Links for Keyword: Alzheimers

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/ By Steven Lubet There is a memorable episode in the now-classic sitcom Scrubs in which the conniving Dr. Kelso unveils a plan to peddle useless “full body scans” as a new revenue stream for the perpetually cash-strapped Sacred Heart Hospital. The irascible but ultimately patient-protecting Dr. Cox objects loudly. “I think showing perfectly healthy people every harmless imperfection in their body just to scare them into taking invasive and often pointless tests is an unholy sin,” he says. Undeterred, Kelso launches an advertising campaign that promotes the scans in a tear-jerking television commercial and a billboard screaming “YOU may already be DYING.” Alarmist medical advertising is pretty funny on television, but it can be far more troubling in real life. Although I’ve never been alerted to impending death, I recently received an advertisement from my own trusted health care provider warning that I may have Alzheimer’s disease, although I have no known symptoms and no complaints. As long-time patients at NorthShore University Health System, which is affiliated with the University of Chicago, my wife and I received two solicitations from its Center for Brain Health touting the development of “ways to slow brain aging and even prevent the onset of Alzheimer’s.” According to the ads, which arrived in both postcard and email form, there is “new hope for delaying — even preventing — aging brain diseases” through “genetic testing, advanced diagnostics, and lifestyle factors.” Copyright 2017 Undark

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: 23978 - Posted: 08.19.2017

By Andy Coghlan Can exercise during childhood protect you against memory loss many decades later? Exercise early in life seems to have lifelong benefits for the brain, in rats at least. “This is an animal study, but it indicates that physical activity at a young age is very important – not just for development, but for the whole lifelong trajectory of cognitive development during ageing,” says Martin Wojtowicz of the University of Toronto, Canada. “In humans, it may compensate for and delay the appearance of Alzheimer’s symptoms, possibly to the point of preventing them.” Wojtowicz’s team spilt 80 young male rats into two equal groups, and placed running wheels in the cages of one group for a period of six weeks. Around four months later – when the rats had reached middle age – the team taught all the rats to associate an electric shock with being in a specific box. When placed in the box, they froze with fear. Two weeks later, the team tested the rats in three scenarios: exactly the same box in the same room, the same box with the room arranged and lit differently, and a completely different box in a different room. The rats without access to a running wheel when they were young now froze the same proportion of times in each of these situations, suggesting they couldn’t remember which one was hazardous. But those that had been able to run in their youth froze 40 to 50 per cent less in both altered box settings. © Copyright New Scientist Ltd

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: 23959 - Posted: 08.15.2017

By Aggie Mika Individuals who possess an innate resilience to age-related brain pathologies may offer molecular clues to unexplored therapeutics for neurodegenerative disease. After having accidentally discovered rapid aging and disease in mice with mutations in the gene that encodes the protein klotho—named after the Greek Fate Clotho, daughter of Zeus and spinner of the thread of life—independent researchers have shown that some people with genetic variants that promote elevated klotho levels live longer and tend to stave off age-related cognitive decline. In a paper published today (August 8) in Cell Reports, scientists report that a fragment of klotho, similar to what winds up in circulation after cleavage from the cell membrane, boosted spatial and short-term memory in young and aging mice and improved both memory and mobility in a transgenic mouse model of neurodegenerative disease. Notably, in each type of mouse, the protein fragment was injected into the animals’ bodies either a day or a few hours before cognitive testing took place. Previously, neurologist and researcher Dena Dubal of the University of California, San Francisco, and others have demonstrated that transgenic overexpression of klotho throughout an organism’s lifespan produces similar cognitive improvements. Dubal’s current work, she says, provides a promising answer to a “big, burning question” of klotho’s therapeutic utility: “could you give it acutely, and would it increase cognition in a rapid way?” © 1986-2017 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: 23942 - Posted: 08.10.2017

Shirley S. Wang Efforts to develop a treatment that stalls the memory-robbing devastation of Alzheimer's disease have so far been unsuccessful, but scientists are making strides in another important area: the development of better tests to tell who has the condition. Their aim is to develop more accurate, cheaper and less invasive tests to detect the biological markers of Alzheimer's-induced changes in the brain. At the recent Alzheimer's Association International Conference in London, scientists presented early but promising data on a new blood test and a novel brain imaging technique. They also unveiled preliminary data on a study to investigate the potential clinical usefulness of a test that's already on the market but isn't widely reimbursed by insurance. Alzheimer's is characterized by changes to the brain involving clumping of a protein called amyloid and another called tau — pathologies that until the last decade or so could only be seen upon autopsy. The biomarker tests available to date focus primarily on detecting amyloid. These tests are generally used only for research purposes because they can be expensive or require special technology. They are meant to be used for ruling out Alzheimer's in patients who already have memory problems. Less invasive, easier to use and cheaper technologies may mean that more people could have access to testing. For public health, this could mean being able to more broadly screen the population to identify people who are at high-risk for getting the illness and then focusing more expensive, involved efforts for testing, prevention and treatment on them. © 2017 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: 23914 - Posted: 08.05.2017

By Ryan Cross Researchers have discovered tell-tale signs of Alzheimer’s disease in 20 elderly chimpanzee brains, rekindling a decades-old debate over whether humans are the only species that develop the debilitating condition. Whether chimps actually succumb to Alzheimer’s or are immune from symptoms despite having the key brain abnormalities is not clear. But either way, the work suggests that chimps could help scientists better understand the disease and how to fight it—if they could get permission to do such studies on these now-endangered animals. A definitive diagnosis of Alzheimer’s includes dementia and two distortions in the brain: amyloid plaques, sticky accumulations of misfolded pieces of protein known as amyloid beta peptides; and neurofibrillary tangles, formed when proteins called tau clump into long filaments that twist around each other like ribbons. Many other primates including rhesus monkeys, baboons, and gorillas also acquire plaques with aging, but tau tangles are either absent in those species or don’t fully resemble those seen in humans. In the new study, researchers led by biological anthropologist Mary Ann Raghanti at Kent State University in Ohio turned to our closest relative, chimpanzees. In 2015, the U.S. Fish and Wildlife Service declared all U.S. chimps endangered, effectively ending all invasive research on them. But thanks to a newly founded center that collects brains from chimps that die at zoos or research centers, the team was able to examine the brains of 20 chimps aged 37 to 62—the oldest recorded age for a chimp, roughly equivalent to a human at the age of 120. Of these chimps, 13 had amyloid plaques, and four also had the neurofibrillary tangles typical of more advanced stages of Alzheimer’s in humans, the team writes [DATE TK] in Neurobiology of Aging. © 2017 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: 23906 - Posted: 08.01.2017

By Tara Bahrampour Older patients who become disoriented or confused after surgery are more than three times more likely to develop dementia later, a new study has found. The report, published Friday by the British Journal of Anaesthesia, assesses the effects of post-operative delirium (POD) on people 65 and older who were cognitively normal before their operations. Of 1,152 such patients, 9.5 percent met criteria for mild cognitive impairment or dementia a median of nine months after surgery. The frequency of being diagnosed with MCI or dementia after surgery was much higher – 33.3 percent – among those who had experienced post-operative delirium, compared with 9 percent among those who had not. While earlier studies have showed a relationship between POD and dementia, this is the first to look entirely at subjects who showed no cognitive decline in pre-surgery assessments, said David Warner, an anesthesiologist at Mayo Clinic in Rochester, Minnesota and the study’s senior author. Delirium is defined by an acute state of confusion, inattention, disorganized thinking, and a fluctuating mental state. Older patients are more likely than younger ones to develop it after surgery, as are people with lower education levels and those who undergo vascular procedures. Further study is needed to determine whether delirium contributes to later cognitive decline or is an indicator of some underlying factor that made people more likely to develop dementia, Warner said. © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 23888 - Posted: 07.28.2017

Joseph Jebelli The terror of Alzheimer’s is that it acts by degrees, and can therefore bewilder family members as much as its victims. Those who first notice the onset of Alzheimer’s in a loved one tell of forgotten names and unsettling behaviour, of car keys found in the fridge and clothing in the kitchen cabinet, of aimless wanderings. Naturally, they want to understand the boundaries of normal ageing and whether these are being crossed. Often, the answer arrives when they’re greeted as complete strangers, when the patient’s mind becomes irrevocably unmoored from its past. The disease is terrifying for its insidiousness as well as its long-term manifestations. Fear partly explains why Alzheimer’s has been ignored for so long. Yet it is now the leading cause of death among the oldest people, and according to Professor Sir Michael Marmot, an expert in health inequalities, it could be an “important part” of the stagnation in increases in life expectancy since 2010 that he has identified. As a researcher, I have been struck by how many patients speak openly about their condition only after receiving a diagnosis. “I knew something wasn’t right. Sometimes I don’t know what day of the week it is or what I have to do,” one newly diagnosed patient told me. “I look in my calendar but then I think: why am I looking at this? My husband was the one who made me see a GP. I was too frightened. I thought I might have it but I didn’t want to hear it.” © 2017 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: 23862 - Posted: 07.22.2017

By Fergus Walsh Medical correspondent One in three cases of dementia could be prevented if more people looked after their brain health throughout life, according to an international study in the Lancet. It lists nine key risk factors including lack of education, hearing loss, smoking and physical inactivity. The study is being presented at the Alzheimer's Association International Conference in London. By 2050, 131 million people could be living with dementia globally. There are estimated to be 47 million people with the condition at the moment. Nine factors that contribute to the risk of dementia Mid-life hearing loss - responsible for 9% of the risk Failing to complete secondary education - 8% Smoking - 5% Failing to seek early treatment for depression - 4% Physical inactivity - 3% Social isolation - 2% High blood pressure - 2% Obesity - 1% Type 2 diabetes - 1% These risk factors - which are described as potentially modifiable - add up to 35%. The other 65% of dementia risk is thought to be potentially non-modifiable. Source: Lancet Commission on dementia prevention, intervention and care "Although dementia is diagnosed in later life, the brain changes usually begin to develop years before," said lead author Prof Gill Livingston, from University College London. "Acting now will vastly improve life for people with dementia and their families and, in doing so, will transform the future of society." The report, which combines the work of 24 international experts, says lifestyle factors can play a major role in increasing or reducing an individual's dementia risk. It examines the benefits of building a "cognitive reserve", which means strengthening the brain's networks so it can continue to function in later life despite damage. Image caption Eve Laird is taking part in a study on how to prevent dementia © 2017 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: 23856 - Posted: 07.21.2017

By Tara Bahrampour A significant portion of people with mild cognitive impairment or dementia who are taking medication for Alzheimer’s may not actually have the disease, according to interim results of a major study currently underway to see how PET scans could change the nature of Alzheimer’s diagnosis and treatment. The findings, presented Wednesday at the Alzheimer’s Association International Conference in London, come from a four-year study launched in 2016 that is testing over 18,000 Medicare beneficiaries with MCI or dementia to see if their brains contain the amyloid plaques that are one of the two hallmarks of the disease. So far, the results have been dramatic. Among 4,000 people tested so far in the Imaging Dementia-Evidence for Amyloid Scanning (IDEAS) study, researchers from the Memory and Aging Center at the University of California, San Francisco found that just 54.3 percent of MCI patients and 70.5 percent of dementia patients had the plaques. A positive test for amyloid does not mean someone has Alzheimer’s, though its presence precedes the disease and increases the risk of progression. But a negative test definitively means a person does not have it. The findings could change the way doctors treat people in these hard-to-diagnose groups and save money currently being spent on inappropriate medication. “If someone had a putative diagnosis of Alzheimer’s Disease, they might be on an Alzheimer’s drug like Aricept or Namenda,” said James Hendrix, the Alzheimer Association’s director of global science initiatives who co-presented the findings. “What if they had a PET scan and it showed that they didn’t have amyloid in their brain? Their physician would take them off that drug and look for something else.” © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23848 - Posted: 07.19.2017

Shirley S. Wang In nursing homes and residential facilities around the world, health care workers are increasingly asking dementia patients questions: What are your interests? How do you want to address us? What should we do to celebrate the life of a friend who has passed away? The questions are part of an approach to care aimed at giving people with memory loss and other cognitive problems a greater sense of control and independence. At its core is the idea that an individual with dementia should be treated as a whole person and not "just" a patient. Scientists sometimes call this approach an ecopsychosocial intervention. The goal is to create environments that better meet patients' psychological and emotional needs through strategies other than medication. At the Alzheimer's Association International Conference this week in London, researchers from the U.S., the U.K. and Israel presented data from four trials demonstrating that such interventions significantly improve residents' mood and quality of life. The interventions can also reduce their use of antipsychotic drugs and improve their ability to care for themselves. Taken together, these studies and others suggest that relatively simple and potentially cost-effective interventions can yield significant benefits for people with dementia, even those in residential facilities in the later stages of disease. Behavioral Therapy Helps More Than Drugs For Dementia Patients As the population continues to age, and the number of people with dementia continues to rise, these interventions are likely to increase in importance as well. © 2017 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: 23847 - Posted: 07.19.2017

Jon Hamilton Harsh life experiences appear to leave African-Americans vulnerable to Alzheimer's and other forms of dementia, researchers reported Sunday at the Alzheimer's Association International Conference in London. Several teams presented evidence that poverty, disadvantage and stressful life events are strongly associated with cognitive problems in middle age and dementia later in life among African-Americans. The findings could help explain why African-Americans are twice as likely as white Americans to develop dementia. And the research suggests genetic factors are not a major contributor. "The increased risk seems to be a matter of experience rather than ancestry," says Megan Zuelsdorff, a postdoctoral fellow in the Health Disparities Research Scholars Program at the University of Wisconsin-Madison. Scientists have struggled to understand why African-Americans are so likely to develop dementia. They are more likely to have conditions like high blood pressure and diabetes, which can affect the brain. And previous research has found some evidence that African-Americans are more likely to carry genes that raise the risk. But more recent studies suggest those explanations are incomplete, says Rachel Whitmer, an epidemiologist with Kaiser Permanente's Division of Research in Northern California. Whitmer has been involved in several studies that accounted for genetic and disease risks when comparing dementia in white and black Americans. "And we still saw these [racial] differences," she says. "So there is still something there that we are trying to get at." © 2017 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: 23841 - Posted: 07.17.2017

Pagan Kennedy In 2011, Ben Trumble emerged from the Bolivian jungle with a backpack containing hundreds of vials of saliva. He had spent six weeks following indigenous men as they tramped through the wilderness, shooting arrows at wild pigs. The men belonged to the Tsimane people, who live as our ancestors did thousands of years ago — hunting, foraging and farming small plots of land. Dr. Trumble had asked the men to spit into vials a few times a day so that he could map their testosterone levels. In return, he carried their kills and helped them field-dress their meat — a sort of roadie to the hunters. Dr. Trumble wanted to find out whether the hunters who successfully shot an animal would be rewarded with a spike in testosterone. (They were.) As a researcher with the Tsimane Health and Life History Project, he had joined a long-running investigation into human well-being and aging in the absence of industrialization. That day when he left the jungle, he stumbled across a new and more urgent question about human health. He dropped his backpack, called his mom and heard some terrible news: His 64-year-old uncle had learned he had dementia, probably Alzheimer’s. In just a few short years, his uncle, a vibrant former lawyer, would stop speaking, stop eating and die. “I couldn’t help my uncle,” Dr. Trumble said, but he was driven to understand the disease that killed him. He wondered: Do the Tsimane suffer from Alzheimer’s disease like we do? And if not, what can we learn from them about treating or preventing dementia? “There is really no cure yet for Alzheimer’s,” Dr. Trumble told me. “We have nothing that can undo the damage already done.” Why, he wondered, had billions of dollars and decades of research yielded so little? Perhaps major clues were being missed. Dr. Trumble was trained as an anthropologist, and his field — evolutionary medicine — taught him to see our surroundings as a blip in the timeline of human history. He thinks it’s a problem that medical research focuses almost exclusively on “people who live in cities like New York or L.A.” Scientists often refer to these places as “Weird” — Western, educated, industrialized, rich and democratic — and point out that our bodies are still designed for the not-Weird environment in which our species evolved. Yet we know almost nothing about how dementia affected humans during the 50,000 years before developments like antibiotics and mechanized farming. Studying the Tsimane, Dr. Trumble believes, could shed light on this modern plague. © 2017 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: 23839 - Posted: 07.14.2017

By Giorgia Guglielmi Semen has something in common with the brains of Alzheimer’s sufferers: Both contain bundles of protein filaments called amyloid fibrils. But although amyloid accumulation appears to damage brain cells, these fibrils may be critical for reproduction. A new study suggests that semen fibrils immobilize subpar sperm, ensuring that only the fittest ones make it to the egg. “I’m sure that from the very first time scientists described semen fibrils, they must have been speculating what their natural function was,” says Daniel Otzen, an expert in protein aggregates at Aarhus University in Denmark, who did not participate in the research. “This seems to be the smoking gun.” Researchers discovered semen fibrils in 2007. At first, they seemed like mostly bad news. Scientists showed that the fibrils, found in the seminal fluid together with sperm cells and other components, can bind to HIV, helping it get inside cells. But the fibrils are found in most primates, notes Nadia Roan, a mucosal biologist at the University of California, San Francisco. “If fibrils didn’t serve some beneficial purpose, they would have been eliminated over evolutionary time.” Because the way HIV fuses to cells is reminiscent of the way a sperm fuses to the egg, she wondered whether the fibrils facilitated fertilization. © 2017 American Association for the Advancement of Science.

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: 23828 - Posted: 07.12.2017

By James Gallagher Abnormal deposits that build up in the brain during Alzheimer's have been pictured in unprecedented detail by UK scientists. The team at the MRC Laboratory of Molecular Biology says its findings "open up a whole new era" in neurodegenerative disease. Their work should make it easier to design drugs to stop brain cells dying. The researchers used brain tissue from a 74-year-old woman who died after having Alzheimer's disease. The form of dementia leads to tangles of a protein called tau spreading throughout the brain. The more tau tangles there are, the worse the symptoms tend to be. Doctors have known this has happened for decades but what has been missing is a detailed understanding of what the tangles look like. The team took advantage of the "resolution revolution" in microscopy to take thousands of highly detailed images of the tau inside the woman's brain tissues. And using computer software, they figured out the tangles look like this: Image copyright LMB It is pretty meaningless to an untrained eye, but to scientists this could be one of the most important recent discoveries in tackling dementia. Attempts to develop a drug to slow the pace of dementia have been met by repeated failure. But it is hard to come up with a drug when you do not know the precise chemical structure of what you are targeting. Dr Sjors Scheres, one of the researchers, told the BBC News website: "It's like shooting in the dark - you can still hit something but you are much more likely to hit if you know what the structure is. "We are excited - it opens up a whole new era in this field, it really does." © 2017 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: 23807 - Posted: 07.06.2017

By NICHOLAS BAKALAR Poor sleep may be an indication of increased risk for Alzheimer’s disease, a new study of older people suggests. Researchers studied 101 cognitively normal people, average age 63, who completed well-validated sleep questionnaires. They analyzed their spinal fluid for the presence of indicators of the plaques and tangles that are characteristic of Alzheimer’s. The study is in Neurology. After controlling for age, a family history of Alzheimer’s, the ApoE gene that increases Alzheimer’s risk and other factors, they found that poor sleep quality, sleep problems and daytime sleepiness were associated with increased spinal fluid indicators of Alzheimer’s disease. The reason for the association is unclear, but at least one animal study found that during sleep the brain’s capacity to clear toxins like beta amyloid, the toxic protein that forms plaques in the brains of those with Alzheimer’s, improves. It may be that poor sleep interferes with this process in people, too. “Not everyone with sleep problems is destined to develop Alzheimer’s disease,” said the senior author, Barbara B. Bendlin, an associate professor of medicine at the University of Wisconsin School of Medicine and Public Health. “We’re looking at groups of people, and over the whole group we find the association of poor sleep with the markers of Alzheimer’s. But when you look at individuals, not everyone shows that pattern.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 23806 - Posted: 07.06.2017

Rebecca Hersher The first problem with the airplane bathroom was its location. It was March. Greg O'Brien and his wife, Mary Catherine, were flying back to Boston from Los Angeles, sitting in economy seats in the middle of the plane. "We're halfway, probably over Chicago," Greg remembers, "and Mary Catherine said, 'Go to the bathroom.' " "It just sounded like my mother," Greg says. So I said 'no.' " Mary Catherine persisted, urging her husband of 40 years to use the restroom. People started looking at them. "It was kind of funny," says Greg. Mary Catherine was more alarmed than amused. Greg has early-onset Alzheimer's, which makes it increasingly hard for him to keep track of thoughts and feelings over the course of minutes or even seconds. It's easy to get into a situation where you feel like you need to use the bathroom, but then forget. And they had already been on the plane for hours. Finally, Greg started toward the restroom at the back of the plane, only to find the aisle was blocked by an attendant serving drinks. Mary Catherine gestured to him. "Use the one in first class!" At that point, on top of the mild anxiety most people feel when they slip into first class to use the restroom, Greg was feeling overwhelmed by the geography of the plane. He pulled back the curtain dividing the seating sections. "This flight attendant looks at me like she has no use for me. I just said 'Look, I really have to go the bathroom,' and she says 'OK, just go.' " © 2017 npr

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: 23772 - Posted: 06.26.2017

By Sharon Begley, STAT To anyone who’s aware that efforts to develop Alzheimer’s drug treatments have met failure after failure, and to have therefore decided that prevention is the only hope, a U.S. panel of experts issued a sobering message on Thursday: Don’t count on it. From physical activity to avoiding high blood pressure to brain training, a 17-member committee assembled by the National Academies of Sciences concluded, no interventions are “supported by high-strength evidence.” Instead, some high-quality studies found that one or another intervention worked, but other equally rigorous studies found they didn’t. 1. Cognitive training The evidence for programs aimed at boosting reasoning, problem-solving, memory, and speed of processing does include randomized trials that reported benefits from brain training, but the report calls that evidence “low to moderate strength.” One problem: There seemed to be benefits for two years, but not after five or 10. Results in other randomized studies were even more equivocal. There are also data from studies that are less rigorous, leading the committee to conclude that brain training (computer-based or not) can delay or slow age-related cognitive decline—but not Alzheimer’s. 2. Controlling blood pressure Evidence that this helps is weaker still. © 2017 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: 23763 - Posted: 06.23.2017

By David Noonan Sight and hearing get all the glory, but the often overlooked and underappreciated sense of smell—or problems with it—is a subject of rapidly growing interest among scientists and clinicians who battle Alzheimer’s and Parkinson’s diseases. Impaired smell is one of the earliest and most common symptoms of both, and researchers hope a better understanding will improve diagnosis and help unlock some of the secrets of these incurable conditions. The latest offering from the burgeoning field is a paper published this month in Lancet Neurology. It proposes neurotransmitter dysfunction as a possible cause of smell loss in a number of neurodegenerative diseases, including Alzheimer’s and Parkinson’s. More than 90 percent of Parkinson’s patients report some level of olfactory dysfunction. And because problems with smell progress in Alzheimer’s, nearly all of those diagnosed with moderate to severe forms of the illness have odor identification issues. “It’s important, not just because it’s novel and interesting and simple but because the evidence is strong,” says Davangere Devanand, a professor of psychiatry and neurology at Columbia University. His most recent paper on the subject, a review, was published in The American Journal of Geriatric Psychiatry in December. Studies have shown impaired smell to be even stronger than memory problems as a predictor of cognitive decline in currently healthy adults. It is especially useful for forecasting the progression from mild cognitive impairment (MCI) to full-blown Alzheimer’s. According to the Alzheimer’s Association, approximately 15 to 20 percent of people over 65 have MCI. About half of them go on to develop Alzheimer’s, Devanand says—and the sooner they are identified, the earlier doctors can begin interventions, including treatment with the few existing Alzheimer’s drugs. © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 23729 - Posted: 06.12.2017

By PHILIP S. GUTIS My husband, Tim, and a duo of Jack Russell terriers arrived in my life 13 years ago. They were a package deal that included Osceola Jack, a champion Frisbee player who once was the Mighty Dog actor in the famous commercials, and his pup, the equally mighty Samantha. Later our family grew with Beatrice, a sweet cattle dog mix from Florida who belonged to Tim’s brother but needed a new home. As an introvert, I have not always had the best people skills, but my ability to connect with animals has never flagged. Many of my best memories involve animals. But now things are changing. Last summer, at age 54, I learned I had early onset Alzheimer’s. Amid the many worries that accompany this diagnosis, I am afraid that I will lose my cherished ability to bond with — or even remember — my animal companions much longer. Since my 20s and 30s, I’ve had some weird memory gaps. I once forgot that a childhood best friend worked for me at the school newspaper at Penn State. I wrote off these memory holes to a busy life and career. I worked long days, spent hours on airplanes and trains, managed dozens of people and grappled with complicated issues. I told myself that all of that work, stress and the sheer volume of information that I was expected to retain had to take a toll on my ability to remember everything. But a few years ago, I started to notice that I just wasn’t performing as well as I used to. Keeping track of big projects became increasingly difficult. Skills that were sometimes challenging (simple math, remembering names, understanding maps and directions) became all but impossible. Some days my memory was so bad that I wanted to wear a shirt that said, “Sorry, I just cannot remember your name.” My sister found an online advertisement for people concerned about memory loss. I called the phone number and scheduled an in-person screening. Bring someone familiar with you, the woman on the phone said. I brought Tim, who stayed close as a neurologist poked and prodded me, and vials and vials of blood were drawn. And then came the memory tests. © 2017 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: 23724 - Posted: 06.09.2017

By NICHOLAS BAKALAR Chronic pain may be linked to an increasing risk for dementia. Researchers interviewed 10,065 people over 62 in 1998 and 2000, asking whether they suffered “persistent pain,” defined as being often troubled with moderate or severe pain. Then they tracked their health through 2012. After adjusting for many variables, they found that compared with those who reported no pain problems, people who reported persistent pain in both 1998 and 2000 had a 9 percent more rapid decline in memory performance. Moreover, the probability of dementia increased 7.7 percent faster in those with persistent pain compared with those without. The study, in JAMA Internal Medicine, does not prove cause and effect. But chronic pain may divert attention from other mental activity, leading to poor memory, and some studies have found that allaying pain with opioids can lead to cognitive improvements. Still, the lead author, Dr. Elizabeth L. Whitlock, an anesthesiologist at the University of California at San Francisco, acknowledged that treatment with opioids is problematic, and that safely controlling chronic pain is a problem that so far has no satisfactory solution. “I’d encourage clinicians to be aware of the cognitive implications of a simple report of pain,” she said. “It’s a simple question to ask, and the answer can be used to identify a population at high risk of functional and cognitive problems.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 23719 - Posted: 06.08.2017