Links for Keyword: Alzheimers

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Jon Hamilton Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one. Neuroscientists Robert Moir and Rudolph Tanzi were sipping Coronas in separate offices during "attitude adjustment hour" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system. Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. "I cruise wherever my fancy takes me," he says. And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain. One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized. These peptides are "extremely important," Moir says. "They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours." As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia. © 2018 npr

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: 24680 - Posted: 02.19.2018

By John Carroll, For years now the gold standard for R&D in Alzheimer’s disease has focused on generating convincing evidence that any new therapy being studied could slow the cognitive decline of patients and help preserve their ability to perform the kind of daily functions that can keep a patient independent for a longer period of time. That’s a hurdle no one has managed to clear for well over a decade. So now, with late-stage clinical failures piling up, the U.S. Food and Drug Administration (FDA) has set off down a path to adapt those standards as researchers are pushed inexorably into earlier and earlier forms of the disease, ahead of the brain damage inflicted by Alzheimer’s. In a set of draft guidances, the agency essentially proposed to offer an approval pathway for new drugs that could prevent the onset of the devastating symptoms of Alzheimer’s if drug developers could hit acceptable biomarkers that indicate the drug is working. And they’re likely going to continue with a new gold standard that will focus on long-term cognition alone, lowering the bar for drugs for an enormous and growing market. David Miller, the clinical vice president of Bracket, a Washington, D.C.-based tech provider which specializes in Alzheimer’s studies, tells me the draft guidance hit just after a meeting of the Washington, D.C.-based Alzheimer’s Association research group, which was discussing how you might be able to use a mix of markers for amyloid β and tau—two toxic proteins frequently cited as likely triggers—alongside neurodegenerative markers to identify patients who could be enrolled at a very early point in the disease. © 2018 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: 24674 - Posted: 02.17.2018

Aimee Cunningham Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine. The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques. Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear. One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients. |© Society for Science & the Public 2000 - 2018.

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: 24666 - Posted: 02.15.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

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: 24665 - Posted: 02.15.2018

The supplement nicotinamide riboside (NR) – a form of vitamin B3 – prevented neurological damage and improved cognitive and physical function in a new mouse model of Alzheimer’s disease. The results of the study, conducted by researchers at the National Institute on Aging (NIA) part of the National Institutes of Health, suggest a potential new target for treating Alzheimer’s disease. The findings appear in the Feb. 5, 2018, issue of Proceedings of the National Academy of Sciences. NR acts on the brain by normalizing levels of nicotinamide adenine dinucleotide (NAD+), a metabolite vital to cellular energy, stem cell self-renewal, resistance to neuronal stress and DNA repair. In Alzheimer’s disease, the brain’s usual DNA repair activity is impaired, leading to mitochondrial dysfunction, lower neuron production, and increased neuronal dysfunction and inflammation. “The pursuit of interventions to prevent or delay Alzheimer’s and related dementias is an important national priority,” said Richard J. Hodes, M.D., director of the NIA. “We are encouraging the testing of a variety of new approaches, and this study’s positive results suggest one avenue to pursue further.” Based on their studies in human postmortem brain, they developed a new strain of mice mimicking major features of human Alzheimer’s such as tau pathology, failing synapses, neuronal death and cognitive impairment. Using this animal model, the researchers tested the effects of an NR supplement by adding it to the drinking water of the mice. Over a three-month period, researchers found that mice who received NR showed reduced tau in their brains, but no change in amyloid-beta.

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: 24627 - Posted: 02.07.2018

Ina Jaffe A study published Monday by Human Rights Watch finds that about 179,000 nursing home residents are being given antipsychotic drugs, even though they don't have schizophrenia or other serious mental illnesses that those drugs are designed to treat. Most of these residents have Alzheimer's disease or another form of dementia and antipsychotics aren't approved for that. What's more, antipsychotic drugs come with a "black box warning" from the FDA, stating that they increase the risk of death in older people with dementia. The study concluded that antipsychotic drugs were often administered without informed consent and for the purpose of making dementia patients easier to handle in understaffed facilities. Researchers focused on six states, including California and Texas, which have the most skilled nursing facilities. They used publicly available data, along with hundreds of interviews with residents, families and state ombudsmen, the officials who deal with complaints about long term care facilities. In 2012, the federal government began a program to reduce the use of antipsychotic drugs in nursing homes, in partnership with the nursing home industry, and advocacy organizations. Since then, the use of the drugs has dropped by about a third nationwide, from 23.9 percent of residents in 2012 to 15.7 percent at the beginning of 2017. The Centers for Medicare and Medicaid Services have called for an additional 15 percent reduction by 2019 for those nursing homes that have lagged in curtailing their use of antipsychotics. © 2018 npr

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 24620 - Posted: 02.06.2018

Allison Aubrey To age well, we must eat well — there's been a lot of evidence that heart-healthy diets help protect the brain. The latest good news: A study recently published in Neurology finds that healthy seniors who had daily helpings of leafy green vegetables — such as spinach, kale and collard greens — had a slower rate of cognitive decline, compared to those who tended to eat little or no greens. "The association is quite strong," says study author Martha Clare Morris, a professor of nutrition science at Rush Medical College in Chicago. She also directs the Rush Institute for Healthy Aging. The research included 960 participants of the Memory and Aging Project. Their average age is 81, and none of them have dementia. Each year the participants undergo a battery of tests to assess their memory. Scientists also keep track their eating habits and lifestyle habits. To analyze the relationship between leafy greens and age-related cognitive changes, the researchers assigned each participant to one of five groups, according to the amount of greens eaten. Those who tended to eat the most greens comprised the top quintile, consuming, on average, about 1.3 servings per day. Those in the bottom quintile said they consume little or no greens. After about five years of follow-up/observation, "the rate of decline for [those] in the top quintile was about half the decline rate of those in the lowest quintile," Morris says. So, what's the most convenient way to get these greens into your diet? © 2018 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: 24615 - Posted: 02.05.2018

By Bret Stetka For the most part, clinical trials in Alzheimer’s disease have been woefully disappointing—failed drug after failed drug. Even colossal drugmaker Pfizer announced earlier this month that it will stop pursuing treatments for the disorder out of scientific and financial frustration. Yet a Japanese study published Jan. 31 in Nature reports on a screening test that could improve the success of Alzheimer’s drug research. The new findings suggest a simple blood test can accurately predict levels of a protein called amyloid beta in the brain that begins appearing early in the course of the disease before symptoms appear. Amyloid buildup is a key pathological feature of Alzheimer’s, and determining the degree to which someone’s brain is riddled with the molecule is essential for designing effective clinical trials. At the moment the only way to accurately measure amyloid in a living person is either via costly positron emission tomography imaging (PET scan) or by sampling cerebrospinal fluid (CSF) with a lumbar puncture, or spinal tap. A blood test would offer a cheaper, far less invasive means of determining a patient’s amyloid status. This could encourage more patients to enter clinical trials. It could also help researchers distinguish people with brewing Alzheimer’s from those with other forms of dementia. Senior study author Katsuhiko Yanagisawa, director general of the National Center for Geriatrics and Gerontology in Japan, is convinced that enough amyloid penetrates the blood–brain barrier to make its way into the bloodstream to be a useful measure of cognitive function. “We think amyloid blood tests could replace costly, invasive amyloid tests, especially when it comes to detecting preclinical Alzheimer’s,” he says. “We hope our biomarker better facilitates clinical trials for [Alzheimer’s] by improving enrollment of participants.” © 2018 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: 24600 - Posted: 02.01.2018

By Clare Wilson Two thin wires implanted in the brain may help treat Alzheimer’s disease by delivering electrical current. In the first test of this technique in people, two out of the three people who received the treatment showed less of a decline in their mental abilities than people at a similar stage of the disease who didn’t have the surgery. However, a larger randomised control trial is needed to know if the treatment really does work. The technique used is called deep brain stimulation, and is already used to treat the tremors and movement problems of some people with severe Parkinson’s disease. As well as having wires surgically inserted into the brain, recipients also get a power supply for the wires implanted under the skin near their collar bones. Depending on the current, the wires can either boost activity in nearby brain cells or reduce it. In Parkinson’s disease, they are used to turn down the excessive firing of discrete clusters of nerve cells that control movement. Alzheimer’s disease, however, is a less obvious target for such a treatment, because what causes this form of dementia is unknown. There has already been a small trial of brain stimulation using wires inserted into the brain’s memory centres, but this failed to help people with the condition. © Copyright New Scientist Ltd.

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: 24593 - Posted: 01.31.2018

LaVonne Moore has Alzheimer's disease, but her doctors hope her dementia symptoms could possibly be kept in check by a new type of treatment. Electric wires implanted deep in her brain stimulate areas involved with decision-making and problem-solving. Unlike many long-term dementia patients, LaVonne, 85, can cook meals, dress herself and organise outings. But it remains unclear whether her deep brain stimulation (DBS) therapy is responsible for her independence. DBS is already helping hundreds of thousands of patients with Parkinson's disease to overcome symptoms of tremor, but its use in Alzheimer's is still very experimental. Image copyright Ohio State University Only a small number of DBS studies have been done for Alzheimer's and they have focused on stimulating brain regions governing memory, rather than judgement. But Dr Douglas Scharre and colleagues at the Ohio State University Wexner Medical Center believe their approach, which targets the decision-making frontal lobe of the brain, might help patients keep their independence for longer. LaVonne's brain pacemaker was implanted three and a half years ago. Since then, her husband, Tom, from Delaware, Ohio, says her dementia has worsened - but more slowly than he had expected. "LaVonne has had Alzheimer's disease longer than anybody I know, and that sounds negative, but it's really a positive thing because it shows that we're doing something right." Two other patients have had the same treatment as LaVonne, but only one of them appeared to benefit significantly, according to the Journal of Alzheimer's Disease. Experts say it is too early to say if the treatment will help counteract cognitive decline. © 2018 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: 24589 - Posted: 01.30.2018

Paula Span When Ann Vandervelde visited her primary care doctor in August, he had something new to show her. Dr. Barak Gaster, an internist at the University of Washington School of Medicine, had spent three years working with specialists in geriatrics, neurology, palliative care and psychiatry to come up with a five-page document that he calls a dementia-specific advance directive. In simple language, it maps out the effects of mild, moderate and severe dementia, and asks patients to specify which medical interventions they would want — and not want — at each phase of the illness. “Patients stumble into the advanced stage of dementia before anyone identifies it and talks to them about what’s happening,” Dr. Gaster told me. “At what point, if ever, would they not want medical interventions to keep them alive longer? A lot of people have strong opinions about this, but it’s hard to figure out how to let them express them as the disease progresses.” One of those with strong opinions, it happens, was Ms. Vandervelde, 71, an abstract painter in Seattle. Her father had died of dementia years before, in a nursing home after her mother could no longer care for him at home. Ms. Vandervelde had also spent time with dementia patients as a hospice volunteer. Further, caring for her mother in her final year, Ms. Vandervelde had seen how family conflicts could flare over medical decisions. “I was not going to leave that choice to my children if I could spare them that,” she said. So when Dr. Gaster explained his directive, “it just made so much sense,” Ms. Vandervelde said. “While I could make these decisions, why not make them? I filled it out right there.” © 2018 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: 24545 - Posted: 01.20.2018

Nicola Davis The quest to develop drugs to treat Alzheimer’s disease has experienced a new setback, with a promising medication failing to show benefits in the latest series of clinical trials. Earlier trials had suggested that the drug idalopirdine, from the Danish international pharmaceutical company Lundbeck, might improve cognition in those with Alzheimer’s disease when taken alongside existing drugs – known as cholinesterase inhibitors – acting to improve symptoms rather than stopping the disease from developing. But the latest trials have dashed such hopes. “I was personally very excited,” said professor Clive Ballard, co-author of the study from the University of Exeter, pointing out that previous trials had appeared promising. “It is very disappointing that it then didn’t pan out.” Analysis This may be a turning point in treating neurodegenerative diseases Success in trials for Huntington’s and Spinal Muscular Atrophy, raises hopes that diseases such as Alzheimer’s and ALS could be tackled using a new class of drugs Read more Writing in the Journal of the American Medical Association, an international team of researchers report how they carried out three clinical trials involving a total of 2,525 participants in 34 countries, to explore the impact of idalopirdine. All participants were aged 50 years or older and had mild to moderate Alzheimer’s disease. © 2018 Guardian News and Media Limited

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: 24514 - Posted: 01.10.2018

By Meredith Wadman For the first time, scientists have produced evidence in living humans that the protein tau, which mars the brain in Alzheimer’s disease, spreads from neuron to neuron. Although such movement wasn’t directly observed, the finding may illuminate how neurodegeneration occurs in the devastating illness, and it could provide new ideas for stemming the brain damage that robs so many of memory and cognition. Tau is one of two proteins—along with β-amyloid—that form unusual clumps in the brains of people with Alzheimer’s disease. Scientists have long debated which is most important to the condition and, thus, the best target for intervention. Tau deposits are found inside neurons, where they are thought to inhibit or kill them, whereas β-amyloid forms plaques outside brain cells. Researchers at the University of Cambridge in the United Kingdom combined two brain imaging techniques, functional magnetic resonance imaging and positron emission tomography (PET) scanning, in 17 Alzheimer’s patients to map both the buildup of tau and their brains’ functional connectivity—that is, how spatially separated brain regions communicate with each other. Strikingly, they found the largest concentrations of the damaging tau protein in brain regions heavily wired to others, suggesting that tau may spread in a way analogous to influenza during an epidemic, when people with the most social contacts will be at greatest risk of catching the disease. © 2018 American Association for the Advancement of Science.

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: 24496 - Posted: 01.06.2018

Brian Mann When Bella Doolittle heard her diagnosis last February of early-onset Alzheimer's, she sat in the car outside the doctor's office and cried. "He said, 'Well, we figured out what's going on with you and this is it.' And I'm like, 'No it's not.' " Doolittle's husband, Will Doolittle, sits next to her on the couch, recalling how she grilled the doctor. "You asked, 'How long does this take? How long do I have?' And he said, 'On average, eight years.' That really upset you." "That really pissed me off," Bella says, laughing now at the memory. "Absolutely. I mean, I was pretty devastated. I'm like, eight years? I'm not even wrinkly yet." Researchers say as many as 200,000 Americans experience Alzheimer's younger than the typical age of 65, developing dementia-like symptoms in their 40s and 50s. For people like Bella, the diagnosis can feel overwhelming and bring feelings of shame. They fear losing memories, careers, and parts of their identity. Bella is a young-looking 59, wearing a T-shirt and a mop of red hair. On the day NPR visited her home in Glens Falls in upstate New York, where they raised four kids, Bella was in the kitchen making her signature Christmas gift. "It's homemade Kahlúa, the best you will ever drink," she says. "I have my vanilla beans imported from Madagascar." Bella Doolittle remembers how she first became aware that something was wrong. For a while before the diagnosis, she just felt "off." Her brain would get fuzzy and then it got worse. © 2018 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: 24478 - Posted: 01.02.2018

Laura Sanders Globs of an inflammation protein beckon an Alzheimer’s protein and cause it to accumulate in the brain, a study in mice finds. The results, described in the Dec. 21/28 Nature, add new details to the relationship between brain inflammation and Alzheimer’s disease. Researchers suspect that this inflammatory cycle is an early step in the disease, which raises the prospect of being able to prevent the buildup of amyloid-beta, the sticky protein found in brains of people with Alzheimer’s disease. “It is a provocative paper,” says immunologist Marco Colonna of Washington University School of Medicine in St. Louis. Finding an inflammatory protein that can prompt A-beta to clump around it is “a big deal,” he says. Researchers led by Michael Heneka of the University of Bonn in Germany started by studying specks made of a protein called ASC that’s produced as part of the inflammatory response. (A-beta itself is known to kick-start this inflammatory process.) Despite being called specks, these are large globs of protein that are created by and then ejected from brain immune cells called microglia when inflammation sets in. A-beta then accumulates around these ejected ASC specks in the space between cells, Haneke and colleagues now propose. Specks of a type of inflammation protein called ASC (red) form the core of amyloid-beta plaques (green) in the brain of a 4-month-old mouse (top) and in the brain of a person who had Alzheimer’s disease (bottom). |© Society for Science & the Public 2000 - 2017.

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: 24448 - Posted: 12.21.2017

By NICHOLAS BAKALAR Eating leafy greens may help slow mental decline. Researchers studied 960 men and women ages 58 to 99 who completed food frequency questionnaires and had two or more cognitive assessments over an average of almost five years of follow-up. Among many other foods, the researchers recorded the number of servings of lettuce, spinach, kale and collard greens. At least twice over the course of the study they administered cognitive tests covering memory, spatial ability and perceptual speed. Those who ate the most leafy vegetables — one to two servings a day — scored the equivalent of 11 years younger on tests of mental ability than those who ate little or none. Greens contain lutein, folate, beta carotene and other nutrients known to affect aging. Could the same effect be obtained with supplements containing these nutrients? Probably not. “The evidence for supplements is not positive, either from observational studies or clinical trials,” said the lead author, Martha Clare Morris, a professor of epidemiology at Rush University in Chicago. “The nutrients in food have many different forms and interactions. A specific formulation put in a pill with the same effect? That’s wishful thinking.” The study, in Neurology, controlled for smoking, physical activity and other factors, but it is observational, and does not prove cause and effect. © 2017 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: 24446 - Posted: 12.21.2017

/ By Rae Ellen Bichell In mid-October, Dr. David Bennett, a neurologist who directs the Alzheimer’s Disease Center at Rush University Medical Center in Chicago, stood in a St. Louis auditorium packed with nuns. His goal: To convince them — particularly the ones without brain disease — to donate their brains to science. “We are beginning to understand how little we actually know about the human brain.” Politicians, Bennett is fond of saying, can walk into a room and separate people from their money. “I can walk into a room and separate people from their brains.” To Bennett, making such acquisitions is, in some ways, more crucial than ever. Demand for brains for scientific research is rising across the board — driven in varying degrees by increased funding for research on brain disorders, rising incidence of age-related brain disease, big technological leaps in scientific tools used to analyze the brain, and a growing sense that sometimes, studying animals just isn’t good enough to understand and fix human disease. But more than this, scientists like Bennett are realizing that the brains they have traditionally studied (Bennett maintains 4,000 square feet of cabinets and freezers full of brain slices in Chicago), are too often riddled with the signs of end stage Alzheimer’s and other maladies that contribute to dementia. Far more rare are comparatively healthy brains that can allow scientists to more accurately identify what causes dementia — and what protects us from it. That deficiency now has Bennett and other scientists working hard to stock their shelves with a particularly precious resource: the brains of people like Sister Carleen Reck, who heard Bennett speak and thought his request for brain donations was a good idea, so she signed an anatomical gift act. Copyright 2017 Undark

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: 24417 - Posted: 12.11.2017

An analysis of more than 800,000 people has concluded that people who remain single for life are 42 per cent more likely to get dementia than married couples. The study also found that people who have been widowed are 20 per cent more likely to develop the condition, but that divorcees don’t have an elevated risk. Previous research has suggested that married people may have healthier lifestyles, which may help explain the findings. Another hypothesis is that married people are more socially engaged, and that this may protect against developing the condition. The stress of bereavement might be behind the increased risk in those who have been widowed. But marriage isn’t always good for the health. While men are more likely to survive a heart attack if they are married, single women recover better than those who are married. Journal reference: Journal of Neurology, Neurosurgery, and Psychiatry © Copyright New Scientist Ltd.

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: 24382 - Posted: 12.01.2017

By Shawna Williams Neurodegenerative diseases are tough nuts to crack, not just because of the inherent difficulties of sorting through what has gone awry, and why, but also due to a dearth of biomarkers that could help spot the diseases and track their progression. This inability to easily diagnose many forms of neurodegeneration means that the diseases can’t be treated early in their progression. The lack of biomarkers also hinders the certainty with which researchers running clinical trials can assess whether and how well experimental treatments of the diseases are working. A simple, noninvasive eye scan now being developed for Alzheimer’s disease (AD), however, may help address both shortcomings. AD researchers already utilize amyloid positron emission tomography (PET), in which tracers are injected into patients’ brains to make the disease’s characteristic amyloid plaques detectable by PET imaging. But the scans are very expensive, spurring the continuing hunt for biomarkers. “What we now know is that the disease essentially occurs about 20 years before a patient becomes symptomatic,” says Cedars-Sinai Medical Center neuroscientist and neurosurgeon Keith Black. “And by the time one is symptomatic, they’ve already lost a lot of their brain weight; they’ve already lost a significant number of brain cells; they’ve already lost a significant amount of connectivity.” What’s needed, he says, is a way to detect the disease early so it can be treated—with drugs, lifestyle interventions, or both—before it’s too late. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 24376 - Posted: 11.29.2017

By Linda Searing Benzodiazepines, also known as benzos, are drugs sometimes prescribed to ease the agitation, anxiety and insomnia often experienced by people with Alzheimer’s disease. Might these powerful medications have an effect beyond their sleep-inducing or calming properties? This study Researchers analyzed data on 31,140 adults with Alzheimer’s, most in their early 80s and predominantly women. The group included 10,380 people who started taking benzodiazepines (6,438), benzodiazepine-related “Z-drugs” (3,826) or both (116) after being diagnosed with Alzheimer’s. None of them had taken these drugs for at least a year before their diagnosis. Prescribed benzos included Valium, Librium, Ativan, Xanax, Restoril, Serax and one drug not approved for use in the United States. Prescribed Z-drugs were Ambien and one non-U.S. drug. Within six months of starting to take the medication, 1,225 people had died. Those taking benzos were 41 percent more likely to have died than were people who did not take these drugs, with the strongest mortality risk occurring within four months of starting the medication. No increased risk was linked to Z-drugs. Who may be affected? People with Alzheimer’s, which usually affects those 60 and older. The researchers noted that benzodiazepines and similar drugs have a stronger effect on the central nervous system of older people than of younger ones, and they have been shown to raise older people’s risk for hip fractures, pneumonia and stroke. Because of this, they wrote, “the observed association with an increased risk of death might result from these outcomes.” Today, about 5 million Americans are living with Alzheimer’s — a number that may triple in the next three decades. © 1996-2017 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: 24369 - Posted: 11.28.2017