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By Elizabeth Anne Brown Forget the soul — it turns out the eyes may be the best window to the brain. Changes to the retina may foreshadow Alzheimer’s and Parkinson’s diseases, and researchers say a picture of your eye could assess your future risk of neurodegenerative disease. Pinched off from the brain during embryonic development, the retina contains layers of neurons that seem to experience neurodegenerative disease along with their cousins inside the skull. The key difference is that these retinal neurons, right against the jellylike vitreous of the eyeball, live and die where scientists can see them. Early detection “is sort of the holy grail,” said Ron Petersen, director of Mayo Clinic’s Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. By the time a patient complains of memory problems or tremors, the machinery of neurodegenerative disease has been at work probably for years or decades. Experts liken it to a cancer that only manifests symptoms at Stage 3 or 4. When patients begin to feel neurodegenerative disease’s impact on their daily life, it’s almost too late for treatment. Catching the warning signs of neurodegenerative disease earlier could give patients more time to plan for the future — whether that’s making caregiving arrangements, spending more time with family or writing the Great American novel. In the longer term, researchers hope the ability to notice brain changes before symptoms begin could eventually lead to early treatments more successful at slowing or stopping the progress of Parkinson’s and Alzheimer’s, since no such treatment is currently available. The hope is that “the sooner we intervene, the better we will be” at preventing cognitive impairment, Petersen said © 1996-2021 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27713 - Posted: 02.28.2021

In a study led by National Institutes of Health researchers, scientists found that five genes may play a critical role in determining whether a person will suffer from Lewy body dementia, a devastating disorder that riddles the brain with clumps of abnormal protein deposits called Lewy bodies. Lewy bodies are also a hallmark of Parkinson’s disease. The results, published in Nature Genetics, not only supported the disease’s ties to Parkinson’s disease but also suggested that people who have Lewy body dementia may share similar genetic profiles to those who have Alzheimer’s disease. “Lewy body dementia is a devastating brain disorder for which we have no effective treatments. Patients often appear to suffer the worst of both Alzheimer’s and Parkinson’s diseases. Our results support the idea that this may be because Lewy body dementia is caused by a spectrum of problems that can be seen in both disorders,” said Sonja Scholz, M.D., Ph.D., investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope that these results will act as a blueprint for understanding the disease and developing new treatments.” The study was led by Dr. Scholz’s team and researchers in the lab of Bryan J. Traynor, M.D., Ph.D., senior investigator at the NIH’s National Institute on Aging (NIA). Lewy body dementia usually affects people over 65 years old. Early signs of the disease include hallucinations, mood swings, and problems with thinking, movements, and sleep. Patients who initially have cognitive and behavioral problems are usually diagnosed as having dementia with Lewy bodies, but are sometimes mistakenly diagnosed with Alzheimer’s disease. Alternatively, many patients, that are initially diagnosed with Parkinson’s disease, may eventually have difficulties with thinking and mood caused by Lewy body dementia. In both cases, as the disease worsens, patients become severely disabled and may die within eight years of diagnosis.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 5: The Sensorimotor System
Link ID: 27694 - Posted: 02.17.2021

By Leslie Nemo Ironically, this tangle of brain cells is helping scientists tease apart a larger problem: how to help people with Alzheimer’s disease. Matheus Victor, a researcher at the Massachusetts Institute of Technology, photographed these neurons after coaxing them to life in a petri dish in the hope that the rudimentary brain tissue will reveal why a new therapy might alleviate Alzheimer’s symptoms. In humans and mice, a healthy memory is associated with a high level of synced neurons that turn on and off simultaneously. Those with neurological conditions such as Alzheimer’s and Parkinson’s disease often have fewer brain cells blinking unanimously. A couple of years ago Victor’s lab leader Li-Huei Tsai and her team at M.I.T. found that when they surrounded mice genetically predisposed to Alzheimer’s with sound pulses beating 40 times a second, the rodents performed better on memory-related tasks. The animals also lost some amyloid plaques, protein deposits in the brain that are characteristic of the disease. The researchers had previously performed a similar study with light flickering at the same rate, and the mice were found to experience additional improvements when the sound and light pulses were combined. Astoundingly, the mouse neurons synced up to the 40-beats-per-second rhythm of the audio pulses, though the mechanism behind this result and the reason the shift improves symptoms remain a mystery. To help solve it, the researchers want to watch how brain tissue responds to the stimulants at the cellular level. The goal is to one day understand how this exposure treatment might work for people, so the team is growing human brain cells in the lab and engineering them to respond to sound and light without eyes and ears. “We are trying to mimic the sensory stimulation in mice but missing a lot of the hardware that makes it possible. So this is a bit of a hack,” Victor says. © 2021 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27690 - Posted: 02.15.2021

By Gina Kolata Is it possible to predict who will develop Alzheimer’s disease simply by looking at writing patterns years before there are symptoms? According to a new study by IBM researchers, the answer is yes. And, they and others say that Alzheimer’s is just the beginning. People with a wide variety of neurological illnesses have distinctive language patterns that, investigators suspect, may serve as early warning signs of their diseases. For the Alzheimer’s study, the researchers looked at a group of 80 men and women in their 80s — half had Alzheimer’s and the others did not. But, seven and a half years earlier, all had been cognitively normal. The men and women were participants in the Framingham Heart Study, a long-running federal research effort that requires regular physical and cognitive tests. As part of it, they took a writing test before any of them had developed Alzheimer’s that asks subjects to describe a drawing of a boy standing on an unsteady stool and reaching for a cookie jar on a high shelf while a woman, her back to him, is oblivious to an overflowing sink. The researchers examined the subjects’ word usage with an artificial intelligence program that looked for subtle differences in language. It identified one group of subjects who were more repetitive in their word usage at that earlier time when all of them were cognitively normal. These subjects also made errors, such as spelling words wrongly or inappropriately capitalizing them, and they used telegraphic language, meaning language that has a simple grammatical structure and is missing subjects and words like “the,” “is” and “are.” The members of that group turned out to be the people who developed Alzheimer’s disease. The A.I. program predicted, with 75 percent accuracy, who would get Alzheimer’s disease, according to results published recently in The Lancet journal EClinicalMedicine. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 27677 - Posted: 02.03.2021

By Gina Kolata In a small clinical trial, an experimental Alzheimer’s drug slowed the rate at which patients lost the ability to think and care for themselves, the drug maker Eli Lilly announced on Monday. The findings have not been published in any form, and not been widely reviewed by other researchers. If accurate, it is the first time a positive result has been found in a so-called Phase 2 study, said Dr. Lon S. Schneider, professor of psychiatry, neurology and gerontology at the University of Southern California. Other experimental drugs against Alzheimer’s were never tested in Phase 2 trials, moving straight to larger Phase 3 trials, or failed to produce positive results. The Phase 3 studies themselves have repeatedly had disappointing results. The two-year study involved 272 patients with brain scans indicative of Alzheimer’s disease. Their symptoms ranged from mild to moderate. The drug, donanemab, a monoclonal antibody, binds to a small part of the hard plaques in the brain made of a protein, amyloid, that are hallmarks of Alzheimer’s disease. Patients received the drug by infusion every four weeks. Participants who received the drug had a 32 percent deceleration in the rate of decline, compared with those who got a placebo. In six to 12 months, plaques were gone and stayed gone, said Dr. Daniel Skovronsky, the company’s chief scientific officer. At that point, patients stopped getting the drug — they got a placebo instead — for the duration of the study. The small study needs to be replicated, noted Dr. Michael Weiner, a leading Alzheimer’s researcher at the University of California, San Francisco. Still, “this is big news,” he said. “This holds out hope for patients and their families.” Eli Lilly did not release the sort of pertinent data needed for a thorough analysis, Dr. Schneider said. For example, the company provided only percentages describing declines in function among the participants, not the actual numbers. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27648 - Posted: 01.15.2021

By Jennie Erin Smith MEDELLÍN, Colombia — Aliria Rosa Piedrahita de Villegas carried a rare genetic mutation that had all but guaranteed she would develop Alzheimer’s disease in her 40s. But only at age 72 did she experience the first symptoms of it. Her dementia was not terribly advanced when she died from cancer on Nov. 10, a month shy of her 78th birthday, in her daughter’s home on a hillside that overlooks the city. Neurology investigators at the University of Antioquia in Medellín, led by Dr. Francisco Lopera, have followed members of Ms. Piedrahita de Villegas’s vast extended family for more than 30 years, hoping to unlock the secrets of early-onset Alzheimer’s disease. In that time they encountered several outliers, people whose disease developed later than expected, in their 50s or even 60s. But none were as medically remarkable as the woman they all knew as doña Aliria. In recent years Aliria traveled to Boston, where investigators at Massachusetts General Hospital conducted nuclear imaging studies of her brain as part of an ongoing study of this Colombian family, the largest in the world with genetic early-onset Alzheimer’s. In Boston it was discovered that Aliria had exceptionally large quantities of one protein seen in Alzheimer’s — amyloid beta — without much tau, the toxic protein that spreads later in the disease cascade. Something had interrupted the usual degenerative process, leaving her day-to-day functioning relatively preserved. Last year, researchers at Harvard Medical School and the University of Antioquia published the surprise finding that while Aliria carried a well-known mutation, unique to Colombia, that causes early Alzheimer’s, she also carried two copies of another rare mutation that appear to have thwarted the activity of the first one. Since then, investigators worldwide have been studying what is known as the Christchurch mutation, a variant on a gene, APOE, that can affect a person’s risk of developing Alzheimer’s. Thus far, drugs targeting amyloid beta have disappointed in clinical trials. If the protective effect of Aliria’s double Christchurch mutation can be replicated, a new avenue for desperately needed therapies could open. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27620 - Posted: 12.12.2020

Carrie Arnold In her job as a physician at the Boston Medical Center in Massachusetts, Sondra Crosby treated some of the first people in her region to get COVID-19. So when she began feeling sick in April, Crosby wasn’t surprised to learn that she, too, had been infected. At first, her symptoms felt like those of a bad cold, but by the next day, she was too sick to get out of bed. She struggled to eat and depended on her husband to bring her sports drinks and fever-reducing medicine. Then she lost track of time completely. For five days, Crosby lay in a confused haze, unable to remember the simplest things, such as how to turn on her phone or what her address was. She began hallucinating, seeing lizards on her walls and smelling a repugnant reptilian odour. Only later did Crosby realize that she had had delirium, the formal medical term for her abrupt, severe disorientation. “I didn’t really start processing it until later when I started to come out of it,” she says. “I didn’t have the presence of mind to think that I was anything more than just sick and dehydrated.” Physicians treating people hospitalized with COVID-19 report that a large number experience delirium, and that the condition disproportionately affects older adults. An April 2020 study in Strasbourg, France, found that 65% of people who were severely ill with coronavirus had acute confusion — a symptom of delirium1. Data presented last month at the annual meeting of the American College of Chest Physicians by scientists at the Vanderbilt University Medical Center in Nashville, Tennessee, showed that 55% of the 2,000 people they tracked who were treated for COVID-19 in intensive-care units (ICUs) around the world had developed delirium. These numbers are much higher than doctors are used to: usually, about one-third of people who are critically ill develop delirium, according to a 2015 meta-analysis2 (see ‘How common is delirium?’). © 2020 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27613 - Posted: 12.07.2020

By Jamie Talan After 20 years of marriage, after raising two kids, after building a farm in Kentucky and tending horses and dogs, Laura Prewitt knew this much about her husband: He was tenderhearted, fun-loving and never let stress land too long on his shoulders. But in 2014, old Ted somehow morphed into a new guy, one who is not so communicative. A guy who lost his social edge and seemed unable to read faces or feelings. Who is tired and withdrawn. “He’s just not the same guy,” she says. “I want him back.” At 59, the old Ted, the sensitive husband who cried during sad movies, is gone. A scan of Ted’s brain helps explain it: Discrete regions of the right temporal lobe that regulate emotion are getting smaller; the tissue is shrinking. Ted can still do some of the things he has done for decades. Until a few years ago, he was the president at a construction company. Lately, he’ll see someone he is supposed to know but forgets who they are. He sleeps a lot. And he can’t be left alone for too long or his wife may find him trying to eat a battery or a hammer. He’s agitated. He’s always putting things in his mouth. Ted Prewitt, who has behavioral variant frontotemporal dementia (bvFTD), is one of a growing number of people in midlife diagnosed with an atypical form of dementia. Unlike Alzheimer’s, which generally occurs in older people, these are rarer dementias — including bvFTD; another frontotemporal variant that leads to language disturbances called primary progressive aphasia; a visual and spatial dementia called posterior cortical atrophy; Lewy body dementia; and early-onset Alzheimer’s in people with no family history. These conditions show up in people in their 50s and 60s, sometimes even earlier and sometimes a bit later. No one knows whether these conditions are becoming more common or doctors are better at diagnosing them. © 1996-2020 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27612 - Posted: 12.07.2020

Alison Abbott Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ. The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. Norins wanted to reward work that would make the infection idea more persuasive. The amyloid hypothesis has become “the one acceptable and supportable belief of the Established Church of Conventional Wisdom”, says Norins. “The few pioneers who did look at microbes and published papers were ridiculed or ignored.” In large part, this was because some early proponents of the infection theory saw it as a replacement for the amyloid hypothesis. But some recent research has provided intriguing hints that the two ideas could fit together — that infection could seed some cases of Alzheimer’s disease by triggering the production of amyloid clumps. The data hint at a radical role for amyloid in neurons. Instead of just being a toxic waste product, amyloid might have an important job of its own: helping to protect the brain from infection. But age or genetics can interrupt the checks and balances in the system, turning amyloid from defender into villain. And that idea suggests new avenues to explore for potential therapies. To test the theory further, scientists are now developing animal models that mimic Alzheimer’s disease more closely. “We are taking the ideas seriously,” says neuroscientist Bart de Strooper, director of the UK Dementia Research Institute at University College London. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27571 - Posted: 11.07.2020

By Laura Sanders The fate of a potential new Alzheimer’s drug is still uncertain. Evidence that the drug works isn’t convincing enough for it to be approved, outside experts told the U.S. Food and Drug Administration during a Nov. 6 virtual meeting that at times became contentious. The scientists and clinicians were convened at the request of the FDA to review the evidence for aducanumab, a drug that targets a protein called amyloid-beta that accumulates in the brains of people with Alzheimer’s. The drug is designed to stick to A-beta and stop it from forming larger, more dangerous clumps. That could slow the disease’s progression but not stop or reverse it. When asked whether a key clinical study provided strong evidence that the drug effectively treated Alzheimer’s, eight of 11 experts voted no. One expert voted yes, and two were uncertain. The FDA is not bound to follow the recommendations of the guidance committee, though it has historically done so. If ultimately approved, the drug would be a milestone, says neurologist and neuroscientist Arjun Masurkar of New York University Langone’s Alzheimer’s Disease Research Center. Aducanumab “would be the first therapy that actually targets the underlying disease itself and slows progression.” Developed by the pharmaceutical company Biogen, which is based in Cambridge, Mass., the drug is controversial. That’s because two large clinical trials of aducanumab have yielded different outcomes, one positive and one negative (SN: 12/5/19). The trials were also paused at one point, based on analyses that suggested the drug didn’t work. © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27570 - Posted: 11.07.2020

By Nicholas Bakalar Some studies have suggested that older people who consistently engage in leisure activities are less likely to develop dementia than those who do not, suggesting that failure to participate in such pastimes could spur cognitive deterioration. A new study suggests another explanation: Failure to participate in leisure activities may be a consequence of dementia, not a cause. Researchers studied 8,280 people, average age 56, who were free of dementia at the start of the analysis. Over the next 18 years, the participants underwent periodic physical and psychological examinations, while researchers tracked their involvement in 13 leisure activities — listening to music, gardening, attending cultural events, playing cards, using a home computer and others. By the end of the project, 360 had developed dementia. The study, in Neurology, controlled for smoking, physical activity, education, coronary heart disease and other health and behavioral characteristics that are tied to dementia risk. They found no association between engagement in leisure activities at age 56 and the incidence of dementia over the following 18 years. The researchers concluded that actively pursuing leisure activities may not provide protection against developing dementia. “Dementia develops over a long period of time, so it’s possible that some changes happen before the diagnosis of dementia,” said the lead author, Andrew Sommerlad, a researcher at University College London. “Elderly people withdrawing from activities that they previously enjoyed may be developing early signs of dementia.” © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27563 - Posted: 11.04.2020

By Nicholas Bakalar Long-term exposure to noise may be linked to an increased risk for Alzheimer’s disease and other forms of dementia. Researchers did periodic interviews with 5,227 people 65 and older participating in a study on aging. They assessed them with standard tests of orientation, memory and language, and tracked average daytime noise levels in their neighborhoods for the five years preceding the cognitive assessments. About 11 percent had Alzheimer’s disease, and 30 percent had mild cognitive impairment, which often progresses to full-blown dementia. Residential noise levels varied widely, from 51 to 78 decibels, or from the level of a relatively quiet suburban neighborhood to that of an urban setting near a busy highway. The study is in Alzheimer’s & Dementia. After controlling for education, race, smoking, alcohol consumption, neighborhood air pollution levels and other factors, they found that each 10 decibel increase in community noise level was associated with a 36 percent higher likelihood of mild cognitive impairment, and a 29 percent increased risk for Alzheimer’s disease. The associations were strongest in poorer neighborhoods, which also had higher noise levels. The reasons for the connection are unknown, but the lead author, Jennifer Weuve, an associate professor of epidemiology at Boston University, suggested that excessive noise can cause sleep deprivation, hearing loss, increased heart rate, constriction of the blood vessels and elevated blood pressure, all of which are associated with an increased risk for dementia. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 27551 - Posted: 10.28.2020

Jon Hamilton Medical research was an early casualty of the COVID-19 pandemic. After cases began emerging worldwide, thousands of clinical trials unrelated to COVID-19 were paused or canceled amid fears that participants would be infected. But now some researchers are finding ways to carry on in spite of the coronavirus. "It's been a struggle of course," says Joshua Grill, who directs the Institute for Memory Impairments and Neurological Disorders at the University of California, Irvine. "But I think there's an imperative for us to find ways to move forward." Grill got a close-up view of the challenge in July when COVID-19 cases were spiking nationwide as he was trying to launch a study. UC Irvine and dozens of other research centers had just begun enrolling participants in the AHEAD study, a global effort that will test whether an investigational drug can slow down the earliest brain changes associated with Alzheimer's disease. Finding individuals willing and able to sign up for this sort of research is difficult even without a pandemic, says Grill, who also co-directs recruitment for the Alzheimer's Clinicals Trial Consortium, funded by the National Institute on Aging. "We're asking people do a lot, including enroll in long studies that require numerous visits," he says, "and in the AHEAD study, taking an investigational drug or placebo that's injected into a vein." Participants will receive either a placebo or a drug called BAN2401, made by Eisai, which is meant to reduce levels of amyloid, a toxic protein associated with Alzheimer's. People in the study will also have positron emission tomography, or PET, scans of their brains to measure changes in amyloid and another toxic protein called tau. © 2020 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27545 - Posted: 10.24.2020

By Jeremy Hsu Artificial intelligence could soon help screen for Alzheimer’s disease by analyzing writing. A team from IBM and Pfizer says it has trained AI models to spot early signs of the notoriously stealthy illness by looking at linguistic patterns in word usage. Other researchers have already trained various models to look for signs of cognitive impairments, including Alzheimer’s, by using different types of data, such as brain scans and clinical test results. But the latest work stands out because it used historical information from the multigenerational Framingham Heart Study, which has been tracking the health of more than 14,000 people from three generations since 1948. If the new models’ ability to pick up trends in such data holds up in forward-looking studies of bigger and more diverse populations, researchers say they could predict the development of Alzheimer’s a number of years before symptoms become severe enough for typical diagnostic methods to pick up. And such a screening tool would not require invasive tests or scans. The results of the Pfizer-funded and IBM-run study were published on Thursday in EClinicalMedicine. The new AI models provide “an augmentation to expert practitioners in how you would see some subtle changes earlier in time, before the clinical diagnosis has been achieved,” says Ajay Royyuru, vice president of health care and life sciences research at IBM. “It might actually alert you to some changes that [indicate] you ought to then go do a more complete exam.” To train these models, the researchers used digital transcriptions of handwritten responses from Framingham Heart Study participants who were asked to describe a picture of a woman who is apparently preoccupied with washing dishes while two kids raid a cookie jar behind her back. These descriptions did not preserve the handwriting from the original responses, says Rhoda Au, director of neuropsychology at the Framingham study and a professor at Boston University. © 2020 Scientific American,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 15: Language and Lateralization
Link ID: 27544 - Posted: 10.24.2020

By Laurie Archbald-Pannone The number of cases of dementia in the United States is rising as baby boomers age, raising questions for boomers themselves and also for their families, caregivers and society. Dementia, which is not technically a disease but a term for impaired ability to think, remember or make decisions, is one of the most feared impairments of old age. Incidence increases dramatically as people move into their 90s. About 5 percent of those 71 to 79 have dementia, and about 37 percent of those about 90 live with it. Older people may worry about their own loss of function as well as the cost and toll of caregiving for someone with dementia. A 2018 study estimated that the lifetime cost of care for a person with Alzheimer’s, the most common form of dementia, to be $329,360. That figure, too, will no doubt rise, putting even more burdens on family, Medicare and Medicaid. There’s also been a good deal of talk and reporting about dementia in recent months because of the presidential election. Some voters have asked whether one or both candidates might have dementia. But is this even a fair question to ask? When these types of questions are posed — adding further stigma to people with dementia — it can unfairly further isolate them and those caring for them. We need to understand dementia and the impact it has on more than 5 million people in the United States who now live with dementia and their caregivers. That number is expected to triple by 2060. First, it is important to know that dementia cannot be diagnosed from afar or by someone who is not a doctor. A person needs a detailed doctor’s exam for a diagnosis. Sometimes, brain imaging is required. And, forgetting an occasional word — or even where you put your keys — does not mean a person has dementia. There are different types of memory loss and they can have different causes, such as other medical conditions, falls or even medication, including herbals, supplements and anything over-the-counter. © 1996-2020 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27532 - Posted: 10.19.2020

By Pam Belluck After contracting the coronavirus in March, Michael Reagan lost all memory of his 12-day vacation in Paris, even though the trip was just a few weeks earlier. Several weeks after Erica Taylor recovered from her Covid-19 symptoms of nausea and cough, she became confused and forgetful, failing to even recognize her own car, the only Toyota Prius in her apartment complex’s parking lot. Lisa Mizelle, a veteran nurse practitioner at an urgent care clinic who fell ill with the virus in July, finds herself forgetting routine treatments and lab tests, and has to ask colleagues about terminology she used to know automatically. “I leave the room and I can’t remember what the patient just said,” she said, adding that if she hadn’t exhausted her medical leave she’d take more time off. “It scares me to think I’m working,” Ms. Mizelle, 53, said. “I feel like I have dementia.” It’s becoming known as Covid brain fog: troubling cognitive symptoms that can include memory loss, confusion, difficulty focusing, dizziness and grasping for everyday words. Increasingly, Covid survivors say brain fog is impairing their ability to work and function normally. “There are thousands of people who have that,” said Dr. Igor Koralnik, chief of neuro-infectious disease at Northwestern Medicine in Chicago, who has already seen hundreds of survivors at a post-Covid clinic he leads. “The impact on the work force that’s affected is going to be significant. Scientists aren’t sure what causes brain fog, which varies widely and affects even people who became only mildly physically ill from Covid-19 and had no previous medical conditions. Leading theories are that it arises when the body’s immune response to the virus doesn’t shut down or from inflammation in blood vessels leading to the brain. © 2020 The New York Times Company

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27522 - Posted: 10.12.2020

By William Wan If only Dan Goerke could hold his wife’s hand. Maybe she would talk again. Maybe she would look at him and smile as she used to. Maybe she would eat and stop wasting away. Since the pandemic began, Goerke’s wife, Denise — 63 years old and afflicted with Alzheimer’s disease — had declined dramatically. Left alone in her nursing home, she had lost 16 pounds, could not form the simplest words, no longer responded to the voices of her children. In recent weeks, she had stopped recognizing even the man she loved. Goerke, 61, could tell the isolation was killing his wife, and there was nothing he could do but watch. “Every day it gets a little worse,” he said. “We’ve lost months, maybe years of her already.” Beyond the staggering U.S. deaths caused directly by the novel coronavirus, more than 134,200 people have died from Alzheimer’s and other forms of dementia since March. That is 13,200 more U.S. deaths caused by dementia than expected, compared with previous years, according to an analysis of federal data by The Washington Post. Overlooked amid America’s war against the coronavirus is this reality: People with dementia are dying not just from the virus but from the very strategy of isolation that’s supposed to protect them. In recent months, doctors have reported increased falls, pulmonary infections, depression and sudden frailty in patients who had been stable for years. Social and mental stimulation are among the few tools that can slow the march of dementia. Yet even as U.S. leaders have rushed to reopen universities, bowling alleys and malls, nursing homes say they continue begging in vain for sufficient testing, protective equipment and help.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27478 - Posted: 09.19.2020

By Nicholas Bakalar Being overweight may be linked to an increased risk for dementia. British researchers used data on 6,582 men and women, age 50 and older, who were cognitively healthy at the start of the study. The analysis, in the International Journal of Epidemiology, tracked the population for an average of 11 years, recording incidents of physician-diagnosed dementia. Almost 7 percent of the group developed dementia. Compared with people of normal weight (body mass index between 18.5 and 24.9), overweight people with a B.M.I. of 25 to 29.9 were 27 percent more likely to develop dementia, and the obese, with a B.M.I. of 30 or higher, were 31 percent more likely to become demented. The researchers also found that women with central obesity — a waist size larger than 34.6 inches — were 39 percent more likely to develop dementia than those with normal waist size. Fat around the middle was not associated with a higher dementia risk in men. The study controlled for age, sex, APOE4 (a gene known to increase the risk of Alzheimer’s disease, the most common form of dementia), education, marital status, smoking and other known dementia risks. The lead author, Yixuan Ma, a student at University College London, said that this observational study does not prove cause and effect. “Being overweight is just a risk,” she said. “It doesn’t mean that an overweight person will necessarily get dementia. But for many reasons, it’s good to maintain a normal weight and engage in vigorous physical activity over a lifetime.” © 2020 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: Development of the Brain
Link ID: 27449 - Posted: 09.05.2020

Although the number of people with dementia continues to increase, the rate of growth has declined by 13 percent in each of the past three decades. The brain disorder currently affects nearly 50 million people worldwide and nearly 6 million in the United States. The new finding, reported by Harvard researchers in the journal Neurology, suggests that the number of people developing dementia in coming years may be less than expected. Nonetheless, that number — known as the prevalence of dementia — is expected to triple in the next 30 years, growing to more than 150 million people worldwide, due in large part to increases in life expectancy and population size. Dementia, which involves deterioration in memory, thinking and behavior beyond what is considered a normal part of aging, includes but is not limited to Alzheimer’s disease, which accounts for 60 to 70 percent of dementia cases. The researchers cited a “somewhat stronger” decline in the rate of growth — referred to as the incidence rate — among men than women (24 percent vs. 8 percent). They projected that, if the trend continues, it is possible that up to 60 million fewer people than expected would develop dementia worldwide by 2040. The researchers did not determine underlying causes of the decline in incidence, but they did note that improvements in lifestyle overall — as well as better control of blood pressure and cardiovascular issues — may have contributed to the decline. Their research was based on data from seven long-term studies, involving 49,202 people 65 and older from six countries in Europe and North America, including the United States. But the database included only people of European ancestry, and other research has found stable or increasing rates of dementia diagnoses in other ethnic and geographic regions. — Linda Searing

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27432 - Posted: 08.26.2020

By Gina Kolata Despite the lack of effective treatments or preventive strategies, the dementia epidemic is on the wane in the United States and Europe, scientists reported on Monday. The risk for a person to develop dementia over a lifetime is now 13 percent lower than it was in 2010. Incidence rates at every age have steadily declined over the past quarter-century. If the trend continues, the paper’s authors note, there will be 15 million fewer people in Europe and the United States with dementia than there are now. The study is the most definitive yet to document a decline in dementia rates. Its findings counter warnings from advocacy groups of a coming tsunami of Alzheimer’s disease, the most common form of dementia, said Dr. John Morris, director of the Center for Aging at Washington University in St. Louis. It is correct that there are now more people than ever with dementia, but that is because there are more and more older people in the population. The new incidence data are “hopeful,” Dr. Morris said. “It is such a strong study and such a powerful message. It suggests that the risk is modifiable.” Researchers at Harvard University in Cambridge, Mass., reviewed data from seven large studies with a total of 49,202 individuals. The studies followed men and women aged 65 and older for at least 15 years, and included in-person exams and, in many cases, genetic data, brain scans and information on participants’ risk factors for cardiovascular disease. The data also include a separate assessment of Alzheimer’s disease. Its incidence, too, has steadily fallen, at a rate of 16 percent per decade, the researchers found. Their study was published in the journal Neurology. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27404 - Posted: 08.06.2020