of the brain changes that are hallmarks of the disease. Last year, those data helped Baker win his first independent National Institutes of Health (NIH) research grant—not from NIH's National Cancer Institute, which he once expected to rely on, but from the National Institute on Aging (NIA) in Bethesda, Maryland. He now has a six-person lab at the Mayo Clinic, working on senescence and Alzheimer's. Baker is the kind of newcomer NIH hoped to attract with its recent Alzheimer's funding bonanza. For years, patient advocates have pointed to the growing toll and burgeoning costs of Alzheimer's as the U.S. population ages. Spurred by those projections and a controversial national goal to effectively treat the disease by 2025, Congress has over 3 years tripled NIH's annual budget for Alzheimer's and related dementias, to $1.9 billion. The growth spurt isn't over: Two draft 2019 spending bills for NIH would bring the total to $2.3 billion—more than 5% of NIH's overall budget. © 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: 25402 - Posted: 08.31.2018

By Christopher F. Schuetze DOETINCHEM, Netherlands — “We’re lost,” said Truus Ooms, 81, to her friend Annie Arendsen, 83, as they rode a city bus together. “As the driver, you should really know where we are,” Ms. Arendsen told Rudi ten Brink, 63, who sat at the wheel of the bus. But she was joking. The three are dementia patients at a care facility in the eastern Netherlands. Their bus ride — a route on the flat, tree-lined country roads of the Dutch countryside — was a simulation that plays out several times a day on three video screens. It is part of an unorthodox approach to dementia treatment that doctors and caregivers across the Netherlands have been pioneering: harnessing the power of relaxation, childhood memories, sensory aids, soothing music, family structure and other tools to heal, calm and nurture the residents, rather than relying on the old prescription of bed rest, medication and, in some cases, physical restraints. “The more stress is reduced, the better,” said Dr. Erik Scherder, a neuropsychologist at the Vrije Universiteit Amsterdam and one of the country’s best-known dementia care specialists. “If you can lower stress and discomfort, it has a direct physiological effect.” Simulated trips in buses or on beaches — like one in a care facility in Haarlem, not far from a real beach — create a gathering point for patients. The shared experience lets them talk about past trips and take a mini holiday from their daily lives. Dementia, a group of related syndromes, manifests itself in a steep decline in brain functions. The condition steals memories and personalities. It robs families of their loved ones and saps resources, patience and finances. © 2018 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: 25361 - Posted: 08.22.2018

By Gretchen Reynolds Sitting for hours without moving can slow the flow of blood to our brains, according to a cautionary new study of office workers, a finding that could have implications for long-term brain health. But getting up and strolling for just two minutes every half-hour seems to stave off this decline in brain blood flow and may even increase it. Delivering blood to our brains is one of those automatic internal processes that most of us seldom consider, although it is essential for life and cognition. Brain cells need the oxygen and nutrients that blood contains, and several large arteries constantly shuttle blood up to our skulls. Because this flow is so necessary, the brain tightly regulates it, tracking a variety of physiological signals, including the levels of carbon dioxide in our blood, to keep the flow rate within a very narrow range. But small fluctuations do occur, both sudden and lingering, and may have repercussions. Past studies in people and animals indicate that slight, short-term drops in brain blood flow can temporarily cloud thinking and memory, while longer-term declines are linked to higher risks for some neurodegenerative diseases, including dementia. Other research has shown that uninterrupted sitting dampens blood flow to various parts of the body. Most of those studies looked at the legs, which are affected the most by our postures, upright or not. Stay seated for several hours, and blood flow within the many blood vessels of the legs can slacken. Whether a similar decline might occur in the arteries carrying blood to our brains was not known, however. So for the new study, which was published in June in the Journal of Applied Physiology, researchers at Liverpool John Moores University in England gathered 15 healthy, adult, male and female office workers. © 2018 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: 25338 - Posted: 08.16.2018

By Damian Garde, In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with new results with an in-development drug. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about. At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have. In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo. To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude. “I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.” But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions. © 2018 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: 25273 - Posted: 07.31.2018

By Kelly Servick In the hunt for a drug to treat Alzheimer’s disease, even a whiff of success can be intoxicating. That helps explain why an experimental drug called BAN2401, which a few months ago seemed like it might join a growing heap of failed candidates, created so much buzz yesterday at the Alzheimer’s Association International Conference in Chicago, Illinois. In a phase II trial, the drug had already failed to show the level of benefit that its developers—Biogen Inc. in Cambridge, Massachusetts; and Eisai Co. Ltd. in Tokyo—set as the study’s primary endpoint. But yesterday the companies presented a series of other analyses from the same trial that suggest BAN2401 might slow the pace of cognitive decline in Alzheimer’s patients, and reverse the buildup of a brain protein thought to drive the disease’s neurodegeneration. But the subset of patients who showed those benefits was relatively small—161 people—and an unexpected change to the way the study was randomized cast some skepticism on the results. For many, the findings are too preliminary to celebrate. “If these results we saw today pan out in phase III clinical trials, then you’re looking at disease-modifying medication—the first one for Alzheimer’s disease,” says Keith Fargo, director of scientific programs & outreach at the Alzheimer’s Association in Chicago, Illinois. “But you don’t know whether they’re going to pan out until you actually do the phase III trial.” © 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: 25257 - Posted: 07.27.2018

Aimee Cunningham Keeping a tight lid on blood pressure isn’t just good for the heart. It may also help the brain. People given intensive drug treatment for high blood pressure were less likely to develop an early form of memory loss, according to preliminary results from a major clinical trial. This approach reduced the rate of early memory loss, called mild cognitive impairment, by around 19 percent, compared with people who received less aggressive treatment. And the intensely treated group developed fewer white matter lesions over time, researchers reported July 25 at the Alzheimer’s Association International Conference in Chicago. White matter lesions, which are associated with dementia, are thought to be caused by blood vessel injuries in white matter, the part of the brain that contains nerve fibers. The brain research is part of SPRINT, the Systolic Blood Pressure Intervention Trial involving more than 9,300 participants. Some received intensive treatment aimed at lowering their systolic blood pressure — the pressure on artery walls when the heart beats — below 120 millimeters of mercury; others got standard treatment to bring it below 140. The trial had already reported that participants who received the intensive treatment dropped their risk of heart attacks and other cardiovascular problems by 25 percent, compared with the standard group (SN Online: 11/9/2015). The results were the basis for revamped blood pressure guidelines, released last year (SN: 12/9/17, p. 13). |© Society for Science & the Public 2000 - 2018

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: 25256 - Posted: 07.26.2018

By Emily Willingham Of all of our organs, our brains and hearts get the most attention. But the liver once held top billing, preeminent over the heart and mind as the seat of emotion and even the soul. As its name implies, we need our liver to live—not only because it works hard as a detox unit but also because it quietly processes components our brains need to thrive. The Alzheimer’s disease (AD) research community is turning its attention to this liver–brain connection. That newfound interest turns up in a quartet of new studies presented July 24 at the Alzheimer’s Association International Conference 2018. The results may help provide clues to both the basic biology of AD and how diet is linked to brain health. More specifically, it may give insight into why human clinical trials of fish oil have failed to protect against AD and other forms of dementia. In the four studies, blood levels of molecules associated with the liver and production of fats, or lipids, were tied to AD risk—a first step toward deeper examination of the liver–brain link. “There seem to be some positive results correlating levels of lipids with cognition and cognitive progression,” says Paul Schulz, director of the Dementia and Memory Disorders Clinic at The University of Texas McGovern Medical School, who was not involved in the studies. “The challenge will be to establish cause and effect.” The brain consists mostly of fats, which contribute to both its form and function. These lipids facilitate communication from neuron to neuron and make up much of the insulation that sheaths these cells. It is the liver that builds the fats the brain needs—and many genes tied to AD are linked to fat production or transport, including a version of a gene associated with high AD risk—APOE ε4. © 2018 Scientific American

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: 25253 - Posted: 07.26.2018

Jon Hamilton There's new evidence that a woman's levels of female sex hormones, including estrogen and progesterone, can influence her risk of Alzheimer's and other forms of dementia. Women are less likely to develop dementia later in life if they begin to menstruate earlier, go through menopause later, and have more than one child, researchers reported Monday at the Alzheimer's Association International Conference in Chicago. And recent studies offer hints that hormone replacement therapy, which fell out of favor more than a decade ago, might offer a way to protect a woman's brain if it is given at the right time, the researchers said. The findings could help explain why women make up nearly two-thirds of people in the U.S. with Alzheimer's, says Maria Carrillo, the association's chief scientific officer. "It isn't just that women are living longer," Carrillo says. "There is some biological underpinning. And because of the large numbers of women that are affected, it is important to find out [what it is]." Scientists have long suspected that sex hormones such as estrogen and progesterone play a role in Alzheimer's. And two studies on dementia and what occurs during a women's reproductive years support that idea. One of the studies looked at nearly 15,000 women in California. And it found an association between a woman's reproductive history and her risk of memory problems later in life. © 2018 npr

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: 25242 - Posted: 07.24.2018

By Gina Kolata The task facing Eli Lilly, the giant pharmaceutical company, sounds simple enough: Find 375 people with early Alzheimer’s disease for a bold new clinical trial aiming to slow or stop memory loss. There are 5.4 million Alzheimer’s patients in the United States. You’d think it would be easy to find that many participants for a trial like this one. But it’s not. And the problem has enormous implications for treatment of a disease that terrifies older Americans and has strained families in numbers too great to count. The Global Alzheimer’s Platform Foundation, which is helping recruit participants for the Lilly trial, estimates that to begin finding participants, it will have to inform 15,000 to 18,000 people in the right age groups about the effort. Of these, nearly 2,000 must pass the initial screening to be selected for further tests to see if they qualify. Just 20 percent will meet the criteria to enroll in Lilly’s trial: They must be aged 60 to 89, have mild but progressive memory loss for at least six months, and have two types of brain scans showing Alzheimer’s is underway. Yet an 80 percent screening failure rate is typical for Alzheimer’s trials, said John Dwyer, president of the foundation. There is just no good way to quickly diagnose the disease. The onerous process of locating just 375 patients illustrates a grim truth: finding patients on whom to test new Alzheimer’s treatments is becoming an insurmountable obstacle — no matter how promising the trial. With brain scans, lab tests and memory tests, the cost per diagnosis alone is daunting — as much as $100,000 for each person who ends up enrolled in a trial, Mr. Dwyer said — even before they begin the experimental treatment. © 2018 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: 25241 - Posted: 07.24.2018

Sukanya Charuchandra Older individuals with high blood pressure are more likely to have brain lesions than those without high blood pressure and may also have protein tangles, a sign of Alzheimer’s disease, according to a study published in Neurology on July 11. Coauthor Zoe Arvanitakis, a neurologist at Rush University Medical Center, says these “preliminary data” need further exploration, according to the Associated Press. “We can’t be alarmist,” she says. According to a statement, the researchers were keen to learn if blood pressure had links to signs of brain aging. They tracked 1,288 people who were over the age of 65 until their deaths, an average of eight years. The scientists measured the blood pressure of the subjects once every year and examined their brains postmortem. Of the total number of subjects, two-thirds of the subjects had high blood pressure, while about half had one or more brain infarcts, necrotic regions caused by a loss of blood flow. With higher blood pressure, the risk of brain lesions went up: people with an upper blood pressure of 147 (normal being 120) had a 46 percent higher chance of having one or more lesions. Additionally, those with high pressure were more likely to have protein tangles in their brains. While the paper has “good information,” it also raises many questions, Ajay Misra, a neurologist at New York University Winthrop Hospital who was not involved in this research, tells Health Day. For instance, is higher blood pressure better in some situations? The researchers found that elderly subjects with lower blood pressure had a greater risk of stroke. Misra suggests the higher pressure may be required to keep blood vessels of older adults clear. He adds that a one-size-fits-all blood-pressure guideline may not be appropriate. © 1986 - 2018 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: 25213 - Posted: 07.17.2018

Leah Rosenbaum Joel Dudley and his colleagues were searching through datasets for Alzheimer’s disease vulnerabilities to exploit in creating a treatment when they stumbled across a surprising correlation: Many of the brains they looked at had signs of herpesvirus infection. But those from people with Alzheimer’s disease had much higher levels of viral DNA than those from healthy people. In particular, the researchers found high levels of HHV-6 and HHV-7, two strains of herpesvirus associated with a common childhood illness called roseola, the team reports online June 21 in Neuron. “We had no intention of looking at viruses,” says Dudley, a biomedical informatics researcher at the Icahn School of Medicine at Mount Sinai in New York City, who gives a talk jokingly titled, “I went looking for drugs and all I found were these stupid viruses.” It is unclear whether the herpesviruses contribute to the development of Alzheimer’s, or if Alzheimer’s patients are just more susceptible to these viruses, which can remain latent in the body long after exposure. Genetic factors also influence a person’s risk of developing Alzheimer’s. The researchers did find that the viruses interacted with genes linked with Alzheimer’s disease, though the implications are still murky. |© Society for Science & the Public 2000 - 2018

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: 25126 - Posted: 06.22.2018

by Judith Graham You’ve turned 65 and exited middle age. What are the chances you’ll develop cognitive impairment or dementia in the years ahead? New research about “cognitive life expectancy” — how long older adults live with good vs. declining brain health — shows that after age 65, men and women spend more than a dozen years in good cognitive health, on average. And, over the past decade, that time span has been expanding. By contrast, cognitive challenges arise in a more compressed time frame in later life, with mild cognitive impairment (problems with memory, decision-making or thinking skills) lasting about four years, on average, and dementia (Alzheimer’s disease or other related conditions) occurring over 1½ to two years. Even when these conditions surface, many seniors retain an overall sense of well-being, according to new research presented in April at the Population Association of America’s annual meeting. “The majority of cognitively impaired years are happy ones, not unhappy ones,” said Anthony Bardo, a co-author of that study and an assistant professor of sociology at the University of Kentucky at Lexington. Recent research finds that: Most seniors don’t have cognitive impairment or dementia. Of Americans 65 and older, about 20 to 25 percent have mild cognitive impairment while about 10 percent have dementia, according to Kenneth Langa, an expert in the demography of aging and a professor of medicine at the University of Michigan. Risks rise with advanced age, and the portion of the population affected is significantly higher for people older than 85. © 1996-2018 The Washington Post

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: 25099 - Posted: 06.18.2018

By Judith Graham, You’ve turned 65 and exited middle age. What are the chances you’ll develop cognitive impairment or dementia in the years ahead? New research about “cognitive life expectancy”—how long older adults live with good versus declining brain health—shows that after age 65 men and women spend more than a dozen years in good cognitive health, on average. And, over the past decade, that time span has been expanding. By contrast, cognitive challenges arise in a more compressed time frame in later life, with mild cognitive impairment (problems with memory, decision-making or thinking skills) lasting about four years, on average, and dementia (Alzheimer’s disease or other related conditions) occurring over 1½ to two years. Even when these conditions surface, many seniors retain an overall sense of well-being, according to new research presented last month at the Population Association of America’s annual meeting. “The majority of cognitively impaired years are happy ones, not unhappy ones,” said Anthony Bardo, a co-author of that study and assistant professor of sociology at the University of Kentucky-Lexington. Recent research finds that: Most seniors don’t have cognitive impairment or dementia. Of Americans 65 and older, about 20 to 25 percent have mild cognitive impairment while about 10 percent have dementia, according to Dr. Kenneth Langa, an expert in the demography of aging and a professor of medicine at the University of Michigan. Risks rise with advanced age, and the portion of the population affected is significantly higher for people over 85. © 2018 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: 25022 - Posted: 05.25.2018

Kelly Crowe · In a darkened room at Toronto's Krembil Research Institute, Dr. Donald Weaver is looking at a screen covered in green fluorescent dots. That's not a good thing. Those glowing green dots are exactly what this Alzheimer's researcher did not want to see. "Weeks if not months of work went into this compound and it failed," he said. "It's done." Weaver, a neurologist and chemist, was testing a compound to see if it could prevent the clumping of a protein called tau which creates distinctive tangles in the brains of people with Alzheimer's disease. If it had worked, it might have been a candidate for a new drug. But it didn't work, just like the thousands of others he's already tried. Failure is normal for researchers engaged in the frustrating search for drugs to treat Alzheimer's disease. "You have to be passionate," Weaver said. "This is a disease in which so many approaches have failed. You really have to deeply believe that your approach is correct just to get up every day and keep working at it." Many promising drugs have failed But after a series of high-profile drug failures over the past few years, scientists are facing the disturbing possibility that their leading theory of Alzheimer's might be fatally flawed. It's called the amyloid hypothesis, and it was an obvious target for researchers because the amyloid protein forms distinctive plaques in the brains of people with Alzheimer's. "That led to the conclusion it must be playing a pretty important role in the disease," Weaver said. The amyloid hypothesis was first proposed in 1992, and for the past 25 years research has focused on finding compounds that clear amyloid from the brain or slow down its production. ©2018 CBC/Radio-Canada.

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: 25015 - Posted: 05.24.2018

by Erin Blakemore Want to cure Alzheimer’s? Get in line. Researchers have long been puzzled by the disease and vexed by how long it’s taking to unravel its mysteries. One group of scientists is helping speed up that process with assistance from the public. “Stall Catchers,” a game created by Cornell University’s Human Computation Institute, turns the hunt for a cure from frustrating to fun. In the game, players watch short movies — made using a multiphoton microscope — that show blood flowing through the brains of living mice. Players work on a data set of thousands of images to point out “stalls” — areas of reduced blood flow caused by white blood cells accumulating on the sides of the vessels. The films might seem far removed from the experience typical of people with Alzheimer’s disease: difficulty concentrating, jumbled speech and confusion. But they may be closely linked: It’s thought that reduced blood flow in the brain is at least partially responsible for Alzheimer’s symptoms. When a blood vessel in the brain gets stalled, blood doesn’t flow as it should. A single stalled capillary might seem like no big deal, but in mice with Alzheimer’s disease, up to 2 percent of brain capillaries can be stalled. Because vessels in the brain are so interconnected, that can restrict overall brain blood flow by up to 30 percent. Reduced blood flow has been found in the brains of humans with Alzheimer’s disease, too. © 1996-2018 The Washington Post

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: 24945 - Posted: 05.07.2018