Links for Keyword: Alzheimers

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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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27222 - Posted: 04.30.2020

By Joel Shurkin I have learned that when someone you love has Alzheimer's, he or she is not the only one facing memory issues. Do we remember the bright, sunny person full of life and creativity, or do we remember the person who no longer recognizes us, who lies in a bed in a nursing home, gasping for air? Do we remember the lover with whom we could share our body, our thoughts and our adventures or the person who cannot finish a sentence or find the bathroom? How do we live with the fact that the individual actually died years before his or her body stopped? The ghastliness of Alzheimer's seems to push out everything else. I am finding it hard to remember ordinary life with Carol before Alzheimer's. My wife, Carol Howard, was diagnosed with early-onset Alzheimer's in her early 60s. I slowly watched her disintegrate, watched her beautiful mind be deconstructed part by part, watched sentience slowly fade until she was, well, not here. When she learned the diagnosis, she was determined to fight the disease. She enlisted in two clinical trials of potential drugs, both of which failed. When we realized what was inevitable, she told me that she wanted me to scream for her when she was gone. She was angry that several decades' worth of Alzheimer's research had produced no hope. There is no cure; there is no good treatment. I will tell you who she was and what she became. She was a woman of great beauty, with eyes of summer-sky blue. She was peaceful and brilliant, gentle and kind. I met her when she took a science communication course I taught at the University of California, Santa Cruz. She always put the right word in precisely the right place. Carol studied marine biology and wrote a popular book about her doctoral work with two Atlantic bottlenose dolphins. For 15 idyllic years we lived in the redwood forest of the Santa Cruz Mountains, writing. She eventually moved with me to Baltimore and worked at the Center for Alternatives to Animal Testing at the Johns Hopkins Bloomberg School of Public Health, an excellent job that she loved. © 2020 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27199 - Posted: 04.16.2020

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 BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27198 - Posted: 04.16.2020

By Kenneth S. Kosik No fundamental obstacle prevents us from developing an effective treatment for Alzheimer's disease. Other troubles of human nature, such as violence, greed and intolerance, have a bewildering variety of daunting causes and uncertainties. But Alzheimer's, at its core, is a problem of cell biology whose solution should be well within our reach. There is a fairly good chance that the scientific community might already have an unrecognized treatment stored away in a laboratory freezer among numerous vials of chemicals. And major insights may now reside, waiting to be noticed, in big databases or registries of clinical records, neuropsychological profiles, brain-imaging studies, biological markers in blood and spinal fluid, genomes, protein analyses, neuron recordings, or animal and cell culture models. But we have missed those clues because for decades we have spent too much time chasing every glossy new finding in Alzheimer's research and too little time thinking deeply about the underlying biology of this ailment. Instead our work has been driven by a number of assumptions. Among those assumptions has been the central and dominant role of the protein fragment called beta-amyloid. A large amount of data supports the idea that beta-amyloid plays an important part in the disease. We have developed drugs that can reduce concentrations of the protein fragments in people with Alzheimer's, yet by and large they have not stopped patients' cognitive decline in any meaningful way. It now seems simplistic to conclude that eliminating or inhibiting beta-amyloid will cure or treat those suffering from the disease, especially without far deeper and more comprehensive knowledge of how it develops and progresses [see “The Amyloid Drug Struggle”]. We have not been barking up a completely wrong research tree, but our zeal has led us to ignore other trees and even the roots of this particular one. © 2020 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27193 - Posted: 04.15.2020

According to a recent analysis of data from two major eye disease studies, adherence to the Mediterranean diet – high in vegetables, whole grains, fish, and olive oil – correlates with higher cognitive function. Dietary factors also seem to play a role in slowing cognitive decline. Researchers at the National Eye Institute (NEI), part of the National Institutes of Health, led the analysis of data from the Age-Related Eye Disease Study (AREDS) and AREDS2. They published their results today in Alzheimer’s and Dementia: the Journal of the Alzheimer’s Association. “We do not always pay attention to our diets. We need to explore how nutrition affects the brain and the eye” said Emily Chew, M.D., director of the NEI Division of Epidemiology and Clinical Applications and lead author of the studies. The researchers examined the effects of nine components of the Mediterranean diet on cognition. The diet emphasizes consumption of whole fruits, vegetables, whole grains, nuts, legumes, fish, and olive oil, as well as reduced consumption of red meat and alcohol. AREDS and AREDS2 assessed over years the effect of vitamins on age-related macular degeneration (AMD), which damages the light-sensitive retina. AREDS included about 4,000 participants with and without AMD, and AREDS2 included about 4,000 participants with AMD. The researchers assessed AREDS and AREDS2 participants for diet at the start of the studies. The AREDS study tested participants’ cognitive function at five years, while AREDS2 tested cognitive function in participants at baseline and again two, four, and 10 years later. The researchers used standardized tests based on the Modified Mini-Mental State Examination to evaluate cognitive function as well as other tests. They assessed diet with a questionnaire that asked participants their average consumption of each Mediterranean diet component over the previous year.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27192 - Posted: 04.15.2020

By Gary Stix Consumer genetic tests can sometimes result in a terrible surprise appearing in the same report that divulges whether one has a cilantro aversion or wet or dry earwax. Test takers may receive the devastating news that they have a version of a gene—apolipoprotein E epsilon 4 (APOE e4)—that greatly increases their chances of getting Alzheimer’s disease. The shock can be so great that some will seek solace in a support group to help them adjust to the possibility that they could run into cognitive problems beginning in their 50s or 60s. One thing that makes the information so difficult to absorb is that there is no certainty about it. A person with one copy of the APOE e4 gene is more than three times as likely to wind up with Alzheimer’s (one copy can be inherited from each parent). A hit of two copies increases the risk by 10 times or more. APOE e4 may also reduce the age of the disease’s onset by up to a decade. Still, not everyone who is an APOE e4 carrier will ultimately receive a diagnosis for Alzheimer’s, the most common form of dementia. Given the ambiguities, scientists have long wondered whether other genes might counterbalance APOE e4's effects. A new paper may have found a candidate for just such a gene. Advertisement An analysis across multiple studies—with results from more than 20,000 individuals—found that APOE e4 carriers between the ages of 60 and 80 who also had a particular variant of a gene called klotho (named for Clotho, one of the Greek Fates, who spins the thread of life) were 30 percent less likely to receive an Alzheimer's diagnosis than carriers without it. People in their late 70s with a single copy of the klotho variant were also less apt to experience the initial cognitive losses (mild cognitive impairments) that often precede an Alzheimer’s diagnosis. Study participants with the relevant variant also had reduced signs of the hallmark clumps of beta-amyloid protein that turn up in the brain before symptoms arise. © 2020 Scientific American,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27191 - Posted: 04.15.2020

The first published data from the Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease (A4) study supports the hypothesis that higher levels of the amyloid protein in the brain represent an early stage of Alzheimer’s disease. Results of an analysis of participant screening data for the study, published April 6 in JAMA Neurology, also show that amyloid burden in clinically normal older adults is associated with a family history of disease, lower cognitive test scores, and reports of declines in daily cognitive function. Major funding was provided by the National Institute on Aging (NIA), part of the National Institutes of Health; all data is now freely available to the broader research community. With completion expected in late 2022, the A4 study is an ongoing prevention trial launched in 2014 to test whether the drug solanezumab, a monoclonal antibody, could slow cognitive decline associated with elevated brain amyloid if started before clinical symptoms appear. Amyloid, long considered a hallmark of Alzheimer’s disease, has been the target of therapies in clinical trials in people who already show symptoms of the disease. “A major issue for amyloid-targeting Alzheimer’s disease clinical trials, and one that is being addressed with the A4 study, is that previous trials may have been intervening too late in the disease process to be effective,” said NIA Director, Richard J. Hodes, M.D. “A4 is pioneering in the field because it targets amyloid accumulation in older adults at risk for developing dementia before the onset of symptoms."

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27176 - Posted: 04.07.2020

By Christie Aschwanden In February, pharmaceutical companies Roche and Eli Lilly announced that two experimental drugs they had developed for Alzheimer’s disease had failed in clinical trials. Roche’s drug, gantenerumab, and Eli Lilly’s solanezumab joined more than 100 other potential Alzheimer’s drugs that have flopped, including aducanumab, a much-heralded drug from Biogen. In March 2019, Biogen announced that it had halted two clinical trials of the drug early after an interim analysis showed they weren’t working, but the company has since changed course, saying it intends to seek approval from the Food and Drug Administration based on a new analysis of the data. A lot is riding on Biogen's experimental drug. If approved, it "would be the first disease-modifying drug ever," says George Vradenburg, chairman and co-founder of the advocacy group UsAgainstAlzheimer's. The last time a drug was approved specifically for Alzheimer's was 2003, and since then, the Alzheimer's drug pipeline has spit out a bunch of duds. More than 200 promising leads have fallen through just in the past decade. There has been an ongoing search for Alzheimer's drugs since the 1990s, but "the long and short of it is that it's not been successful," says Lon Schneider, an Alzheimer's researcher at the University of Southern California's Keck School of Medicine. These failures aren’t for lack of trying. Instead, they are evidence that the disease and its causes are much more complex than researchers first appreciated. “We were blind to this [complexity]. Things looked simpler than they really are,” says Richard Hodes, director of the National Institute on Aging (NIA).

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27172 - Posted: 04.06.2020

By Erika Mailman In summer 2014, when he was 54, Sacramento artist David Wetzl was exhibiting the behaviors of an elderly man with Alzheimer’s. “I have a bad brain,” he told everyone repeatedly, using a simple phrase to explain his diagnosis to the world. Two years before that, his wife, Diana Daniels, had asked for an MRI because she was suspicious that things weren’t right and fearful when he couldn’t remember the word “shoelaces.” The scan showed with horrific clarity how sections of his brain had shriveled. “The devastation began on his left temporal lobe, working its greatest damage,” says Diana. “By the time of diagnosis, his right temporal lobe also had significant atrophy.” David was diagnosed with frontotemporal dementia, or FTD, part of a group of disorders caused by nerve cell damage to the brain. The disease comes with a dispiriting prognosis. There is no cure (although symptoms can be treated), and patients usually die within seven to 13 years from the onset of symptoms. As FTD progresses, behavior can become strange and antisocial, says Matt Ozga, communications manager at the Association for Frontotemporal Degeneration in King of Prussia, Pa. Patients lose their filter and can make embarrassing remarks. For the spouses who are caught off guard, thinking their mate’s worst setback for the next few decades will be graying hair and a paunch, it’s a shock. The couple may find themselves confronted  by different challenges than those who encounter dementia later in life.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27150 - Posted: 03.30.2020

By Nicholas Bakalar There is good evidence that a daily baby aspirin reduces the risk for heart disease and stroke, and some have thought its inflammation-lowering effect might also help in delaying cognitive decline. But taking a daily low-dose aspirin did not appear to be effective in lowering the risk of Alzheimer’s disease or other forms of dementia, a new study reports. For the study, in Neurology, researchers set up a controlled trial with 19,114 men and women older than 70 who were free of cardiovascular disease and dementia at the start. Half were randomly assigned to take a daily 100-milligram aspirin, while the other half took a placebo. After an average follow-up of almost five years with annual examinations, the researchers found no difference between the groups in diagnoses of Alzheimer’s disease or mild cognitive impairment. They did find declining cognitive function over time, but the speed and degree of that decline was the same in both groups. The researchers found no effect in various subgroups either — people with hypertension or diabetes, smokers or people with high cholesterol, or those who were overweight or obese. A limitation of the study was that patients were followed for less than five years. “If you’re 70 or older and healthy, without evidence of cardiovascular disease, it’s very difficult to improve on your success. The relatively low risk of dementia in this study was not further lowered with aspirin,” said a co-author, Dr. Anne B. Newman, a professor of epidemiology at the University of Pittsburgh. © 2020 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 27147 - Posted: 03.30.2020