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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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning; 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 13: Memory and Learning; 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 13: Memory and Learning; Chapter 13: Memory and Learning
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 13: Memory and Learning
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 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27326 - Posted: 06.26.2020

By Nicholas Bakalar Five behaviors are associated with a lower risk for Alzheimer’s disease, a new study in Neurology suggests, and the more of them you follow, the lower your risk. Researchers used detailed diet and lifestyle information from two databases, one of 1,845 people whose average age was 73, the other of 920 people whose average age was 81. All were free of Alzheimer’s disease at the start of the study. They followed them for an average of about six years, during which 608 developed Alzheimer’s disease. The researchers scored the participants on their adherence to five behaviors: not smoking, consistent moderate or intense physical activity, light to moderate alcohol consumption, a high-quality Mediterranean-style diet, and engagement in late-life cognitively challenging activity. Compared to those with none or one of the healthy lifestyle factors, those with two or three had a 37 percent reduced risk for Alzheimer dementia, and those with four or five had a 60 percent reduced risk. The lead author, Dr. Klodian Dhana, an assistant professor of medicine at Rush Medical College, said that the paper focuses on modifiable risk factors. All five of these factors are related to each other, he added, and work best in combination. “My top recommendations are to engage in cognitively stimulating activities such as reading books and newspapers and playing brain-stimulating games, like chess and checkers,” he said. “Also, exercising regularly and following a diet for a healthy brain that includes green leafy vegetables every day, berries, nuts, poultry, fish, and limited fried food.” © 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 13: Memory and Learning
Link ID: 27317 - Posted: 06.24.2020

Combining more healthy lifestyle behaviors was associated with substantially lower risk for Alzheimer’s disease in a study that included data from nearly 3,000 research participants. Those who adhered to four or all of the five specified healthy behaviors were found to have a 60% lower risk of Alzheimer’s. The behaviors were physical activity, not smoking, light-to-moderate alcohol consumption, a high-quality diet, and cognitive activities. Funded by the National Institute on Aging (NIA), part of the National Institutes of Health, this research was published in the June 17, 2020, online issue of Neurology, the medical journal of the American Academy of Neurology. The research team reviewed data from two NIA-funded longitudinal study populations: The Chicago Health and Aging Project (CHAP)(link is external) and the Memory and Aging Project (MAP)(link is external). They selected participants from those studies who had data available on their diet, lifestyle factors, genetics, and clinical assessments for Alzheimer’s disease. The resulting data pool included 1,845 participants from CHAP and 920 from MAP. The researchers scored each participant based on five healthy lifestyle factors, all of which have important health benefits: At least 150 minutes per week of moderate- to vigorous-intensity physical activity – Physical activity is an important part of healthy aging. Not smoking – Established research has confirmed that even in people 60 or older who have been smoking for decades, quitting will improve health. Light-to-moderate alcohol consumption – Limiting use of alcohol may help cognitive health. A high-quality, Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, which combines the Mediterranean diet and Dietary Approaches to Stop Hypertension (DASH) diet – The MIND diet focuses on plant-based foods linked to dementia prevention. Engagement in late-life cognitive activities – Being intellectually engaged by keeping the mind active may benefit the brain.

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: 27309 - Posted: 06.19.2020

By Tina Hesman Saey A genetic variant that raises one’s risk of developing Alzheimer’s disease may also make people more susceptible to COVID-19. People with two copies of a version of the APOE gene called APOE4 are 14 times as likely to develop Alzheimer’s disease as people with two copies of the APOE3 version of the gene (SN: 9/22/17). Those people were also more than twice as likely to test positive for the coronavirus than people with two copies of the APOE3 version, researchers report May 26 in the Journals of Gerontology: Series A. The results come from a study of more than 600 people in England diagnosed with COVID-19 from March 16 to April 26. Two previous studies showed that people with dementia were more likely to have severe cases or to die of COVID-19. This new study found that even people with no signs of dementia or other diseases associated with having APOE4 were still more susceptible to COVID-19 than people with the APOE3 version. Among nearly 400,000 participants in the large genetic database called the UK Biobank, only 3 percent have two copies of APOE4, while 69 percent have two copies of APOE3. The remainder have one of each version. But the APOE4 version was more common than expected among people diagnosed with COVID-19, the study found. Of 622 people who tested positive for the coronavirus, 37 had two copies of APOE4. On a population scale, that means about 410 of every 100,000 people with two copies of that version of the gene would test positive, the researchers calculate. That compares with 179 of every 100,000 people with two copies of APOE3 testing positive. © 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 13: Memory and Learning
Link ID: 27271 - Posted: 06.01.2020

Jef Akst The APOE ε4 gene variant that puts people at a greater risk of developing Alzheimer’s disease also has a link to COVID-19. According to a study published today (May 26) in The Journals of Gerontology, Series A, carrying two copies of the variant, often called APOE4, makes people twice as likely to develop a severe form of the disease, which is caused by the SARS-CoV-2 coronavirus currently spreading around the world. David Melzer of Exeter University and colleagues used genetic and health data on volunteers in the UK Biobank to look at the role of the APOE4 variant, which affects cholesterol transport and inflammation. Of some 383,000 people of European descent included in the study, more than 9,000 carried two copies. The researchers cross-referenced this list with people who tested positive for COVID-19 between March 16 and April 26—the assumption being that most such cases were severe because testing at the time was largely limited to hospital settings. The analysis suggested that the APOE4 homozygous genotype was linked to a doubled risk of severe disease, compared with people who had two copies of another variant called ε3. The result isn’t due to nursing home settings or to a greater likelihood of having a diagnosis of dementia, which none of the 37 people with two copies of APOE4 who tested positive for COVID-19 had. “It is pretty bulletproof—whatever associated disease we remove, the association is still there,” Melzer tells The Guardian. “So it looks as if it is the gene variant that is doing it.” © 1986–2020 The Scientist.

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: 27267 - Posted: 05.29.2020

R. Douglas Fields Discoveries that transcend boundaries are among the greatest delights of scientific research, but such leaps are often overlooked because they outstrip conventional thinking. Take, for example, a new discovery for treating dementia that defies received wisdom by combining two formerly unrelated areas of research: brain waves and the brain’s immune cells, called microglia. It’s an important finding, but it still requires the buy-in and understanding of researchers to achieve its true potential. The history of brain waves shows why. In 1887, Richard Caton announced his discovery of brain waves at a scientific meeting. “Read my paper on the electrical currents of the brain,” he wrote in his personal diary. “It was well received but not understood by most of the audience.” Even though Caton’s observations of brain waves were correct, his thinking was too unorthodox for others to take seriously. Faced with such a lack of interest, he abandoned his research and the discovery was forgotten for decades. Flash forward to October 2019. At a gathering of scientists that I helped organize at the annual meeting of the Society for Neuroscience in Chicago, I asked if anyone knew of recent research by neuroscientists at the Massachusetts Institute of Technology who had found a new way to treat Alzheimer’s disease by manipulating microglia and brain waves. No one replied. I understood: Scientists must specialize to succeed. Biologists studying microglia don’t tend to read papers about brain waves, and brain wave researchers are generally unaware of glial research. A study that bridges these two traditionally separate disciplines may fail to gain traction. But this study needed attention: Incredible as it may sound, the researchers improved the brains of animals with Alzheimer’s simply by using LED lights that flashed 40 times a second. Even sound played at this charmed frequency, 40 hertz, had a similar effect. All Rights Reserved © 2020

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 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27264 - Posted: 05.28.2020

By Nicholas Bakalar Eating foods high in flavonoids — a group of nutrients found in many fruits and vegetables — may lower your risk for dementia, researchers report. The study, in the American Journal of Clinical Nutrition, looked at 2,801 men and women who were 50 and older and free of dementia at the start. Over an average of 20 years of follow-up, researchers gathered diet information at five periodic health examinations; during that time, 193 of the participants developed Alzheimer’s disease or other forms of dementia. Compared with those in the 15th percentile or lower for flavonoid intake, those in the 60th or higher had a 42 to 68 percent lower risk for dementia, depending on the type of flavonoid consumed. Intake of one type of flavonoid, anthocyanins, abundant in blueberries, strawberries and red wine, had the strongest association with lowered risk. Apples, pears, oranges, bananas and tea also contributed. The study controlled for many health and behavioral characteristics, including how strongly participants adhered to the government’s Dietary Guidelines for Americans, which in addition to fruits and vegetables emphasize whole grains, lean meats and other heart-healthy foods. The senior author, Paul F. Jacques, a scientist with the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, said that the amount consumed by those who benefited the most was not large. Their monthly average was about seven half-cup servings of strawberries or blueberries, eight apples or pears, and 17 cups of tea. “It doesn’t take much,” he said. “A couple of servings of berries a week, maybe an apple or two.” © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27255 - Posted: 05.20.2020

By Ellen Ruppel Shell My first day in Mexico City was tough. The smog was so thick that I gasped for breath while climbing the stairs to my hotel room. I had braced for headaches from the high altitude and thin air, but I was not prepared for how dirty that air was or for the bloodshot eyes and burning lungs. Declared the world's most polluted metropolis by the United Nations in 1992, greater Mexico City has worked hard to clean up its act. To some degree it has: the city is rightfully proud of its miles of bike paths and lush parks. Yet a casual glance at the smudged horizon shows that those efforts are not enough. Most days the area has levels of airborne sooty particles that greatly exceed standards set by the World Health Organization, as well as elevated amounts of other pollutants. Clogged with more than 9.6 million vehicles and an estimated 50,000 smokestacks, Mexico City stews in a toxic brew known to corrode human lungs and hearts. Now many scientists agree that this pollution also damages the brain. In 2018 a study found lesions known to be hallmarks of Alzheimer's disease in the brains of Mexico City residents in their 30s and 40s—decades before signs of the disease normally can be detected—and tied this damage to exposure to the city's bad air. The researchers who did that work, who are from institutions in Mexico and the U.S., have also found early forms of this frightening damage in infants and young children. And Mexico City is not the only place where bad air has been linked to Alzheimer's. Just a few years ago a team of Harvard scientists released data from a large study of 10 million Medicare recipients ages 65 and older living in 50 different cities in the northeastern U.S. The researchers reported a strong correlation between exposure to specific air pollutants and a number of neurodegenerative disorders, including Alzheimer's. © 2020 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27247 - Posted: 05.14.2020

By Tanya Lewis In March 2019 biotechnology giant Biogen stopped two big trials of its experimental Alzheimer's disease drug aducanumab because it did not appear to improve memory in declining patients. Then, in a surprise reversal several months later, the company and its partner, Japanese drugmaker Eisai, said they would ask the U.S. Food and Drug Administration to approve the treatment. A new analysis, Biogen said, showed that a subset of people on the highest doses in one trial did benefit from the compound, which dissolves clumps of a protein called beta-amyloid within the brain. The back-and-forth decisions, along with the failure of a slew of other amyloid-clearing compounds, have left experts divided about whether treating amyloid buildup—long thought to be the best target for an Alzheimer's therapy—is still a promising approach. Some of the scientists rethinking the so-called amyloid hypothesis helped to generate it in the first place. “I would say it has legs, but it's limping,” says geneticist John Hardy, who co-authored the genetic studies that pioneered the idea more than two decades ago. According to Hardy, who runs a molecular neuroscience program at University College London's Institute of Neurology, “the [concept] we drew in 1998 is cartoonishly oversimplistic. There were lots of question marks. We thought those questions would be filled in within a couple of years. And yet 20 years later they are not filled in.” Other experts, though, still contend that the amyloid hypothesis is a strong explanation and that treatments targeting the protein are the right way to go. © 2020 Scientific American

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: 27222 - Posted: 04.30.2020