Links for Keyword: Alzheimers

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By Minaz Kerawala, For years, gamers, athletes and even regular people trying to improving their memory have resorted, with electrified enthusiasm, to "brain zapping" to gain an edge. The procedure, called transcranial direct current stimulation (tDCS), uses a battery and electrodes to deliver electrical pulses to the brain, usually through a cap or headset fitted close to the scalp. Proponents say these currents are beneficial for a range of neurological conditions like Alzheimer's and Parkinson's diseases, stroke and schizophrenia, but experts are warning that too little is known about the safety of tDCS. "You might end up with a placement of electrodes that doesn't do what you think it does and could potentially have long-lasting effects," said Matthew Krause, a neuroscientist at the Montreal Neurological Institute. All functions of the brain—thought, emotion and coordination—are carried out by neurons using pulses of electricity. "The objective of all neuroscience is to influence these electrical processes," Krause said. The brain's activity can be influenced by drugs that alter its electrochemistry or by external external electric fields. While mind-altering headsets may seem futuristic, tDCS is not a new procedure. Much of the pioneering work in the field was done in Montreal by Dr. Wilder Penfield in the 1920s and 30s. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 22464 - Posted: 07.21.2016

By Maggie Koerth-Baker When former Tennessee women’s basketball coach Pat Summitt died Tuesday morning, news outlets, including ESPN, reported the cause of her death as “early-onset dementia, Alzheimer’s type.” That’s more than just a long-winded way of saying “Alzheimer’s.” By using five words instead of one, journalists were trying to point a big, flashing neon arrow at the complex realities of dementia. Dementia is more of a symptom than a diagnosis, and it can be caused by a number of different diseases. Even Alzheimer’s, the most common type of dementia, doesn’t seem to have a single cause. Instead, what ties Summitt to millions of other Alzheimer’s patients all over the world is the physical damage it wrought in her brain. Worldwide, 47.5 million people are living with some kind of dementia. Alzheimer’s represents 60 percent to 70 percent of those cases. Imagine a map of a city — roads branching out, intersecting with other roads, creating a network that allows mail to be delivered, food to be sold and brought home, people to get to their jobs. What would happen to that town if random intersections were suddenly barricaded and impassible? That’s the dystopian chaos Alzheimer’s causes, as damaged proteins clog the neurons and inhibit the flow of information from one neuron to another. Cut off from food, as well as data, the cells die. The brain shrinks. Eventually, the person dies, too. Afterward, doctors can cut into their brain and see the barriers, which are called plaques.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22426 - Posted: 07.12.2016

By Edd Gent, The devastating neurodegenerative condition Alzheimer's disease is incurable, but with early detection, patients can seek treatments to slow the disease's progression, before some major symptoms appear. Now, by applying artificial intelligence algorithms to MRI brain scans, researchers have developed a way to automatically distinguish between patients with Alzheimer's and two early forms of dementia that can be precursors to the memory-robbing disease. The researchers, from the VU University Medical Center in Amsterdam, suggest the approach could eventually allow automated screening and assisted diagnosis of various forms of dementia, particularly in centers that lack experienced neuroradiologists. Additionally, the results, published online July 6 in the journal Radiology, show that the new system was able to classify the form of dementia that patients were suffering from, using previously unseen scans, with up to 90 percent accuracy. [10 Things You Didn't Know About the Brain] "The potential is the possibility of screening with these techniques so people at risk can be intercepted before the disease becomes apparent," said Alle Meije Wink, a senior investigator in the center's radiology and nuclear medicine department. "I think very few patients at the moment will trust an outcome predicted by a machine," Wink told Live Science. "What I envisage is a doctor getting a new scan, and as it is loaded, software would be able to say with a certain amount of confidence [that] this is going to be an Alzheimer's patient or [someone with] another form of dementia." © 2016 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22425 - Posted: 07.12.2016

By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: 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: 22420 - Posted: 07.11.2016

By Nancy Stearns Bercaw In her memoir “Aliceheimer’s: Alzheimer’s Through the Looking Glass,” Dana Walrath uses drawings and stories to chronicle three years of caregiving for her mother, Alice, who was in the middle stages of Alzheimer’s disease. The experience turned out to be a magical trip down the rabbit hole of memory loss, an outcome that inspired Dr. Walrath, a medical anthropologist who taught at the University of Vermont College of Medicine and who also studied art and writing, to share their tale. Refusing to accept the dominant narrative of Alzheimer’s disease as a horror story, Dr. Walrath used the techniques of graphic medicine to create “Aliceheimer’s,” an 80-page, 35-picture tribute to her mother’s animated mind. Graphic medicine uses text and graphics to, as she writes in the book’s introduction, “let us better understand those who are hurting, feel their stories, and redraw and renegotiate those social boundaries.” We spoke with Dr. Walrath to learn more about graphic medicine, how the book came into being, and what it can teach others about caring for someone with Alzheimer’s disease. Here’s an edited excerpt of our conversation. Q. You say that “Aliceheimer’s” found you, not the other way around. What’s the backstory of your story? A. After a lifetime of mutually abrasive interaction, my mother moved into my home when a lock-down memory-care unit was her only other option. The years of living together not only brought us closure, but it also integrated my disparate career threads. Medical anthropology, creative writing, visual art — who knew they were connected? I sure didn’t. But Alice must have. During dementia, she said to me, “You should quit your job and make art full time.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22350 - Posted: 06.23.2016

By Aleszu Bajak Can the various puzzles and quizzes associated with commercial brain-training games really improve cognitive function — or better yet, stave off cognitive decline? To date, the scientific evidence is murky, but that hasn’t kept companies from trying to cash-in on consumers’ native desire for quick fixes to complex health problems. The most famous among such companies is probably Lumosity, a product of San Francisco-based Lumos Labs, which once marketed its suite of web-based games and mobile apps as being “built on proven neuroscience,” and by encouraging users to “harness your brain’s neuroplasticity and train your way to a brighter life.” Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Exercising your brain with online brain-training games like Lumosity (above) or Smart Brain Aging sounds like a great idea, but the science is still murky. Those claims were among several that attracted the attention of the Federal Trade Commission, which earlier this year filed a complaint against the company. Lumosity was ultimately slapped with $50 million in fines for deceiving consumers — although $48 million of that was reportedly suspended by a district court, because the company was financially unable to pay the full amount. “Lumosity preyed on consumers’ fears about age-related cognitive decline, suggesting their games could stave off memory loss, dementia, and even Alzheimer’s disease,” said Jessica Rich, Director of the FTC’s Bureau of Consumer Protection, in a statement accompanying the settlement. “But Lumosity simply did not have the science to back up its ads.” Copyright 2016 Undark

Related chapters from BP7e: 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: 22328 - Posted: 06.16.2016

By Sandra G. Boodman Richard McGhee and his family believed the worst was behind them. McGhee, a retired case officer at the Defense Intelligence Agency who lives near Annapolis, had spent six months battling leukemia as part of a clinical trial at MD Anderson Cancer Center in Houston. The experimental chemotherapy regimen he was given had worked spectacularly, driving his blood cancer into a complete remission. But less than nine months after his treatment ended, McGhee abruptly fell apart. He became moody, confused and delusional — even childish — a jarring contrast with the even-keeled, highly competent person he had been. He developed tremors in his arms, had trouble walking and became incontinent. “I was really a mess,” he recalled. Doctors suspected he had developed a rapidly progressive and fatal dementia, possibly a particularly aggressive form of Alzheimer’s disease. If that was the case, his family was told, his life span would be measured in months. Luckily, the cause of McGhee’s precipitous decline proved to be much more treatable — and prosaic — than doctors initially feared. “It’s really a pleasure to see somebody get better so rapidly,” said Michael A. Williams, a professor of neurology and neurosurgery at the University of Washington School of Medicine in Seattle. Until recently, Williams was affiliated with Baltimore’s Sinai Hospital, where he treated McGhee in 2010. “This was a diagnosis waiting to be found.”

Related chapters from BP7e: 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: 22293 - Posted: 06.07.2016

By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.

Related chapters from BP7e: 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: 22265 - Posted: 05.31.2016

By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,

Related chapters from BP7e: 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: 22257 - Posted: 05.28.2016

By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company

Related chapters from BP7e: 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: 22255 - Posted: 05.26.2016

By Emily Underwood One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia. Although this evidence won’t itself resolve the amyloid-tau debate, the finding could spur more research into new, tau-targeting treatments and lead to better diagnostic tools, researchers say. Scientists have long used an imaging technique called positron emission tomography (PET) to visualize ß-amyloid deposits marked by radioactive chemical tags in the brains of people with AD. Combined with postmortem analyses of brain tissue, these studies have demonstrated that people with AD have far more ß-amyloid plaques in their brains than healthy people, at least as a general rule. But they have also revealed a puzzle: Roughly 30% of people without any signs of dementia have brains “chock-full” of ß-amyloid at autopsy, says neurologist Beau Ances at Washington University in St. Louis in Missouri. That mystery has inspired many in the AD field to ask whether a second misfolded protein, tau, is the real driver of the condition’s neurodegeneration and symptoms, or at least an important accomplice. Until recently, the only ways to test that hypothesis were to measure tau in brain tissue after a person died, or in a sample of cerebrospinal fluid (CSF) extracted from a living person by needle. But in the past several years, researchers have developed PET imaging agents that can harmlessly bind to tau in the living brain. The more tau deposits found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team reports today in Science Translational Medicine. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: 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: 22210 - Posted: 05.12.2016

Patricia Neighmond Hoping to keep your mental edge as you get older? Look after your heart, a recent analysis suggests, and your brain will benefit, too. A research team led by Hannah Gardener, an epidemiologist at the University of Miami, analyzed a subset of data from the Northern Manhattan Study, a large, ongoing study of risk factors for stroke among whites, blacks and Hispanics living in the Washington Heights neighborhood of New York City. The scientists wanted to see how people in their 60s and 70s would do on repeated tests of memory and mental acuity six years later — and, specifically, what sort of subtle differences a heart-healthy lifestyle might make to the brain, beyond the prevention of strokes. Their findings appear in a recent issue of the Journal of the American Heart Association. In this particular study, the researchers started with more than a thousand people who'd had their cardiovascular health assessed using measures that the American Heart Association has dubbed Life's Simple 7. These seven factors known to benefit the heart and blood vessels include maintaining a normal body weight and good nutrition, not smoking, getting exercise regularly and keeping blood pressure, cholesterol and blood sugar levels under control. To measure thinking skills, Gardener's team used a variety of tests of memory, judgement, the ability to plan, mental quickness and other sorts of problem solving. The results were striking: Across all demographic groups, the people who had higher scores on the measures of cardiovascular health did better on the mental tests than those who scored low. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22167 - Posted: 05.02.2016

By n. r. kleinfield IT BEGAN WITH what she saw in the bathroom mirror. On a dull morning, Geri Taylor padded into the shiny bathroom of her Manhattan apartment. She casually checked her reflection in the mirror, doing her daily inventory. Immediately, she stiffened with fright. Huh? What? She didn’t recognize herself. She gazed saucer-eyed at her image, thinking: Oh, is this what I look like? No, that’s not me. Who’s that in my mirror? This was in late 2012. She was 69, in her early months getting familiar with retirement. For some time she had experienced the sensation of clouds coming over her, mantling thought. There had been a few hiccups at her job. She had been a nurse who climbed the rungs to health care executive. Once, she was leading a staff meeting when she had no idea what she was talking about, her mind like a stalled engine that wouldn’t turn over. “Fortunately I was the boss and I just said, ‘Enough of that; Sally, tell me what you’re up to,’” she would say of the episode. Certain mundane tasks stumped her. She told her husband, Jim Taylor, that the blind in the bedroom was broken. He showed her she was pulling the wrong cord. Kept happening. Finally, nothing else working, he scribbled on the adjacent wall which cord was which. Then there was the day she got off the subway at 14th Street and Seventh Avenue unable to figure out why she was there. So, yes, she had had inklings that something was going wrong with her mind. She held tight to these thoughts. She even hid her suspicions from Mr. Taylor, who chalked up her thinning memory to the infirmities of age. “I thought she was getting like me,” he said. “I had been forgetful for 10 years.”

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22160 - Posted: 04.30.2016

By PAM BELLUCK Alzheimer’s disease can seem frightening, mysterious and daunting. There are still a lot of unknowns about the disease, which afflicts more than five million Americans. Here are answers to some common questions: Sometimes I forget what day it is or where I put my glasses. Is this normal aging, or am I developing Alzheimer’s? Just because you forgot an item on your grocery list doesn’t mean you are developing dementia. Most people have occasional memory lapses, which increase with age. The memory problems that characterize warning signs of Alzheimer’s are usually more frequent, and they begin to interfere with safe or competent daily functioning: forgetting to turn off the stove, leaving home without being properly dressed or forgetting important appointments. Beyond that, the disease usually involves a decline in other cognitive abilities: planning a schedule, following multistep directions, carrying out familiar logistical tasks like balancing a checkbook or cooking a meal. It can also involve mood changes, agitation, social withdrawal and feelings of confusion, and can even affect or slow a person’s gait. How is Alzheimer’s diagnosed? Diagnosing Alzheimer’s usually involves a series of assessments, including memory and cognitive tests. Clinicians will also do a thorough medical work-up to determine whether the thinking and memory problems can be explained by other diagnoses, such as another type of dementia, a physical illness or side effects from a medication. Brain scans and spinal taps may also be conducted to check for corroborating evidence like the accumulation of amyloid, the hallmark protein of Alzheimer’s, in the brain or spinal fluid. The cause is unknown for most cases. Fewer than 5 percent of cases are linked to specific, rare gene mutations. Those are usually early-onset cases that develop in middle age. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22159 - Posted: 04.30.2016

By Esther Landhuis Peer inside the brain of someone with Alzheimer’s disease, and you’ll see some striking features: shriveled nerve cells and strange protein clumps. According to a leading theory, proteins called amyloid beta and tau build up in the brain and choke nerve cell communication, setting the disease in motion years before people suspect anything is wrong with their recall. Yet the Alzheimer’s brain has another curious aspect. Some of the clusters of toxic amyloid proteins are entangled with octopus-like immune cells called microglia, cells that live in the brain to clear unwanted clutter. By munching on amyloid plaques, microglia are thought to help keep the disease at bay. But these housekeeping cells have an additional role—they switch on inflammatory pathways. Inflammation is critically important when the immune system encounters infection or needs to repair tissue. If left unchecked, however, the inflammatory process churns out toxic substances that can kill surrounding cells, whose death triggers more inflammation and creates a vicious cycle. For years scientists have probed how neuroinflammation contributes to Alzheimer’s disease and other neurodegenerative ailments. Researchers face a number of immediate questions: Is neuroinflammation a driving force? Does it kick in when the disease is already underway and worsen the process? Could it be harnessed for good in the early stages? Those questions are far from settled, but research is starting to reveal a clearer picture. “It may not be the amyloid plaques themselves that directly damage neurons and the connections between them. Rather, it may be the immune reaction to the plaques that does the damage,” says Cynthia Lemere, a neuroscientist at Brigham and Women’s Hospital. Still, it is hard to say if microglia are good guys or bad, making it challenging to create therapeutics that target these cells. © 2016 Scientific American

Related chapters from BP7e: 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: 22124 - Posted: 04.21.2016

Nicola Davis The proportion of older people suffering from dementia has fallen by a fifth over the past two decades with the most likely explanation being because men are smoking less and living healthier lives, according to new scientific research. A team from three British universities concluded that as a result the number of new cases of dementia is lower than had been predicted in the 1990s, estimated at around 210,000 a year in the UK as opposed to 250,000. The findings are potentially significant because they suggest that it is possible to take preventative action, such as stopping smoking and reducing cholesterol, that could help avoid the condition. “Physical health and brain health are clearly highly linked,” said Carol Brayne of Cambridge University, who co-authored the study. Nick Fox, professor of neurology at University College, London, who was not involved in the study, agrees: “This does suggest that our risk, in any particular age in later life, can be reduced probably by what we do 10, 20 or 30 years before.” The scientists found that new cases of dementia had dropped from 20.1 in every 1,000 people per year in the first study conducted in the early 1990s to 17.7 in the second, which looked at new cases between 2008 and 2013. When sex and age differences were taken into account, the dementia rates were found to have dropped by 20%. The trend emerges from a dramatic drop in new cases for men across all age groups. In the 1990s study, for every 1,000 men aged 70-74, 12.9 went on to develop dementia within a year. In the second study, 20 years later, that figure had dropped to only 8.7 men. For men aged 65-69 the rate of new cases had more than halved between the two studies. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22122 - Posted: 04.20.2016

Scientists believe injections of a natural protein may lessen the symptoms and progress of Alzheimer's dementia after promising early trials in mice. The treatment - IL 33 - appeared to improve memory and help clear and prevent brain deposits similar to those seen in people with Alzheimer's. Tentative human studies of the treatment will soon begin, but experts say it will take many years to know if it could help patients in real life. The work is published in PNAS journal. Interleukin 33, or IL 33 for short, is made by the body as part of its immune defence against infection and disease, particularly within the brain and spinal cord. And patients with Alzheimer's have been found to have lower amounts of IL 33 in their brains than healthy adults. The researchers from the University of Glasgow and the Hong Kong University of Science and Technology tested what effect a boost of IL 33 might have on mice bred to have brain changes akin to Alzheimer's. The rodents rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week of having the injections. Prof Eddy Liew, who led the work at the University of Glasgow, is excited but cautious about his findings. "Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done." © 2016 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22115 - Posted: 04.19.2016

By Jordana Cepelewicz The brain relies on a system of chemical messengers, known as neurotransmitters, to carry missives from cell to cell. When all is well, these communications enable the brain to coordinate various functions, from complex thought to quick, knee-jerk reactions—but when the system is out of whack, serious disease or disorder can ensue. A team of researchers at the Technical University of Denmark (D.T.U.) and University of Oxford have for the first time identified the molecular structure of dopamine beta-hydroxylase (DBH), the enzyme that controls the conversion between dopamine and norepinephrine, two major neurotransmitters. Understanding the crystal structure of the enzyme could provide an ideal target for drug development. Dopamine and norepinephrine play key roles in many brain functions such as learning, memory, movement and the fight-or-flight response. Imbalances in the levels of these neurotransmitters—and the role DBH plays in regulating them—have been implicated in a wide range of disorders, including hypertension, congestive heart failure, anxiety, depression, post-traumatic stress disorder, Alzheimer’s, schizophrenia, Parkinson’s and even cocaine addiction. DBH has long intrigued biochemists but it has been challenging to perform the analyses needed to determine the protein’s structure. “This enzyme has been particularly difficult,” says Hans Christensen, a chemist at D.T.U. and the study’s lead researcher. “We tried many different expression systems before we finally succeeded. Now that we have the structure it is clear why—[it] is very intricate, with different parts of the enzyme interacting very tightly.” © 2016 Scientific American,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22087 - Posted: 04.09.2016

By Roni Caryn Rabin Alzheimer’s disease is a progressive brain disorder that causes dementia, destroying memory, cognitive skills, the ability to care for oneself, speak and walk, said Ruth Drew, director of family and information services at the Alzheimer’s Association. “And since the brain affects everything, Alzheimer’s ultimately affects everything,” she said, “including the ability to swallow, cough and breathe.” Once patients reach the advanced stages of Alzheimer’s, they may stop eating and become weak and susceptible to infections, said Dr. Jason Karlawish, a professor of medicine at the University of Pennsylvania. Unable to swallow or cough, they are at high risk of choking, aspirating food particles or water into the lungs and developing pneumonia, which is often the immediate cause of death, he said. “You see a general decline in the contribution the brain makes, not just in thinking, but in maintaining the body’s homeostasis,” Dr. Karlawish said. Using a feeding tube to nourish patients and hospitalizing them for infections does not significantly extend life at the advanced stages of the disease and is discouraged because it can prolong suffering with no hope of recovery, he said. Alzheimer's is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention, but that figure may underestimate the actual number of cases, Dr. Karlawish said, since some deaths may be attributed to other causes like pneumonia. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22071 - Posted: 04.06.2016

The mystery is starting to untangle. It has long been known that twisted fibres of a protein called tau collect in the brain cells of people with Alzheimer’s, but their exact role in the disease is unclear. Now a study in mice has shown how tau interferes with the strengthening of connections between neurons – the key mechanism by which we form memories. In healthy cells, the tau protein helps to stabilise microtubules that act as rails for transporting materials around the cell. In people with Alzheimer’s, these proteins become toxic, but an important unanswered question is what forms of tau are toxic: the tangles may not be the whole story. In the new study, Li Gan and her colleagues at the Gladstone Institute of Neurological Disease in San Francisco found that the brains of those with Alzheimer’s have high levels of tau with a particular modification, called acetylated tau. They then looked at what acetylated tau does in a mouse model of Alzheimer’s, finding that it accumulates at synapses – the connections between neurons. When we form memories, synapses become strengthened through extra receptors inserted into the cell membranes, and this heightens their response. But acetylated tau depletes another protein called KIBRA, which is essential for this synapse-strengthening mechanism. “We’re excited because we think we now have a handle on the link between tau and memory,” says Gan. “We’re also cautious because we know this may not be the only link. It’s still early days in understanding the mechanism.” © Copyright Reed Business Information Ltd.

Related chapters from BP7e: 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: 22064 - Posted: 04.04.2016