Links for Keyword: Alzheimers

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 1132

Sarah DeVos Targeting tangles of tau protein in mice with Alzheimer’s-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer’s disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer’s have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. “Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial,” says Tim Miller of Washington University in St Louis, Missouri. Now Miller’s team has purged tau tangles from the brains of Alzheimer’s-like mice for the first time. They used fragments of RNA called antisense oligonucleotides to sabotage the gene that makes tau, preventing it from being fully translated into protein. Once a day for four weeks, the team injected the antisense treatment, named Tau-ASO12, into the fluid at the base of each mouse’s spine. The mice had been genetically engineered to make a rogue form of tau similar to what is seen in people with Alzheimer’s, predisposing the mice to developing tau-related brain problems. The drug successfully spread throughout the brain, and was linked to a reduction in levels of tau that was made. It also seemed to destroy existing tau tangles, and prevent tau from spreading around the brain in older mice. © Copyright Reed Business Information Ltd.

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: 23148 - Posted: 01.26.2017

By Joshua A. Krisch At the core of Alzheimer’s disease are amyloid-beta (Aβ) peptides, which self-assemble into protein fibrils that form telltale plaques in the brain. Now, the results of a study published today (January 4) in Nature suggest that certain fibril formations are more likely to appear in cases of rapidly progressive Alzheimer’s disease, as opposed to less-severe subtypes. The findings increase scientists’ understanding of the structure of these fibrils, and may eventually contribute to new tests and treatments for Alzheimer’s disease. “It is generally believed that some form of the aggregated Aβ peptide leads to Alzheimer’s disease, and it’s conceivable that different fibril structures could lead to neurodegeneration with different degrees of aggressiveness,” said coauthor Robert Tycko, a principal investigator at the National Institute of Diabetes and Digestive Kidney Disease. “But the mechanism by which this happens is uncertain. Some structures may be more inert and benign. Others may be more inherently toxic or prone to spread throughout the brain tissue.” Prior research has demonstrated that Aβ fibrils with various molecular structures exhibit different levels of toxicity in neuronal cell cultures, a finding confirmed in subsequent mouse trials. One study even demonstrated that Aβ fibrils cultured from patients with rapidly progressive Alzheimer’s disease are different in size and resistance to chemical denaturation than those isolated from patients with more slowly progressing disease. Building on these observations, Tycko and colleagues set out to better characterize the structures of these fibrils and get a better handle on the potential correlations between structure and disease subtype. © 1986-2017 The Scientist

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: 23066 - Posted: 01.07.2017

By Gary Stix The last six months have witnessed the failure of two drugs in late-stage clinical trials for which the research community had high hopes. In truth, these new reports should not have come as too much of a surprise. Drug after drug continues to show little or no effect in helping the more than 5 million patients in the U.S. diagnosed with Alzheimer’s. Scientists who study neurodegenerative diseases have started to call for new approaches that go beyond targeting the amyloid in plaques and the tau in tangles, proteins that have been thought to be culprits in killing brain cells. One organization—The Alzheimer’s Drug Discovery Foundation (ADDF)—has for years provided funding to move untried ideas into clinical trials. Howard Fillit, the organization’s executive director, recently gave Scientific American his surprisingly optimistic view of where research and drug development for Alzheimer’s is headed. There have been recent failures of late-stage clinical trials and a figure often cited is that more than 99 percent of Alzheimer's drugs fail. Given all that, what level of confidence do you have for the field moving forward? There's a lot of reason for hope. There are over 130 different clinical trials going on now. I remember the days when there were none. We have had many failures. But I think one of the big advances that is creating hope is that we know how to do clinical trials better now. In a study that is being conducted by Biogen, everyone who was recruited into that study actually had Alzheimer's disease, for the first time. © 2017 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: 23062 - Posted: 01.06.2017

Hannah Devlin Science correspondent People living near a busy road have an increased risk of dementia, according to research that adds to concerns about the impact of air pollution on human health. Roughly one in 10 cases of Alzheimer’s in urban areas could be associated with living amid heavy traffic, the study estimated – although the research stopped short of showing that exposure to exhaust fumes causes neurodegeneration. Hong Chen, the scientist who led the work at Public Health Ontario, said: “Increasing population growth and urbanisation has placed many people close to heavy traffic, and with widespread exposure to traffic and growing rates of dementia, even a modest effect from near-road exposure could pose a large public health burden.” Previously, scientists have linked air pollution and traffic noise to reduced density of white matter (the brain’s connective tissue) and lower cognition. A recent study suggested that magnetic nano-particles from air pollution can make their way into brain tissue. The latest study, published in The Lancet, found that those who live closest to major traffic arteries were up to 12% more likely to be diagnosed with dementia – a small but significant increase in risk. The study, which tracked roughly 6.6 million people for more than a decade, could not determine whether pollution is directly harmful to the brain. The increased dementia risk could also be a knock-on effect of respiratory and cardiac problems caused by traffic fumes or due to other unhealthy life-style factors associated with living in built-up urban environments. © 2017 Guardian News and Media Limited

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: 23058 - Posted: 01.05.2017

By LISA FELDMAN BARRETT Think about the people in your life who are 65 or older. Some of them are experiencing the usual mental difficulties of old age, like forgetfulness or a dwindling attention span. Yet others somehow manage to remain mentally sharp. My father-in-law, a retired doctor, is 83 and he still edits books and runs several medical websites. Why do some older people remain mentally nimble while others decline? “Superagers” (a term coined by the neurologist Marsel Mesulam) are those whose memory and attention isn’t merely above average for their age, but is actually on par with healthy, active 25-year-olds. My colleagues and I at Massachusetts General Hospital recently studied superagers to understand what made them tick. Our lab used functional magnetic resonance imaging to scan and compare the brains of 17 superagers with those of other people of similar age. We succeeded in identifying a set of brain regions that distinguished the two groups. These regions were thinner for regular agers, a result of age-related atrophy, but in superagers they were indistinguishable from those of young adults, seemingly untouched by the ravages of time. What are these crucial brain regions? If you asked most scientists to guess, they might nominate regions that are thought of as “cognitive” or dedicated to thinking, such as the lateral prefrontal cortex. However, that’s not what we found. Nearly all the action was in “emotional” regions, such as the midcingulate cortex and the anterior insula. My lab was not surprised by this discovery, because we’ve seen modern neuroscience debunk the notion that there is a distinction between “cognitive” and “emotional” brain regions. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 23045 - Posted: 01.02.2017

Bret Stetka With a president-elect who has publicly supported the debunked claim that vaccines cause autism, suggested that climate change is a hoax dreamed up by the Chinese, and appointed to his Cabinet a retired neurosurgeon who doesn't buy the theory of evolution, things might look grim for science. Yet watching Patti Smith sing "A Hard Rain's a-Gonna Fall" live streamed from the Nobel Prize ceremony in early December to a room full of physicists, chemists and physicians — watching her twice choke up, each time stopping the song altogether, only to push on through all seven wordy minutes of one of Bob Dylan's most beloved songs — left me optimistic. Taking nothing away from the very real anxieties about future funding and support for science, neuroscience in particular has had plenty of promising leads that could help fulfill Alfred Nobel's mission to better humanity. In the spirit of optimism, and with input from the Society for Neuroscience, here are a few of the noteworthy neuroscientific achievements of 2016. One of the more fascinating fields of neuroscience of late entails mapping the crosstalk between our biomes, brains and immune systems. In July, a group from the University of Virginia published a study in Nature showing that the immune system, in addition to protecting us from a daily barrage of potentially infectious microbes, can also influence social behavior. The researchers had previously shown that a type of white blood cells called T cells influence learning behavior in mice by communicating with the brain. Now they've shown that blocking T cell access to the brain influences rodent social preferences. © 2016 npr

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 23041 - Posted: 12.31.2016

By Heather M. Snyder For more than 25 years, Mary Read was a successful nurse in Lititz, Pennsylvania. But in 2010, at the age of 50, she started having trouble with her memory and thinking, making it difficult for her to complete routine tasks and follow instructions at work. The problems worsened, bringing her career to an abrupt end. In 2011, her doctor conducted a comprehensive evaluation, including a cognitive assessment, and found that she was in the early stages of younger-onset Alzheimer’s, which affects hundreds of thousands of people under 65. A year earlier, Elizabeth Wolf faced another sort of upheaval. The 36-year-old community health program director was forced to abandon her own career, home and community in Vermont when both of her parents were diagnosed with Alzheimer’s three months apart. Wolf took the difficult decision to move back into her childhood home in Mount Laurel, New Jersey in order to become their primary caregiver. These stories are not unusual. Alzheimer’s dementia disproportionately affects women in a variety of ways. Compared with men, 2.5 times as many women as men provide 24-hour care for an affected relative. Nearly 19 percent of these wives, sisters and daughters have had to quit work to do so. In addition, women make up nearly two-thirds of the more than 5 million Americans living with Alzheimer’s today. According to the Alzheimer’s Association 2016 Alzheimer’s Disease Facts and Figures, an estimated 3.3 million women aged 65 and older in the United States have the disease. To put that number in perspective, a woman in her sixties is now about twice as likely to develop Alzheimer’s as breast cancer within her lifetime. © 2016 Scientific American

Related chapters from BP7e: 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: 23034 - Posted: 12.29.2016

Ian Sample Science editor The first subtle hints of cognitive decline may reveal themselves in an artist’s brush strokes many years before dementia is diagnosed, researchers believe. The controversial claim is made by psychologists who studied renowned artists, from the founder of French impressionism, Claude Monet, to the abstract expressionist Willem de Kooning. While Monet aged without obvious mental decline, de Kooning was diagnosed with Alzheimer’s disease more than a decade before his death in 1997. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Alex Forsythe at the University of Liverpool analysed more than 2,000 paintings from seven famous artists and found what she believes are progressive changes in the works of those who went on to develop Alzheimer’s. The changes became noticeable when the artists were in their 40s. Though intriguing, the small number of artists involved in the study means the findings are highly tentative. While Forsythe said the work does not point to an early test for dementia, she hopes it may open up fresh avenues for investigating the disease. The research provoked mixed reactions from other scientists. Richard Taylor, a physicist at the University of Oregon, described the work as a “magnificent demonstration of art and science coming together”. But Kate Brown, a physicist at Hamilton College in New York, was less enthusiastic and dismissed the research as “complete and utter nonsense”. © 2016 Guardian News and Media Limited

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: 23033 - Posted: 12.29.2016

Anna Gorman Rosemary Navarro was living in Mexico when her brother called from California. Something wasn't right with their mom, then in her early 40s. She was having trouble paying bills and keeping jobs as a food preparer in convalescent homes. Navarro, then 22, sold her furniture to pay for a trip back to the U.S. for herself and her two young children. Almost as soon as she arrived, she knew her mother wasn't the same person. "She was there but sometimes she wasn't there," she said. "I thought, 'Oh man this isn't going to be good.' " Before long, Navarro was feeding her mom, then changing her diapers. She put a special lock on the door to keep her from straying outside. Unable to continue caring for her, Navarro eventually moved her mom to a nursing home, where she spent eight years. Near the end, her mom, a quiet woman who had immigrated to the U.S. as a teenager and loved telenovelas, could communicate only by laughing or crying. Navarro was there when she took her last breath in 2009, at age 53. "What I went through with my mom I wouldn't wish on anyone," she said. Article continues after sponsorship It has happened again and again in her family — relatives struck by the same terrible disease, most without any clue what it was. An aunt, an uncle, a cousin, a grandfather, a great grandfather. "Too many have died," Navarro said. All in their early 50s. © 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: 23023 - Posted: 12.27.2016

Laura Sanders Flickering light kicks off brain waves that clean a protein related to Alzheimer’s disease out of mice’s brains, a new study shows. The results, described online December 7 in Nature, suggest a fundamentally new approach to counteracting Alzheimer’s. Many potential therapies involve drugs that target amyloid-beta, the sticky protein that accumulates in the brains of Alzheimer’s patients. In contrast, the new method used on mice causes certain nerve cells to fire at a specific rhythm, generating brain waves that researchers believe may clear A-beta. “This is a very creative and innovative new approach to targeting brain amyloid load in Alzheimer’s,” says geriatric psychiatrist Paul Rosenberg of Johns Hopkins Medicine. But he cautions that the mouse results are preliminary. Neuroscientist Li-Huei Tsai of MIT and colleagues saw that mice engineered to produce lots of A-beta don’t produce as many gamma waves in the hippocampus, a brain structure important for memory. Using a method called optogenetics, the researchers genetically designed certain nerve cells in the hippocampus to fire off signals in response to light. In this way, the researchers induced gamma waves — rhythmic firings 40 times per second. After just an hour of forced gamma waves, the mice had less A-beta in the hippocampus, the researchers found. Further experiments revealed that gamma waves packed a double whammy — they lowered A-beta by both reducing production and enhancing the brain’s ability to clear it. © Society for Science & the Public 2000 - 2016

Related chapters from BP7e: 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: 22966 - Posted: 12.08.2016

Alison Abbott & Elie Dolgin A drug that was seen as a major test of the leading theory behind Alzheimer’s disease has failed in a large trial of people with mild dementia. Critics of the ‘amyloid hypothesis’, which posits that the disease is triggered by a build-up of amyloid protein in the brain, have seized on the results as evidence of its weakness. But the jury is still out on whether the theory will eventually yield a treatment. Proponents of the theory note that the particular way in which solanezumab, the drug involved in the trial, works could have led to the failure, rather than a flaw in the hypothesis itself. And many trials are ongoing to test whether solanezumab — or others that target amyloid — could work in people at risk of the disease who have not yet shown symptoms, or even in people with Alzheimer’s, despite the latest negative result. “I’m extremely disappointed for patients, but this, for me, doesn’t change the way I think about the amyloid hypothesis,” says Reisa Sperling, a neurologist at the Brigham and Women’s Hospital in Boston, Massachusetts. She is leading one of several ongoing ‘prevention’ trials that is testing solanezumab, and other drugs that aim to reduce the build-up of amyloid ‘plaques’, in people at risk of developing Alzheimer’s. Solanezumab is an antibody that mops up amyloid proteins from the blood and cerebrospinal fluid. The proteins can go on to form plaques in the brain. Eli Lilly, the company that developed solanezumab, announced on 23 November that it would abandon the drug as a treatment for patients with mild dementia. The outcome adds to a long list of promising Alzheimer’s drugs that have flopped in the clinic, many of which, like solanezumab, targeted amyloid. © 2016 Macmillan Publishers 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: 22912 - Posted: 11.25.2016

By GINA KOLATA Despite fears that dementia rates were going to explode as the population grows older and fatter, and has more diabetes and high blood pressure, a large nationally representative survey has found the reverse. Dementia is actually on the wane. And when people do get dementia, they get it at older and older ages. Previous studies found the same trend but involved much smaller and less diverse populations like the mostly white population of Framingham, Mass., and residents of a few areas in England and Wales. The new study found that the dementia rate in Americans 65 and older fell by 24 percent over 12 years, to 8.8 percent in 2012 from 11.6 percent in 2000. That trend is “statistically significant and impressive,” said Samuel Preston, a demographer at the University of Pennsylvania who was not associated with the study. In 2000, people received a diagnosis of dementia at an average age of 80.7; in 2012, the average age was 82.4. “The dementia rate is not immutable,” said Dr. Richard Hodes, director of the National Institute on Aging. “It can change.” And that “is very good news,” said John Haaga, director of the institute’s division of behavioral and social research. It means, he said, that “roughly a million and a half people aged 65 and older who do not have dementia now would have had it if the rate in 2000 had been in place.” Keith Fargo, director of scientific programs and outreach at the Alzheimer’s Association, said the group had been encouraged by some of the previous research showing a decline but had also been “a little bit nervous” about drawing conclusions because the populations in the earlier studies were so homogeneous. Now, he said of the new data, “here is a nationally representative study. It’s wonderful news.” © 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: 22896 - Posted: 11.22.2016

Nicola Davis Smart bottles that dispense the correct dose of medication at the correct time, digital assistants, and chairs that know how long you’ve sat in them are among the devices set to change the face of care for those living with dementia. Dementia is now the leading cause of death in England and Wales, and is thought to affect more than 850,000 people in the UK. But a new wave of connected devices, dubbed “the internet of things”, could offer new ways to help people live independently for longer. “We have got an elderly population, and children in their 40s and 50s are looking after their elderly parents – and they may not have the capabilities to coordinate that care effectively,” said Idris Jahn, head of health and data at IoTUK, a programme within the government-backed Digital Catapult. While phone calls and text messages help to keep people in touch, says Jahn, problems can still arise, from missed appointments to difficulties in taking medication correctly. But he adds, connected sensors and devices that collect and process data in real time could help solve the problem. “For [people living with dementia] the sensors would be more in the environment itself, so embedded into the plug sockets, into the lights – so it is effectively invisible. You carry on living your life but in the background things will monitor you and provide feedback to people who need to know,” he said. “That might be your carer, it might be your family, it might be your clinician.” The approach, he added, has the potential to change the way care is given. “It is having that cohesive mechanism to put everyone into the loop, which I think hasn’t existed in the past and it is something that people need.” © 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: 22887 - Posted: 11.19.2016

By Alice Klein Alzheimer’s disease can be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer’s disease, the protein goes haywire, clumping together to form twisted tangles and, it is thought, releasing toxic chemicals that harm the brain. Now Lars Ittner at the University of New South Wales, Australia, and his colleagues have pinpointed a crucial enzyme that controls how tau proteins behave in the brain. The enzyme, called p38γ kinase, helps keep tau in a healthy, tangle-free state, preventing the onset of memory loss and other symptoms in mice that have been bred to develop Alzheimer’s disease. The enzyme seems to block Alzheimer’s by interfering with the action of another problem protein, called beta-amyloid. Like tau, clumps of this protein accumulate in the brains of people with Alzheimer’s, making it another suspected cause of the disease. When beta-amyloid forms these sticky plaques, it can also modify the structure of tau proteins, causing them to form tangles and release toxic chemicals. But Ittner’s team found that p38γ kinase makes a different kind of structural change to tau. If this change is made first, it prevents beta-amyloid from being able to turn tau bad, and mice do not develop the disease. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 22883 - Posted: 11.18.2016

By Jessica Hamzelou Having an agile mind in your 90s might sound like wishful thinking, but some people manage to retain youthful memories until their dying days. Now post mortems have revealed that these “superagers” manage to do this even when their brains have the hallmarks of Alzheimer’s diseases. Superagers have the memory and cognition of the average person almost half their age, and manage to avoid Alzheimer’s symptoms. Aras Rezvanian at Northwestern University in Chicago, Illinois, and his colleagues have been looking at brain samples donated by such people to try to understand what their secret might be. The group looked at eight brains, all from people who had lived into their 90s, and had memory and cognition scores of the average 50-year-old until their final days. Specifically, the team studied two brain regions – the hippocampus, which is involved in memory, and the prefrontal cortex, which is key for cognition. They found that the brain samples of the superagers had plaques and tangles in them to varying degrees. These are sticky clumps and twisted fibres of protein that seem to be linked to the death of neurons, and are usually found in the brains of people with Alzheimer’s disease after they die. Of the eight superager samples, two had such a high density and distribution of these proteins that they resembled the most severe cases of Alzheimer’s. © Copyright Reed Business Information Ltd.

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: 22868 - Posted: 11.15.2016

Kathleen Taylor The global rise in dementia should surprise no one. The figures — such as the 9.9 million new diagnoses each year — have been known for decades. As slow as we are to accept such vast changes on a personal, societal and political level, so research is slow to uncover why our brains become fragile with age. Neuroscientist and writer Kathleen Taylor's The Fragile Brain is about that research. But it is much more than a simple reflection on the best published hypotheses. Taylor has crafted a personal, astonishingly coherent review of our current state of knowledge about the causes of Alzheimer's disease and dementia, as well as possible solutions, from lifestyle adjustments to drug developments. Filled with elegant metaphors, her study covers the detail of molecular biology and larger-scale analysis, including epidemiological observations and clinical studies. It extends to dementia due to multiple sclerosis, stroke and encephalitis. For instance, some 5–30% of people who have a first stroke develop dementia. But the book's focus is Alzheimer's disease, and rightly so: it is what up to 80% of people with dementia are diagnosed with. Taylor begins with a shocking juxtaposition, setting the costs of age-related disorders and of dementia alongside the scarcity in funding. In Britain, Australia and the United States, for example, funding for dementia research is a fraction of that for cancer — in the United States, just 18%. She contextualizes with reflections on the history of dementia research, deftly unravelling the roles of pioneering scientists Alois Alzheimer, Franz Nissl and Emil Kraepelin in describing the condition. © 2016 Macmillan Publishers Limited,

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: 22851 - Posted: 11.10.2016

Elie Dolgin There are not a lot of things that could bring together people as far apart on the US political spectrum as Republican Newt Gingrich and Democrat Bob Kerrey. But in 2007, after leading a three-year commission that looked into the costs of care for elderly people, the political rivals came to full agreement on a common enemy: dementia. At the time, there were fewer than 30 million people worldwide diagnosed with the condition, but it was clear that the numbers were set to explode. By 2050, current predictions suggest, it could reach more than 130 million, at which point the cost to US health care alone from diseases such as Alzheimer’s will probably hit US$1 trillion per year in today’s dollars. “We looked at each other and said, ‘You know, if we don’t get a grip on Alzheimer’s, we can’t get anything done because it’s going to drown the system,’” recalls Gingrich, the former speaker of the US House of Representatives. He still feels that sense of urgency, and for good reason. Funding has not kept pace with the scale of the problem; targets for treatments are thin on the ground and poorly understood; and more than 200 clinical trials for Alzheimer’s therapies have been terminated because the treatments were ineffective. Of the few treatments available, none addresses the underlying disease process. “We’re faced with a tsunami and we’re trying to deal with it with a bucket,” says Gingrich. But this message has begun to reverberate around the world, which gives hope to the clinicians and scientists. Experts say that the coming wave can be calmed with the help of just three things: more money for research, better diagnostics and drugs, and a victory — however small — that would boost morale. © 2016 Macmillan Publishers 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: 22848 - Posted: 11.09.2016

By Simon Makin Cerebral autopsy specimen of a patient diagosed having Alzheimer Disease. In the HE stain numerous plaque formations within the neuropil background are visible. Credit: WIKIPEDIA, CC BY-SA 3.0 On Monday Pres. Barack Obama proclaimed November “National Alzheimer's Disease Awareness Month.” The administration’s ambitious goal is to prevent and treat Alzheimer's by 2025. Although there are currently no approved therapies that slow or stop progression of the disease, several approaches are showing promise. In a study published today in Science Translational Medicine, a team from Merck Research Laboratories reports results of early human and animal trials of a drug called verubecestat, which targets the production of protein plaques associated with the disease. “It's a summary of the discovery and early-stage profiling of what we hope is going to be a new therapeutic for Alzheimer's,” says team leader Matthew Kennedy. “It represents well over a decade of investment in this project by many, many scientists.” Definitive conclusions will have to await the results of larger, ongoing phase III clinical trials to assess their efficacy, effectiveness and safety, but the results are promising, experts say. Verubecestat is a so-called BACE1 inhibitor. BACE1 (for Beta-site Amyloid precursor protein Cleaving Enzyme 1, aka beta-secretase 1) is an enzyme involved in producing amyloid beta (Ab), a protein that clumps together, eventually forming the plaques surrounding neurons that are the disease's key hallmark. The amyloid hypothesis of Alzheimer's proposes that the accumulation of amyloid beta aggregates in the brain drives a cascade of biological events leading to neurodegeneration. By blocking BACE1, the hope is this approach could prevent the buildup of these clumps in the first place. But until now, development of these drugs has been hindered by problems finding molecules with the right characteristics, and concerns over theoretical and actual side effects. © 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: 22827 - Posted: 11.03.2016

By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,

Related chapters from BP7e: 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: 22754 - Posted: 10.13.2016

By Smitha Mundasad Health reporter People who experience frequent drops in blood pressure or dizziness when suddenly standing up are at increased risk of dementia, scientists say. Writing in Plos Medicine they suggest that less blood reaches the brain during these moments, leading to brain cell damage over time. Dementia experts say this is a "robust study" and "plausible explanation" that needs further investigation. Charities point out that factors such as smoking carry higher risks. But they say the work adds to growing evidence that changes in blood pressure have an impact on the brain. Previous studies have linked high blood pressure to types of dementia. But in this paper scientists focused on transient periods of low blood pressure - also known as postural hypotension - which become more common in older age. These episodes can sometimes leave people feeling dizzy or give them "head rushes" when standing up suddenly. Researchers from the Erasmus Medical Center, in the Netherlands, tracked 6,000 people for an average of 15 years. They found those who suffered repeated periods of low blood pressure on standing were more likely to develop dementia in the years that followed. Researcher Dr Arfan Ikram said: "Even though the effect can be seen as subtle - with an increased risk of about 4% for people with postural hypotension compared to those without it - so many people suffer from postural hypotension as they get older that it could have a significant impact on the burden of dementia across the world." He told the BBC: "If people experience frequent episodes of dizziness on standing, particularly as they get older, they should see their GPs for advice." © 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: 22753 - Posted: 10.13.2016