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

Nicola Davis Excessive drinking, exposure to air pollution and head injuries all increase dementia risk, experts say in a report revealing that up to 40% of dementia cases worldwide could be delayed or prevented by addressing 12 such lifestyle factors. Around 50 million people around the world live with dementia, including about 850,000 people in the UK. By 2040, it has been estimated there will be more than 1.2 million people living with dementia in England and Wales. There is currently no cure. However, while some risk factors for dementia cannot be changed, for example particular genes or ethnicity, many are down to lifestyle. “Dementia is potentially preventable – you can do things to reduce your risk of dementia, whatever stage of life you are at,” said Gill Livingston, professor of psychiatry of older people at University College London and a co-author of the report. She added such lifestyle changes could reduce the chances of developing dementia in both those with and without a high genetic risk for such conditions. The report from the Lancet Commission on dementia prevention, intervention and care builds on previous work revealing that about a third of dementia cases could be prevented by addressing nine lifestyle factors, including midlife hearing loss, depression, less childhood education and smoking. The research weighs up the latest evidence, largely from high-income countries, supporting the addition of a further three risk factors to the list. It suggests that 1% of dementia cases worldwide are attributable to excessive mid-life alcohol intake, 3% to mid-life head injuries and 2% a result of exposure to air pollution in older age – although they caution that the latter could be an underestimate. © 2020 Guardian News & Media 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: 27394 - Posted: 07.31.2020

By Nicholas Bakalar Severe gum disease and tooth loss may be linked to an increased risk for developing dementia, a new study has found. Researchers looked at 8,275 men and women whose average age was 63 at the start of the study. Over an average follow-up of more than 18 years, 19 percent of them developed Alzheimer’s disease or other forms of dementia. After controlling for various characteristics, including age, sex, education, cholesterol, high blood pressure, coronary heart disease, smoking and body mass index, they found that compared with people with healthy gums, those who had severe gingivitis with tooth loss had a 22 percent increased relative risk for dementia. Being toothless was associated with a 26 percent increased risk. The report is in the journal Neurology. Previous studies have shown that bacteria present in periodontal disease, particularly certain spirochetes, can travel along the trigeminal nerve that connects the mucous membranes of the mouth to the brain, potentially causing brain damage. The researchers also suggest that the connection could be more indirect, with the inflammation of gum disease leading to cardiovascular disease or diabetes, which are known risk factors for dementia. “We haven’t proven causation,” said the lead author, Ryan T. Demmer, an associate professor of epidemiology at the University of Minnesota. “But if it is causal, the population impact could be significant. Half the population has periodontal disease severe enough to put them at higher risk.” © 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: 27392 - Posted: 07.31.2020

By Pam Belluck A newly developed blood test for Alzheimer’s has diagnosed the disease as accurately as methods that are far more expensive or invasive, scientists reported on Tuesday, a significant step toward a longtime goal for patients, doctors and dementia researchers. The test has the potential to make diagnosis simpler, more affordable and widely available. The test determined whether people with dementia had Alzheimer’s instead of another condition. And it identified signs of the degenerative, deadly disease 20 years before memory and thinking problems were expected in people with a genetic mutation that causes Alzheimer’s, according to research published in JAMA and presented at the Alzheimer’s Association International Conference. Such a test could be available for clinical use in as little as two to three years, the researchers and other experts estimated, providing a readily accessible way to diagnose whether people with cognitive issues were experiencing Alzheimer’s, rather than another type of dementia that might require different treatment or have a different prognosis. A blood test like this might also eventually be used to predict whether someone with no symptoms would develop Alzheimer’s. “This blood test very, very accurately predicts who’s got Alzheimer’s disease in their brain, including people who seem to be normal,” said Dr. Michael Weiner, an Alzheimer’s disease researcher at the University of California, San Francisco, who was not involved in the study. “It’s not a cure, it’s not a treatment, but you can’t treat the disease without being able to diagnose it. And accurate, low-cost diagnosis is really exciting, so it’s a breakthrough.” Nearly six million people in the United States and roughly 30 million worldwide have Alzheimer’s, and their ranks are expected to more than double by 2050 as the population ages. Blood tests for Alzheimer’s, which are being developed by several research teams, would provide some hope in a field that has experienced failure after failure in its search for ways to treat and prevent a devastating disease that robs people of their memories and ability to function independently. © 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: 27388 - Posted: 07.29.2020

Jon Hamilton For years, public health officials have been trying to dispel the myth that people who get a flu shot are more likely to get Alzheimer's disease. They are not. And now there is evidence that vaccines that protect against the flu and pneumonia may actually protect people from Alzheimer's, too. The evidence comes from two studies presented Monday at this year's Alzheimer's Association International Conference, which is being held as a virtual event. "We've always known that vaccines are very important to our overall health," says Maria Carrillo, chief science officer of the Alzheimer's Association. "And maybe they even contribute to protecting our memory, our cognition, our brain." The first study came from a team at the University of Texas that combed through millions of medical records in a national database. The goal was to find factors that affected a person's risk of getting certain diseases, including Alzheimer's. "And one of the things that came back was flu shots," says Albert Amran, a medical student of the McGovern Medical School at the University of Texas Health Science Center in Houston and an author of the study. That seemed odd. So Amran and a team of researchers took a closer look at the medical records of about 9,000 people who were at least 60 years old. Some had received a seasonal flu shot. Some hadn't. "We [tried] to make sure that both groups had an equal amount of, say, smoking status, obesity, diabetes, cardiovascular disease," Amran says. Those are known risk factors for Alzheimer's. The team also looked at factors like education and income, and indicators like the number of prescriptions a person had received, to make sure that people who got vaccines weren't just healthier overall. They weren't. © 2020 npr

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: 27385 - Posted: 07.27.2020

By Jocelyn Kaiser It’s well established that exercise can sharpen the mind: People and mice who work out do better on cognitive tests, and elderly people who are physically active reduce their risk of dementia. Now, in a surprising finding, researchers report that blood from a mouse that exercises regularly can perk up the brain of a “couch potato” mouse. This effect, traced to a specific liver protein in the blood, could point the way to a drug that confers the brain benefits of exercise to an old or feeble person who rarely leaves a chair or bed. “Can your brain think that you exercised, from just something in your blood?” asks aging researcher Saul Villeda of the University of California, San Francisco (UCSF), who led the rodent research. The study grew out of research in Villeda’s lab and others suggesting blood from a young mouse can rejuvenate the brain and muscles of an old mouse. Some teams have since claimed to find specific proteins that explain the benefits of this “young blood.” Graduate student Alana Horowitz and postdoc Xuelai Fan in Villeda’s group wondered whether exercise—not just youth—could confer similar benefits via the blood. It was easy to enough to test: Put a wheel in a cage full of mice, and the mostly inactive animals will run for miles at night. The researchers collected blood from elderly or middle-aged mice that had an exercise wheel in their cage for 6 weeks and then transfused this blood into old mice without a wheel in their cage. Couch potato mice receiving this blood eight times over 3 weeks did nearly as well on learning and memory tests, such as navigating through a maze, as the exercising mice. A control group of couch potatoes receiving blood from similarly old, nonexercising mice saw no boost. The rodents getting the blood from the active mice also grew roughly twice as many new neurons in the hippocampus, a brain region involved in learning and memory, Villeda’s team reports today in Science. That change is comparable to what’s seen in rodents that directly exercise. © 2020 American Association for the Advancement of Science.

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 4: Development of the Brain; Chapter 5: The Sensorimotor System
Link ID: 27357 - Posted: 07.11.2020

By Melinda Wenner Moyer For three months, Chelsea Alionar has struggled with fevers, headaches, dizziness and a brain fog so intense it feels like early dementia. She came down with the worst headache of her life on March 9, then lost her sense of taste and smell. She eventually tested positive for the coronavirus. But her symptoms have been stranger, and lasted longer, than most. “I tell the same stories repeatedly; I forget words I know,” she told me. Her fingers and toes have been numb, her vision blurry and her fatigue severe. The 37-year-old is a one of the more than 4,000 members of a Facebook support group for Covid survivors who have been ill for more than 80 days. The more we learn about the coronavirus, the more we realize it’s not just a respiratory infection. The virus can ravage many of the body’s major organ systems, including the brain and central nervous system. Among patients hospitalized for Covid-19 in Wuhan, China, more than a third experienced nervous system symptoms, including seizures and impaired consciousness. Earlier this month, French researchers reported that 84 percent of Covid patients who had been admitted to the I.C.U. experienced neurological problems, and that 33 percent continued to act confused and disoriented when they were discharged. According to Dr. Mady Hornig, a psychiatrist and epidemiologist at the Columbia University Mailman School of Public Health, the possibility that neurological issues “will persist and create disability, or difficulties, for individuals downstream is really looking more and more likely.” Infections have long been implicated in neurological diseases. Syphilis and H.I.V. can induce dementia. Zika is known to invade developing brains and limit their growth, while untreated Lyme disease can cause nerve pain, facial palsy and spinal cord inflammation. One man with SARS developed delirium that progressed into coma, and was found to have the virus in his brain tissue after his death. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 4: Development of the Brain
Link ID: 27335 - Posted: 06.29.2020

Jon Hamilton A research effort based at the Allen Institute in Seattle, Wash., will tap leading scientists from several institutions to dive even deeper into brain genetics and physiology. The aim: Find clues to the earliest beginnings of Alzheimer's. Allen Institute Three research institutions in Seattle have joined forces to study how Alzheimer's disease takes root in the brain. The consortium will create a new research center at the Allen Institute for Brain Science to study tissue from brains donated by people who died with Alzheimer's. UW Medicine and the Kaiser Permanente Washington Health Research Group are also part of the effort, which will be funded by a five-year $40.5 million grant from the National Institute on Aging, a part of the National Institutes of Health. The project, with its emphasis on basic research, represents part of a global do-over for the Alzheimer's field, which has weathered a series of failed attempts to develop a drug that could slow or stop the disease. "The premise of this project here is that we need to take a step back," says Ed Lein, a senior scientist at the Allen Institute and the center's lead investigator. That's a marked change from a decade ago, when there was great excitement about experimental drugs that could scrub away the sticky brain plaques thought to cause Alzheimer's. Studies have shown that the drugs do their job, removing a toxic protein called amyloid-beta from the brain. But they don't help patients avoid memory loss or cognitive problems. © 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: 27331 - Posted: 06.27.2020

Nicola Davis People living with inflammatory bowel disease (IBD) have more than twice the risk of developing dementia, researchers have revealed in the latest study to link gut health to neurological diseases. A growing body of research suggests changes in the gastrointestinal tract may affect the brain through two-way communication known as the gut-brain axis. Scientists have previously found signs that the abnormally folded proteins involved in Parkinson’s disease may arise in the gut and travel to the brain via the vagus nerve, while changes to the microbial community in the gut – the gut microbiome – have been linked with conditions ranging from mental health problems to motor neurone disease and Parkinson’s disease. In addition, previous work has shown people with IBD have a higher risk of Parkinson’s disease. Researchers now say they have found that people with IBD – inflammatory conditions including ulcerative colitis and Crohn’s disease, which have symptoms including stomach pain and bloody stools – have a greater chance of developing dementia than those without, and tend to be diagnosed with dementia several years earlier. “The findings suggest that there may be a connection between IBD and neurocognitive decline,” said Dr Bing Zhang, first author of the research from the University of California San Francisco. While the study does not prove IBD causes dementia, Zhang and his colleagues outlined a number of ways the two may be linked, noting chronic inflammation has been suggested to trigger processes involved in Alzheimer’s disease, and blood clots and stroke – features involved in vascular dementia. © 2020 Guardian News & Media Limited or its affiliated companies.

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: 27326 - Posted: 06.26.2020