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Laura Sanders Alzheimer’s disease destroys command centers in the brain that keep people awake. That finding could explain why the disease often brings daytime drowsiness. Sleep problems can precede dementias, including Alzheimer’s, sometimes by decades. But the new result, described online August 12 in Alzheimer’s & Dementia, suggests that disordered sleeping isn’t just an early harbinger of Alzheimer’s. Instead, sleep trouble is “part of the disease,” says Lea Grinberg, a neuropathologist at the University of California, San Francisco. Grinberg and colleagues focused on the brain stem and a structure perched above it called the hypothalamus. Together, these parts of the nervous system oversee crucial jobs such as keeping people awake and paying attention. Though important, the brain stem and its neighbors have been largely overlooked in studies of dementia, Grinberg says. In particular, the researchers searched for evidence of tau, a protein that can form tangles inside nerve cells, in postmortem brains of people who died with Alzheimer’s disease. Three small regions of the hypothalamus and brain stem, all of which usually contain nerve cells that keep people awake during the day, were packed with tau, the team found. And two of the three areas had lost over 70 percent of their nerve cells, or neurons. These areas “are hit hard, and they are hit by tau,” Grinberg says. That destruction could be part of the reason people with Alzheimer’s disease often feel tired during the day, even if they slept the night before. |© Society for Science & the Public 2000 - 2019.

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: 26509 - Posted: 08.17.2019

By John Williams The first, startling epigraph in Nicci Gerrard’s new book, “The Last Ocean,” comes from Emily Dickinson: “Abyss has no Biographer.” Gerrard sets out to tell the story of dementia, a disease that can appear to consume those it afflicts. After her father, John, died in 2014, the author — who writes best-selling thrillers with her husband under the name Nicci French — embarked on learning more about the disease as both a journalist and an activist. The result is a tender, inquisitive tour of a subject that can be raw and painful. Below, Gerrard talks about loss, art that punches you in the solar plexus and the experience of writing a book that doesn’t answer questions. When did you first get the idea to write this book? I first had the idea when my father, who’d been living with dementia for over 10 years, went into hospital in February 2014. After four weeks without anyone to see him — we were allowed in for very limited times and then not at all, because of a norovirus outbreak — I barely recognized him. I will, for the rest of my life, feel terribly that I didn’t get him out earlier. Then he lived at home for nine months. He had become skeletal, immobile, inarticulate, and in a way he felt utterly lost, like a ghost in our lives and in his own life. He would lay downstairs in a hospital bed, looking outside at the garden he used to love. There was this clear sense that he’d already lost everything he had, everything he was, all his capacity, there was nothing left — and yet somehow that he didn’t lose himself. In the book I say that if I were religious, I would call that self he retained his soul. Something very indelible remained. © 2019 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: 26508 - Posted: 08.17.2019

By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 26504 - Posted: 08.15.2019

­­­In a nationwide study, researchers used magnetic resonance imaging (MRI) to scan the brains of hundreds of participants in the National Institutes of Health’s Systolic Blood Pressure Intervention Trial (SPRINT) and found that intensively controlling a person’s blood pressure was more effective at slowing the accumulation of white matter lesions than standard treatment of high blood pressure. The results complement a previous study published by the same research group which showed that intensive treatment significantly lowered the chances that participants developed mild cognitive impairment. “These initial results support a growing body of evidence suggesting that controlling blood pressure may not only reduce the risk of stroke and heart disease but also of age-related cognitive loss,” said Walter J. Koroshetz, M.D., director of the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “I strongly urge people to know your blood pressure and discuss with your doctors how to optimize control. It may be a key to your future brain health.” Brain white matter is made up of billions of thin nerve fibers, called axons, that connect the neurons with each other. The fibers are covered by myelin, a white fatty coating that protects axons from injury and speeds the flow of electrical signals. White matter lesions, which appear bright white on MRI scans, represent an increase in water content and reflect a variety of changes deep inside the brain, including the thinning of myelin, increased glial cell reactions to injury, leaky brain blood vessels, or multiple strokes. These changes are associated with high blood pressure, or “hypertension”.

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: 26496 - Posted: 08.14.2019

Todd Golde and Steven DeKosky Dr. Todd Golde is a co-founder of Lacerta Therapeutics, Inc. and serves on their scientific advisory board (SAB). He is on the SAB for Promis Neuroscience, Inc. In the past he has served, ad hoc, on SABs related to neurodegenerative disease programs for Eli Lilly, Novartis, Bristol Myers Squib, Abbvie, Lundbeck, Biogen and Pfizer. He is co-editor in chief of Alzheimer’s Research and Therapy for which he receives an honorarium. He has served on the medical and scientific advisory board for the Alzheimer’s Association. He serves as a scientific advisor and participates in grant reviews for BrightFocus Foundation and the American Federation for Aging Research. He is a co-inventor on multiple patents and patent applications relating to AD therapeutics. He currently receives funding from the NIH. Steven DeKosky receives grant funding from the National Institute of Aging, serves as a consultant for Amgen, Biogen, and Cognition Therapeutics, and serves as editor for dementia for Up-To-Date, a point-of-care electronic textbook. He has chaired study sections for the NIH, served on two NIH councils, for the National Center for Complementary and Alternative Medicine (now the National Center for Complementary and Integrative Health; NCCIH) and the Director's Council (Council of Councils). He has served on the board of the Alzheimer's Association and chaired their Medical and Scientific Advisory Council, as well as chairing the Medical and Scientific Advisory Panel of Alzheimer's Disease International. © 2010–2019, The Conversation US, Inc.

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: 26495 - Posted: 08.14.2019

By Paula Span Juli Engel was delighted when a neurologist recommended a PET scan to determine whether amyloid — the protein clumps associated with an increased risk of Alzheimer’s disease — was accumulating in her mother’s brain. “My internal response was, ‘Yay!’” said Ms. Engel, 65, a geriatric care manager in Austin, Tex., who has been making almost monthly trips to help her mother in Florida. “He’s using every tool to try to determine what’s going on.” Sue Engel, who’s 83 and lives in a retirement community in Leesburg, Fla., has been experiencing memory problems and other signs of cognitive decline for several years. Her daughter checked off the warning signs: her mother has been financially exploited, suffered an insurance scam, caused an auto accident. Medicare officials decided in 2013, shortly after PET (positron emission tomography) amyloid imaging became available, that they lacked evidence of its health benefits. So outside of research trials, Medicare doesn’t cover the scans’ substantial costs ($5,000 to $7,000, the Alzheimer’s Association says); private insurers don’t, either. Juli Engel thinks Medicare should reimburse for the scan, but “if necessary, we’ll pay for it out of pocket,” she said. Her mother already has an Alzheimer’s diagnosis and is taking a commonly prescribed dementia drug. So she probably doesn’t meet the criteria developed by the Alzheimer’s Association and nuclear medicine experts, which call for PET scans only in cases of unexplained or unusual symptoms and unclear diagnoses. But as evidence mounts that brain damage from Alzheimer’s begins years before people develop symptoms, worried patients and their families may start turning to PET scans to learn if they have this biomarker. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26484 - Posted: 08.03.2019

By Gina Kolata For decades, researchers have sought a blood test for beta amyloid, the protein that is a hallmark of Alzheimer’s disease. Several groups and companies have made progress, and on Thursday, scientists at Washington University in St. Louis reported that they had devised the most sensitive blood test yet. The test will not be available for clinical use for years, and in any event, amyloid is not a perfect predictor of Alzheimer’s disease: Most symptomless older people with amyloid deposits in their brains will not develop dementia. But the protein is a significant risk factor, and the new blood test identified patients with amyloid deposits before brain scans did. That will be important to scientists conducting trials of drugs to prevent Alzheimer’s. They need find participants in the earliest stages of the disease. At present, a diagnosis of Alzheimer’s disease is not easy to make. Doctors rely mostly on tests of mental acuity and interviews with the patient and family members. Studies have shown that community doctors are only 50 to 60 percent accurate in diagnosing the condition — about the same as tossing a coin. Methods that can improve accuracy, like PET scans of the brain, are expensive and often not available. The new test relies on mass spectrometry, a tool used in analytical chemistry that, with recent technical advances, can find elusive beta amyloid molecules in blood with high precision. The lead investigator, Dr. Randall Bateman, a neurologist at Washington University, has been working on a mass spectrometry test for 20 years. He and a colleague, Dr. David Holtzman, founded a company ten years ago and licensed patents from their university to commercialize a mass spectrometry test if they ever developed one. © 2019 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: 26481 - Posted: 08.02.2019

By Judith Graham By all accounts, the woman, in her late 60s, appeared to have severe dementia. She was largely incoherent. Her short-term memory was terrible. She couldn’t focus on questions that medical professionals asked her. But Malaz Boustani, a doctor and professor of aging research at Indiana University School of Medicine, suspected something else might be going on. The patient was taking Benadryl for seasonal allergies, another antihistamine for itching, Seroquel (an antipsychotic medication) for mood fluctuations, as well as medications for urinary incontinence and gastrointestinal upset. To various degrees, each of these drugs blocks an important chemical messenger in the brain, acetylcholine. Boustani thought the cumulative impact might be causing the woman’s cognitive difficulties. He was right. Over six months, Boustani and a pharmacist took the patient off those medications and substituted alternative treatments. Miraculously, she appeared to recover completely. Her initial score on the Mini-Mental State Examination had been 11 of 30 — signifying severe dementia — and it shot up to 28, in the normal range. An estimated 1 in 4 older adults take anticholinergic drugs — a wide-ranging class of medications used to treat allergies, insomnia, leaky bladders, diarrhea, dizziness, motion sickness, asthma, Parkinson’s disease, chronic obstructive pulmonary disease and various psychiatric disorders. Older adults are highly susceptible to negative responses to these medications. Since 2012, anticholinergics have been featured prominently on the American Geriatrics Society Beers Criteria list of medications that are potentially inappropriate for seniors. © 1996-2019 The Washington Post

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: 26479 - Posted: 08.02.2019

By Lydia Denworth An elderly woman suffering from late-stage Alzheimer’s disease had neither talked to nor reacted to any of her family members for years. Then, one day, she suddenly started chatting with her granddaughter, asking for news of other family members and even giving her granddaughter advice. “It was like talking to Rip van Winkle,” the granddaughter told University of Virginia researchers of her astonishment. Unfortunately, the reawakening did not last—the grandmother died the next week. That event got written up as what the case study authors called terminal lucidity—a surprising, coherent episode of meaningful communication just before death in someone presumed incapable of social interaction. Yet it was by no means unique. Physician Basil Eldadah, who heads the geriatric branch at the National Institute on Aging (NIA), had heard such stories and filed them away as intriguing accounts. But in 2018, spurred by the need to make progress combatting Alzheimer’s, Eldadah began to think it was time to do more and organized a workshop for interested scientists. After all, if the grandmother was able to tap into mysterious neural reserves, cases such as hers might help scientists explore how cognition could possibly be restored—even briefly—in patients with the most advanced neurodegenerative disease. This summer Eldadah and the scientists he assembled have taken the first steps toward systematic and rigorous study of what they are now calling paradoxical lucidity, a broader label intended to capture the dramatic, unexpected and puzzling nature of the phenomenon. The workshop participants published two papers on it in the August issue of Alzheimer’s and Dementia, and the NIA announced plans to fund relevant research next year. The early goals are modest—the formulation of an operational definition and a gauging of the phenomenon’s prevalence. The possible long-term implications, however, are tantalizing. “If the brain were able to access that normal state, even if it’s transient, it would suggest that there’s some requisite level of machinery that can work under some kind of unique circumstance,” anesthesiologist and neuroscientist George Mashour, director of the Center for Consciousness Science at the University of Michigan and lead author of one of the papers, says. © 2019 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: 26474 - Posted: 08.01.2019

By Nicholas Bakalar A new study confirms earlier reports that anemia — a condition caused by having too little hemoglobin, the oxygen-carrying component of red blood cells — increases the risk for dementia. It found that having high hemoglobin levels does so as well. Dutch researchers looked at 12,305 people without dementia at the start of the study, measuring their hemoglobin levels and following them for an average of 12 years. Over the period, 1,520 developed dementia, including 1,194 with Alzheimer’s disease. The study is in Neurology. The scientists divided the hemoglobin levels into five groups, low to high. Compared with those in the middle one-fifth, those in the highest fifth had a 20 percent increased risk for any dementia type, and a 22 percent increased risk for Alzheimer’s. Those in the lowest were at a 29 percent increased risk for dementia and a 36 percent increased risk for Alzheimer’s. The researchers controlled for education level, blood pressure, diabetes, lipid-lowering medication, alcohol intake and other health and behavioral characteristics. “We don’t have the intervention studies that would show that modifying hemoglobin could prevent dementia,” said the lead author, Frank J. Wolters, a researcher at Erasmus University Medical Center in Rotterdam, “and we can’t recommend interventions based on this study. In the meantime, given the other beneficial effects of treating anemia, this study provides an extra incentive.” © 2019 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: 26473 - Posted: 08.01.2019

By Sarah White | Some five ounces of clear fluid fills the spaces between your brain and your skull. This brain juice, or cerebrospinal fluid, cushions against injury, supplies nutrients and clears away waste. Your body can make as much as a pint of fresh stuff every day to replace the old. But for 150 years, scientists have puzzled over how the used cerebrospinal fluid leaves the brain to make room for more. New research, published Wednesday in Nature, has finally deciphered this brain drain process. As a result, it’s also inching us closer to understanding Alzheimer’s and other neurodegenerative diseases. South Korean scientists, led by Gou Young Koh, completed the puzzle by studying our immune system’s superhighway, dubbed the lymphatic system. They were able to trace the cerebrospinal fluid’s one-directional path in mice, from its origin in the brain into lymph nodes in the neck. The key conduit? Lymphatic vessels at the bottom of the skull, in the brain’s outer layers. Before now, neuroscientists thought cerebrospinal fluid drained through lymphatic vessels on top of the brain or ones exiting through the nasal cavity. No one had managed to carefully examine the lymphatic vessels on the bottom of the brain because they’re so close to bones and delicate blood vessels. But by having a neurosurgeon on their team, the researchers could get close enough to identify what was so special about these bottom lymphatic vessels and see what makes them ideal for draining cerebrospinal fluid.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26455 - Posted: 07.27.2019

By Lauren Aguirre, STAT Scientists who study Alzheimer’s disease have mostly ignored the role of seizures, but that is beginning to change, and new research suggests they may provide insight into the progression of the disease and pave the way for treatments. It’s no surprise to neurologists that some people experience convulsive seizures in the later stages of the disease. In fact, the second patient ever to receive an Alzheimer’s diagnosis more than a century ago suffered from them. But because brain damage can cause seizures, they were long thought to be just one more casualty of a deteriorating brain. Now evidence is accumulating that such abnormal electrical activity is far more common and occurs much earlier—and perhaps even precedes obvious signs of memory loss. This raises the possibility that seizures may be intimately tied up with the progression of the disease. New research that lends credence to this hypothesis was shared at the Alzheimer’s Association International Conference in Los Angeles this week. One study looked at 55 patients between the ages of 50 and 69 who were admitted to an Israeli medical center with their first known seizure. A quarter of them went on to develop dementia—with a mean time to the diagnosis of eight and a half years. Another study of nearly 300,000 U.S. veterans over the age of 55 found that seizures were associated with twice the risk for developing dementia between one and nine years later. © 2019 Scientific American,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26441 - Posted: 07.23.2019

Scientists say they may have discovered why more women than men have Alzheimer's disease and dementia. It has always been thought that women living longer than men was the reason. But new research presented at an international conference suggests this may not be the whole story. Differences in brain connectivity and sex-specific genes linked to risk could explain the numbers, the researchers say. Most people living with Alzheimer's - the most common cause of dementia - are women. In the UK, about 500,000 women have dementia, compared with 350,000 men. Most people who develop the disease are over the age of 65 but it is not a normal part of ageing. Alzheimer's disease can affect younger people too. Researchers from Vanderbilt University Medical Centre studied brain scans of hundreds of men and women, looking at the pattern of a protein called tau. One of the characteristic features of Alzheimer's is the build-up of proteins called tau and amyloid in the brain. When they form toxic, tangled clumps, this causes brain cells to die, leading to memory problems. The researchers found differences between the sexes in how tau was spread across regions of the brain. Women appeared to have better connectivity between the regions where tau protein builds up - and this had implications for the brain, the study said. With this higher connectivity, women's brains may be at risk of faster spread of tau - and of cognitive decline. Dr Jana Voigt, head of research at Alzheimer's Research UK, said the study revealed "sex-specific differences in brain connectivity that could contribute to differing Alzheimer's risk in men and women". © 2019 BBC.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26434 - Posted: 07.20.2019

Jon Hamilton Researchers are prescribing exercise as if it were a drug in a study that aims to see if it can prevent Alzheimer's disease. "We are testing if exercise is medicine for people with a mild memory problem," says Laura Baker, principal investigator of the nationwide EXERT study and associate director of the Alzheimer's Disease Research Center at Wake Forest School of Medicine. The study, funded by the National Institute on Aging, could help determine whether exercise can protect people from the memory and thinking problems associated with Alzheimer's. "The evidence in science has been building for the last 20 years to suggest that exercise at the right intensity could protect brain health as we age," Baker says. But much of that evidence has come from studies that were small, ran for only a few months or relied on people's own estimates of how much they exercised. The EXERT study is different. It's taking 300 people at high risk for Alzheimer's and randomly assigning them to one of two groups for 18 months. Half the participants do aerobic exercise, like running on a treadmill. The other half do stretching and flexibility exercises for comparison. By subscribing, you agree to NPR's terms of use and privacy policy. This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply. © 2019 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: 26430 - Posted: 07.19.2019

By Susan Berger Julie Staple was a child when her dad, Mark Womack, began exhibiting odd behavior. An award-winning violin, viola and cello maker, Womack was not following through for clients nor returning phone calls promptly. He was watching more TV and taking more breaks from work. He began drinking and was quick to become angry. The behavior lasted years and took its toll. Staple and her mom, Ginny Womack, a professional violinist, thought Mark Womack was depressed. Her parents got divorced. Mark Womack was fired from two jobs making instruments in Nebraska and Texas. There were other disturbing events. A body shop wouldn’t fix his car because he couldn’t recall insurance information. A drive to his parents’ home that normally took two hours took five. And then came a phone call from his boss to the family — Mark Womack was crying and couldn’t remember how to make a violin. The boss took him to a clinic. At age 53, Mark Womack was diagnosed with early onset Alzheimer’s in September 2015. Further evaluation a few months back revealed instead a diagnosis of frontotemporal dementia or FTD. Ginny Womack became his caregiver. “Had my mom known, she would never have divorced him and been his caretaker from the beginning,” Staple, of Deerfield, Ill., said. FTD often is misdiagnosed as a psychiatric disorder or Alzheimer’s. It affects the area of the brain generally associated with personality, behavior and language and is often diagnosed in people between the ages of 40 and 45. About 5.8 million people in the United States are living with Alzheimer’s and dementia, said Heather Snyder, senior director for medical and scientific operations for the Alzheimer’s Association. The number is expected to rise to 14 million by 2050. Approximately 16 million people are caregivers. © 1996-2019 The Washington Post

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: 26417 - Posted: 07.15.2019

Jon Hamilton In a waiting room at the Banner Alzheimer's Institute in Phoenix, a 74-year-old woman named Rubie is about to find out whether she has a gene that puts her at risk for Alzheimer's. "I'm a little bit apprehensive about it, and I hope I don't have it," she says. "But if I do, I want to be able to plan for my future." The gene is called APOE E4, and it's the most powerful known genetic risk factor for Alzheimer's after age 65. APOE E4 doesn't cause the disease, and many of those who carry it never develop Alzheimer's. Still, about 1 in 4 people who carries a single copy will develop Alzheimer's by 85. Among people who get two copies (one from each parent) up to 55% will develop Alzheimer's by age 85. Rubie is one of several participants in a research study at Banner who agreed to speak both before and after learning their APOE E4 status. The participants are identified only by first name to protect their privacy. Like many people in their 60s and 70s, Rubie has seen dementia up close. "My mother had Alzheimer's in the last stage of her life, and I've got friends and family that have Alzheimer's," she says. "It's a terrible sickness." Rubie wanted to do something to help researchers find a treatment for Alzheimer's. So she volunteered for the Generation Program, which is testing an experimental drug meant to prevent or delay the disease. © 2019 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: 26413 - Posted: 07.13.2019

Jon Hamilton The squiggly blue lines visible in the neurons are an Alzheimer's biomarker called tau. The brownish clumps are amyloid plaques. Courtesy of the National Institute on Aging/National Institutes of Health Alzheimer's disease begins altering the brain long before it affects memory and thinking. So scientists are developing a range of tests to detect these changes in the brain, which include an increase in toxic proteins, inflammation and damage to the connections between brain cells. The tests rely on biomarkers, shorthand for biological markers, that signal steps along the progression of disease. These new tests are already making Alzheimer's diagnosis more accurate, and helping pharmaceutical companies test new drugs. "For the future, we hope that we might be able to use these biomarkers in order to stop or delay the memory changes from ever happening," says Maria Carrillo, chief science officer of the Alzheimer's Association. (The association is a recent NPR sponsor.) The first Alzheimer's biomarker test was approved by the Food and Drug Administration in in 2012. It's a dye called Amyvid that reveals clumps of a protein called amyloid. These amyloid plaques are a hallmark of Alzheimer's. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26390 - Posted: 07.05.2019

Two nationally renowned neurosurgeons at Washington University School of Medicine in St. Louis will present “BrainWorks,” a live theatrical performance that explores the wonders of the human brain by dramatizing real-life neurological cases. The performance, comprised of four one-act plays, will debut July 19-21 at the Loretto-Hilton Center for the Performing Arts at Webster University. Albert Kim, PhD, MD, associate professor of neurological surgery, and Eric C. Leuthardt, MD, professor of neurological surgery, will guide the audience through each scene as they explain the mysteries of the human brain and the neuroscience of diseases such as Alzheimer’s disease, epilepsy, brain tumors and stroke. Kim and Leuthardt teamed up with playwrights from the New Dramatists to write each one-act play; the scenarios are based on patients the doctors have treated. “We have involved conversations about what’s going to happen – the course of treatment, the risks and benefits,” Kim said. “We also ensure the families become involved in those conversations. Together, the patient and family members become a part of the process that transforms and heals them. It’s this kind of conversation we want to bring to others through ‘BrainWorks.’” ©2019 Washington University in St. Louis

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26386 - Posted: 07.04.2019

Laura Sanders Immune cells can storm into the brains of older mice, where these normally helpful cells seem to be up to no good. The result, described July 3 in Nature, raises the possibility that immune cells may have a role in aging. Anne Brunet of Stanford University School of Medicine and colleagues studied gene activity to identify all sorts of cells in a particular spot in mice brains — the subventricular zone, where new nerve cells are born. Compared with young mice, old mice had many more killer T cells in that area. These immune system fighters take out damaged or infected cells in the rest of the body, but aren’t usually expected to show up in the brain. Experiments on postmortem human brain tissue suggest that a similar thing happens in old people. T cells were more abundant in tissue from people ages 79 to 93 than in tissue from people ages 20 to 44, the researchers found. In the brains of mice, killer T cells churn out a compound called interferon-gamma. This molecule might be responsible for the falling birthrate of new nerve cells that comes with old age, experiments on mice’s stem cells in dishes suggest. The results come amid a debate over whether human brains continue to make new nerve cells as adults (SN Online: 3/8/2018). If so, then therapies that shut T cells out of the brain might help keep nerve cell production rates high, even into old age — a renewal that might stave off some of the mental decline that comes with aging. |© Society for Science & the Public 2000 - 2019

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: 26385 - Posted: 07.04.2019

By Nicholas Bakalar Hormone therapy for prostate cancer is associated with an increased risk for dementia, a new study has found. Androgen deprivation therapy, or A.D.T., is used to treat prostate cancer of varying degrees of severity. It can significantly reduce the risk for cancer progression and death. The study, in JAMA Network Open, included 154,089 men whose average age was 74 and who had diagnoses of prostate cancer. Of these, 62,330 received A.D.T. and the rest did not. In an average follow-up of eight years, the scientists found that compared with men who had no hormone therapy, one to four doses of A.D.T. was associated with a 19 percent increased risk for both Alzheimer’s disease and other forms of dementia, and the risk increased with the number of doses. At five to eight doses the increased risk was 28 percent for Alzheimer’s and 24 percent for other dementias. The lead author, Ravishankar Jayadevappa, an associate professor at the University of Pennsylvania Perelman School of Medicine, said that for advanced cancer, A.D.T. can be a lifesaving treatment and should not be avoided because of any increased risk for dementia. But, he said, “Patients with localized cancer should be looking at the risks of dementia, and possibly avoiding A.D.T.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 26384 - Posted: 07.04.2019