Links for Keyword: Alzheimers

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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

Some commonly-prescribed drugs for depression, epilepsy and a few other conditions may increase a person's risk of dementia, according to researchers. The medicines, which belong to a family of drugs called anticholinergics, have already been linked to short-term problems with thinking. Now a large study of UK patients raises concerns about possible long-term brain side effects. Experts stress the findings, in JAMA Internal Medicine, external, do not prove there is a direct risk or mean that patients should come off the drugs. What are anticholinergics? Anticholinergic drugs block the action of a chemical messenger used by the brain to control signals around the body. Doctors prescribe them for a wide range of conditions and millions of people in the UK are on them. They can be used to treat overactive bladder, chronic obstructive pulmonary disease, depression, epilepsy, psychosis, Parkinson's disease and some allergies. These medications include some antidepressants, antipsychotics and muscle relaxants. What are the concerns? The study, led by Prof Carol Coupland at the University of Nottingham, included more than 58,000 people with dementia and 225,000 without the condition. The researchers looked at medication use going back over 20 years, before any dementia was diagnosed. This revealed the link between strong anticholinergic medications and increased risk of dementia in the people aged 55 and older. Only certain drugs in this class of medicine - antidepressants, anti-Parkinson drugs, antipsychotics, bladder drugs and epilepsy drugs - were implicated. © 2019 BBC.

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: 26355 - Posted: 06.25.2019

Brian Mann On a warm early summer day, Bella Doolittle sits on the doorstep of her house feeding biscuits to her dog Pepper. Bella was in her mid-50s when she was diagnosed with Alzheimer's. That was two years ago and the symptoms are advancing, with more memory loss and a new painful anxiety. "Have you ever watched a really terrible horror movie where you know any moment now someone's going to get torn to pieces in a very evil, painful way?" she says, describing the tension she often feels. These are the struggles and setbacks that Bella and Will Doolittle, her husband, talk about in their podcast, the Alzheimer's Chronicles. They say they decided to share their experiences because they know many couples and families are struggling with the same challenges. In all, more than 16 million Americans provide unpaid care for someone living with Alzheimer's or another form of dementia. On a recent episode, Bella and Will described how their life is getting harder, bit by bit. "It definitely has been a very tough period," she recounted. "I became almost suicidal. It was horrible." "Yeah, you were in bad shape," Will said. Anxiety medication is helping, but at times their podcasts are raw, vulnerable and intimate, recorded over their kitchen table. During each episode, they pull back the curtain on aspects of Bella's illness, but they've also been increasingly open about the inner workings of their two-decade long marriage. © 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: 26346 - Posted: 06.22.2019

By Christopher Rowland A team of researchers inside Pfizer made a startling find in 2015: The company’s blockbuster rheumatoid arthritis therapy Enbrel, a powerful anti-inflammatory drug, appeared to reduce the risk of Alzheimer’s disease by 64 percent. The results were from an analysis of hundreds of thousands of insurance claims. Verifying that the drug would actually have that effect in people would require a costly clinical trial — and after several years of internal discussion, Pfizer opted against further investigation and chose not to make the data public, the company confirmed. Researchers in the company’s division of inflammation and immunology urged Pfizer to conduct a clinical trial on thousands of patients, which they estimated would cost $80 million, to see if the signal contained in the data was real, according to an internal company document obtained by The Washington Post. “Enbrel could potentially safely prevent, treat and slow progression of Alzheimer’s disease,’’ said the document, a PowerPoint slide show that was prepared for review by an internal Pfizer committee in February 2018. The company told The Post that it decided during its three years of internal reviews that Enbrel did not show promise for Alzheimer’s prevention because the drug does not directly reach brain tissue. It deemed the likelihood of a successful clinical trial to be low. A synopsis of its statistical findings prepared for outside publication, it says, did not meet its “rigorous scientific standards.’’ The surprising reasons why drug prices in the U.S. are higher than in the rest of the world © 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: 26307 - Posted: 06.06.2019

/ By Jennie Erin Smith Piedad’s house sits above the cemetery in Girardota, Colombia, just north of Medellín. From her front porch, the view gives way to green hills, each home to hamlets with sugarcane plots and tile-roofed houses tucked in among the trees. One of these hillside hamlets is where Piedad and her 11 siblings grew up. Their father, Horacio, worked in cane fields and sugar mills, and their mother sold fruit from her orchard; their grandmother made pots from clay she dug across the river. When earthquakes destroyed their home in 1979, the family moved into town and left rural life behind. Why should two families with parallel mutations co-exist in one tiny corner of the Andes? Horacio showed the first symptoms of dementia soon afterward. He ignored the food he was served and got lost returning from church. He grew aggressive and delusional, and Piedad would return from her job at a sugar-packing plant to help bathe him, holding back tears as he kicked and punched. Horacio died in 1984 from what his doctors called senile dementia, the same disease that killed his father and three of his siblings. By the early 2000s, four of Piedad’s own siblings, then in their 40s and 50s, were showing signs of dementia. A local doctor referred them to a group of investigators in Medellín who studied families with a unique genetic mutation that causes early-onset Alzheimer’s disease. Nicknamed the Paisa mutation after the people of Colombia’s Antioquia region, who call themselves paisas, it occurred on a gene, called presenilin-1, implicated in familial Alzheimer’s. The families affected tended to be white farmers living in remote mountain towns that felt untouched by time. Copyright 2019 Undark

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: 26271 - Posted: 05.28.2019

By Simon Makin Something in elderly blood is bad for brains. Plasma from old mice or humans worsens cognition and biological indicators of brain health, when infused into young mice. Conversely, plasma from young mice (or humans) rejuvenates old brains. Much of this research has come from neurobiologist Tony Wyss-Coray’s group at Stanford University, which is pursuing what constituents of blood might be responsible. One previous study identified a protein, which declines with age, that has powerful beneficial effects. That protein can cross from the blood into the brain, but Wyss-Coray wondered how certain molecules contained in blood typically “talk” to the brain. Must they interact with brain cells directly, or can they communicate indirectly, through the gateway to the brain, the blood-brain barrier? To investigate, Wyss-Coray’s team tried a new approach in their latest study, published May 13 in Nature Medicine. “We reasoned that the most obvious way plasma would interact with the brain is through blood vessels,” Wyss-Coray says. “So, we looked at proteins that change with age and had something to do with the vasculature.” One protein that becomes more abundant with age, VCAM1, stood out, and the team showed that it appears to play a pivotal role in the effects of aged blood on the brain. Biological and cognitive measures alike indicated that blocking VCAM1 not only prevents old plasma from damaging young mouse brains but can even reverse deficits in old mice. The work has important implications for age-related cognitive decline and brain diseases. “Cognitive dysfunction in aging is one of our biggest biomedical challenges, and we have no effective medical therapies. None,” says neuroscientist Dena Dubal, of the University of California, San Francisco, who was not involved in the study. “It’s such an important line of investigation; it has tremendous implications.” © 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: 26237 - Posted: 05.15.2019

Jon Hamilton Scientists are setting a new course in their quest to treat Alzheimer's disease. The shift comes out of necessity. A series of expensive failures with experimental drugs aimed at a toxic protein called amyloid-beta have led to a change in approach. The most recent disappointment came in March, when drugmaker Biogen and its partner Eisai announced they were halting two large clinical trials of an amyloid drug called aducanumab. "It was like being punched in the stomach," says Phil Gutis, 57, an Alzheimer's patient in one of the trials. "Participating in this trial, it gave me hope for the future." Gutis, who once was a reporter for The New York Times and worked as an advocate at the American Civil Liberties Union, had hoped the experimental drug would preserve some of his remaining memories. "I'm just being erased," he says. The day before the aducanumab trial ended, Gutis had been leafing through pictures of his dog, Abe, a Jack Russell terrier who died last year. He was trying to remember the companion who'd shared his life for 12 years. © 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: 26208 - Posted: 05.04.2019

By James Gallagher Health and science correspondent, BBC News Dementia is the greatest health challenge of our time, the charity Alzheimer's Research UK has warned. Dementia was first described by the German doctor Alois Alzheimer in 1906 after he performed an autopsy on a woman with profound memory loss. What he found was a dramatically shrunken brain and abnormalities in and around nerve cells. At the time dementia was rare and was then barely studied for decades. But today somebody is diagnosed with it every three seconds, it is the biggest killer in some wealthier countries and is completely untreatable. So what is this disease? Why is it becoming more common? And is there any hope? Is dementia the same as Alzheimer's? No - dementia is a symptom found in many diseases of the brain. Memory loss is the most common feature of dementia, particularly the struggle to remember recent events. Other symptoms can include changes to behaviour, mood and personality, becoming lost in familiar places or being unable to find the right word in a conversation. It can reach the point where people don't know they need to eat or drink. Alzheimer's disease is by far the most common of the diseases that cause dementia. Others include vascular dementia, dementia with Lewy bodies, fronto-temporal dementia, Parkinson's disease dementia, amyotrophic lateral sclerosis and the newly discovered Late. © 2019 BBC

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: 26207 - Posted: 05.04.2019

Laura Sanders A newly described dementia strikes people in their last decades of life. The disease, aptly named LATE, comes with symptoms that resemble Alzheimer’s disease, but is thought to be caused by something completely different. An international team of scientists and clinicians describe the disease and officially christen it LATE, which stands for the more technical description, “limbic-predominant age-related TDP-43 encephalopathy,” online April 30 in Brain. Study coauthor Peter Nelson, a neuropathologist at the University of Kentucky in Lexington, helped organize a meeting last year that addressed a growing realization among doctors and scientists: “There’s this disease, and it doesn’t have a name,” he says. Estimates vary, but it’s possible that about a quarter of people age 85 and older have LATE, Nelson says. “This is a disease that really attacks the very latest portion of the human aging spectrum,” he says. LATE comes with memory trouble and dementia — symptoms that mirror Alzheimer’s, Nelson says. But instead of the plaques and tangles that mark the brains of people with Alzheimer’s disease, LATE is characterized by a lesser-known protein called TDP-43. In LATE, that protein accumulates and spreads through parts of the brain that are key to thinking and memory, including the amygdala and hippocampus. In Brain, Nelson and his colleagues describe the signs of LATE in the brain in a series of stages, from less severe to most severe. But the trouble is that these signs, which include the spread of TDP-43 and occasionally signs of damage to the hippocampus, can be found only after a person has died. There are currently no surefire clinical tests that identify LATE in a living person. |© 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: 26192 - Posted: 05.01.2019

By Lisa Sanders, M.D. “I don’t know where I am,” said a terrified voice on the phone. It was the woman’s husband, and he was scared. “I’m lost,” he said in a panicked tone. It’s O.K., she told him, sounding as calm and reassuring as she could. Her husband, a former high school English teacher in his 60s, left his mother-in-law’s that morning to return to their home several hours away in Pinon Hills, just north of San Bernardino, Calif. It was a route he drove often enough to know well. But after making his way through towns that seemed familiar, he lost his sense of how to get home. With her voice on the speakerphone, she guided him. His voice shook, and she knew he was crying. She wanted to cry, too, but forced herself to be the strength he needed. She still loved her husband, but he’d changed so much. Where was the man she married over 30 years ago? Twenty years earlier, he found out he had multiple sclerosis. It started with numbness in his arms and hands. Sometimes his vision would darken on the periphery, as if he were in a tunnel. And then, after a couple of hours or so, he’d be fine. He was referred to a local neurologist, who did some testing. An M.R.I. of his brain showed patchy white clouds among the normal gray swirls of brain. That finding was suggestive of multiple sclerosis. In M.S., the immune system goes awry and attacks the fatty sleeves that surround the nerves in the brain and spine; that’s what causes the characteristic M.R.I. findings. But it wasn’t a perfect fit. The fluid taken from his spine did not show the proteins that are usually seen in M.S. Moreover, while M.S. is characterized by episodes of unusual neurological symptoms that come and go, they usually last days or weeks rather than hours. Still, there are different forms of the disorder, and they can vary widely in symptom intensity and rate of progression. And there are few diseases that result in the M.R.I. findings and intermittent symptoms that this man had. Subsequent neurologists confirmed the diagnosis of M.S. © 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: 26191 - Posted: 05.01.2019

Nicola Davis Olfactory tests could help doctors spot older adults who are at greater risk of developing dementia, researchers say. The sense of smell is known to deteriorate with age. However, researchers have previously found it might also hint at health problems: older adults who struggle to identify odours have a greater chance of dying in the near future regardless of how old they are. Other studies have found older adults who have difficulties in identifying and remembering smells are more likely to have characteristics linked to a greater risk of developing Alzheimer’s disease even if there is no current sign of cognitive decline. Get Society Weekly: our newsletter for public service professionals Read more It is thought the sense of smell is one of the first faculties affected by certain neurodegenerative diseases. Now experts say they have probed further, and those diseases alone do not explain why a poor sense of smell might bode ill. “My suspicion is [the] process of smell in older adults probably has much broader potential health implications than what we already know about,” said Prof Honglei Chen, a co-author of the research from Michigan State University. He suggested it could be linked to conditions of the immune system and even psychiatric disorders. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 26184 - Posted: 04.30.2019

By Gina Kolata Allan Gallup, a retired lawyer and businessman, grew increasingly forgetful in his last few years. Eventually, he could no longer remember how to use a computer or the television. Although he needed a catheter, he kept forgetting and pulling it out. It was Alzheimer’s disease, the doctors said. So after Mr. Gallup died in 2017 at age 87, his brain was sent to Washington University in St. Louis to be examined as part of a national study of the disease. But it wasn’t just Alzheimer’s disease, the researchers found. Although Mr. Gallup’s brain had all the hallmarks — plaques made of one abnormal protein and tangled strings of another — the tissue also contained clumps of proteins called Lewy bodies, as well as signs of silent strokes. Each of these, too, is a cause of dementia. Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities. For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame. Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia. These questions strike at the very definition of Alzheimer’s disease. And if you can’t define the condition, how can you find a treatment? © 2019 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: 26125 - Posted: 04.09.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 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: 26101 - Posted: 04.01.2019

By Simon Makin Neurodegenerative diseases all involve the accumulation of toxic versions of naturally produced proteins in the brain. Multiple proteins are often abnormal in a patient, and the same aberrant protein can be involved in several different conditions. One common culprit is tau, which is abnormal in various conditions: chronic traumatic encephalopathy, a neurodegenerative disorder caused by repeated head trauma; a group of conditions known collectively as frontotemporal dementia; and, most famously, Alzheimer’s disease (AD). Normally, tau stabilizes structures inside neural connections, called microtubules, which facilitate chemical communication between cells. In disease states, tau is chemically altered, becoming misshapen and breaking away from microtubules. These toxic versions accumulate into structures called “neurofibrillary tangles,” which disrupt cells’ ability to communicate and may trigger other forms of damage, such as inflammation. Tau is involved in AD, but abnormalities in a different protein, amyloid-beta, are thought to be the initial trigger for a chain of biological events (including tau pathology) that underlies neurodegeneration. This is why most AD drugs developed to date have targeted amyloid, although tau has received increasing attention as multiple drugs intended to remove amyloid have failed. A new study, published Wednesday in Science Translational Medicine, suggests that an existing drug, lonafarnib, could be repurposed to treat neurodegenerative diseases that involve tau. A team of researchers, led by neuroscientist Kenneth Kosik of the University of California, Santa Barbara, found the drug had beneficial effects on tau-related pathology in mice, if administered early over an extended period. They also found evidence suggesting it works via a previously unknown biological mechanism. “This opens up a previously completely unsuspected pathway for tau degradation,” says Kosik, a longtime tau researcher. “We don’t have all the molecular details, but as a place to look, this is full of new opportunities.” © 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: 26093 - Posted: 03.29.2019

By Jennifer Couzin-Franke Earlier this week, the Lieber Institute for Brain Development, a nonprofit housed at Johns Hopkins University School of Medicine in Baltimore, Maryland, announced a new neuroscience research initiative that aims to tackle a gaping hole in medicine: the interplay between brain diseases and their genomic drivers among African-Americans. The goal is to better understand how brain diseases play out in this population, which has been profoundly underrepresented in neuroscience research. To build trust among African-Americans in Baltimore and eventually beyond, the venture includes a partnership with the African-American Clergy Medical Research Initiative, a group of clergy leaders in the city. African-American scientists at Lieber are already involved, but project leaders hope to engage those at other institutions as the work expands. The effort builds on Lieber’s rapidly growing brain bank, which now stands at about 3000 brains, with more than 400 new brains collected each year, all donated by next of kin. Many are from young and middle-aged people who die suddenly of suicide, drug overdose, or other causes. Although most of the brains are from people of European ancestry, more than 700 are from African-Americans. Despite growing recognition that African-Americans are underrepresented in medical research—and face discrimination and other hardships that can heighten health risks—study of brain diseases in this population have lagged behind, says Daniel Weinberger, the institute’s director. ScienceInsider spoke with Weinberger, a psychiatrist and schizophrenia researcher who came to the Lieber Institute in 2011 from the National Institute of Mental Health. The conversation has been edited for brevity and clarity. © 2019 American Association for the Advancement of Science

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: 26069 - Posted: 03.23.2019