Links for Keyword: Alzheimers

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Scientists haven’t pinpointed a definitive cause for Alzheimer’s disease—a fatal brain disorder that robs people of their memory and cognitive abilities. But now researchers have uncovered an intriguing clue about why more women than men develop the condition. A particular gene variant, found in a quarter of the population and long known to raise people’s risk for the disease, seems less menacing in men, new research shows. The findings could have implications for potential gender-specific treatments, some Alzheimer’s investigators suggest. Though a small percentage of Alzheimer’s cases arise from genetic mutations that cause obvious disease before the age of 65, the vast majority of people who develop the condition do so later in life from undefined triggers, some thought to be genetic. In 1993, scientists found that people who inherit a gene variant called apolipoprotein E4 (APOE4) are more prone to the common form of Alzheimer’s that strikes in late life. There’s also a “risk-neutral” variant (APOE3) and a much rarer version of the gene (APOE2) that decreases a person’s risk for Alzheimer’s. Shortly thereafter, other research groups replicated the finding and some data hinted that APOE4 raises Alzheimer’s risk more in women than in men. Indeed, when scientists combed through a massive data set containing 5930 Alzheimer’s patients and 8607 dementia-free elderly from 40 independent studies, they reported in 1997 that females with the APOE4 variant were four times more likely to have Alzheimer’s compared with people with the more common, neutral form of the gene. However, in men, APOE4 seemed virtually harmless. “It was a pretty big effect,” says Michael Greicius, a neurologist at Stanford University Medical Center in California, of the analysis. Yet the findings didn’t create much of a stir at the time. © 2014 American Association for the Advancement of Science

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: 19490 - Posted: 04.15.2014

Want to live a long, dementia-free life? Stress your cells out. That’s the conclusion of a new study, which finds that heightened cellular stress causes brain cells to produce a protein that staves off Alzheimer’s disease and other forms of dementia. The work could lead to new ways to diagnose or treat such diseases. “This paper is very impressive,” says neuroscientist Li-Huei Tsai of the Massachusetts Institute of Technology in Cambridge, who was not involved in the new work. “It puts a finger on a particular pathway that can provide some explanation as to why some people are more susceptible to Alzheimer’s.” Alzheimer’s disease, characterized by a progressive loss of memory and cognition, affects an estimated 44.4 million people worldwide, mostly over the age of 65. The illness has been linked to the accumulation of certain proteins in the brain, but what causes symptoms has been unclear. That’s because the brains of some elderly people without dementia have the same clumps of so-called amyloid β and τ proteins typically associated with Alzheimer’s. The new study deals with a protein called repressor element 1-silencing transcription factor (REST), which turns genes and off. Scientists knew that REST played a key role in fetal brain development by controlling the activity of certain genes, but they thought it was absent in adult brains. However, when Bruce Yankner, a neurologist at Harvard Medical School in Boston, looked at all the genes and proteins that change in brains as people age, he found that REST levels begin increasing again when a person hits their 30s. Stumped as to why, he and his colleagues isolated human and mouse brain cells and probed what factors altered REST levels and what consequences those levels had. © 2014 American Association for the Advancement of Science

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: 19389 - Posted: 03.20.2014

By Maggie Fox and Erika Edwards Women are carrying the bigger burden of Alzheimer’s disease in the U.S., according to a new report — making up not only most of the cases, but paying more of the cost of caring for the growing population of people with the mind-destroying illness. The new report from the Alzheimer’s Association paints Alzheimer’s as a disease that disproportionately affects women, both as patients and as caregivers. It points out that women in their 60s are about twice as likely to develop Alzheimer’s over the rest of their lives as they are to develop breast cancer. “So women are at the epicenter of Alzheimer's disease today, not only by being most likely to be diagnosed with Alzheimer's, but also by being the caregiver most of the time,” said Maria Carrillo, vice president of the advocacy group. Alzheimer’s affects more than 5 million Americans, a number projected to soar to 13 million over the next 35 years. A study published earlier this year suggested it’s a big killer, taking down more than 500,000 Americans every year. Three out of five of those living with Alzheimer’s are women, the report finds. “The surprising statistic we pulled out of this report actually is that women over 65 have a one in six chance of developing Alzheimer's disease, in comparison to one out of 11 in men,” Carrillo said. And that compares to a one in eight lifetime risk for developing breast cancer.

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: 19381 - Posted: 03.19.2014

by Colin Barras Amyloid plaques, a hallmark of diseases like Alzheimer's, are bad news for humans – but they could have been drivers of the earliest life on Earth. A new study shows that these amyloid clusters can behave as catalysts, backing a theory that they helped trigger the reactions that sustain life, long before modern enzymes appeared. Without enzymes, life's metabolic reactions simply wouldn't occur. But making enzymes from scratch isn't easy. They are normally large, complicated proteins folded into a specific three-dimensional shape. It's difficult to see how these large proteins could have popped out of the primordial soup fully formed. Even if they did, nature faced another problem. There are 20 naturally occurring amino acids, which are the building blocks for all proteins, and each enzyme is made up of a unique sequence of at least 100 amino acids. This means there is a mind-bogglingly vast number – 20100 – of possible enzymes, each with a different amino acid sequence and a slightly different 3D structure. But very few of these 3D structures will work effectively as enzymes because they have to be an exact fit for the substrate they react with – in the same way that a lock can only be opened by one particular key. Even with millions of years to work at the problem, says Ivan Korendovych at Syracuse University in New York, nature would have struggled to build and test all possible enzyme molecules to identify the relatively few that catalyse today's metabolic reactions. © 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: 19372 - Posted: 03.17.2014

Alison Abbott A simple blood test has the potential to predict whether a healthy person will develop symptoms of dementia within two or three years. If larger studies uphold the results, the test could fill a major gap in strategies to combat brain degeneration, which is thought to show symptoms only at a stage when it too late to treat effectively. The test was identified in a preliminary study involving 525 people aged over 70. The work identified a set of ten lipid metabolites in blood plasma that distinguished with 90% accuracy between people who would remain cognitively healthy from those who would go on to show signs of cognitive impairment. “These findings are potentially very exciting,” says Simon Lovestone, a neuroscientist at the University of Oxford, UK, and a cordinator of a major European public-private partnership seekimg biomarkers for Alzheimer's. But he points out that only 28 participants developed symptoms similar to those of Alzheimer's disease during the latest work. “So the findings need to be confirmed in independent and larger studies.” There is not yet a good treatment for Alzheimer’s disease, which affects 35 million people worldwide. Several promising therapies have been tested in clinical trials over the last few years, but all have failed. However, those trials involved people who had already developed symptoms. Many neuroscientists fear that any benefits of a treatment would be missed in such a study, because it could be impossible to halt the disease once it has manifested. “We desperately need biomarkers which would allow patients to be identified — and recruited into trials — before their symptoms begin,” says Lovestone. © 2014 Nature Publishing Group,

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: 19340 - Posted: 03.10.2014

By Tara Bahrampour, Alzheimer’s disease likely plays a much larger role in the deaths of older Americans than is reported, according to a new study that says the disease may be the third-leading cause of death in the United States. The Centers for Disease Control and Prevention lists Alzheimer’s as the sixth-leading cause of death, far below heart disease and cancer. But the new report, published Wednesday in the medical journal of the American Academy of Neurology, suggests that the current system of relying on death certificates for causes misses the complexity of dying for many older people and underestimates the impact of Alzheimer’s. While the CDC attributed about 84,000 deaths in 2010 to Alzheimer’s, the report estimated that number to be 503,400 among people 75 and older. That puts it in a close third place, behind heart disease and cancer, and well above chronic lung disease, stroke and accidents, which rank third, fourth and fifth. Alzheimer’s is somewhat of a sleeping giant compared with other leading killers that have received more funding over the years. While deaths from these diseases have been going down thanks to better treatment and prevention, the number of people suffering from Alzheimer’s is quickly rising and the disease is always fatal. More than 5 million people in the United States are estimated to have Alzheimer’s. With the aging of the baby-boom generation, this number is expected to nearly triple by 2050 if there are no significant medical breakthroughs, according to the Alzheimer’s Association. © 1996-2014 The Washington Post

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: 19326 - Posted: 03.06.2014

Ian Sample, science correspondent, in Chicago Regular brisk walks can slow down the shrinking of the brain and the faltering mental skills that old age often brings, scientists say. Studies on men and women aged 60 to 80 found that taking a short walk three times a week increased the size of brain regions linked to planning and memory over the course of a year. The prefrontal cortex and hippocampus increased in size by only 2% or 3%, but that was enough to offset the steady shrinkage doctors expected to see over the same period. "It may sound like a modest amount but that's actually like reversing the age clock by about one to two years," said Professor Kirk Erickson, a neuroscientist at the University of Pittsburgh. "While the brain is shrinking, we actually saw not a levelling out but an increase in the size of these regions. It was better than before we started the study." People who took part in the study scored higher on spatial memory tests, and some reported feeling more mentally alert, according to Erickson. "They feel better, they feel as if the fog has lifted. Anecdotally, it seems to benefit these cognitive functions," he said. Erickson recruited more than 100 adults who confessed to doing little if any exercise in their daily lives. Half were randomly assigned to walk for 30 to 45 minutes three days a week. The rest spent a similar amount of time doing stretching exercises. Medical scans showed minor increases in the two brain regions in both groups. But the effect was greater in the walkers, Erickson said at the annual meeting of the American Association for the Advancement of Science. © 2014 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: 19271 - Posted: 02.20.2014

|By Annie Sneed Alzheimer’s disease is now the sixth leading cause of death in the U.S., but researchers still do not know what causes the degenerative neurological disorder. In recent years they have pinpointed several genes that seem largely responsible for those cases in which the disorder develops early on, prior to age 60. They have also identified about 20 genes that can increase or decrease risk for the more common late-onset variety that starts appearing in people older than 60. But genetics simply cannot explain the whole picture for the over five million Americans with late-onset Alzheimer’s. Whereas genetics contribute some risk of developing this version of the disorder, no combination of genes inevitably leads to the disease. Scientists are now urgently searching for the other missing pieces to explain what causes late-onset Alzheimer’s. Some researchers have shifted their attention from genes to the environment—especially to certain toxins. Their studies of pesticides, food additives, air pollution and other problematic compounds are opening a new front in the battle against this devastating malady. Here’s a roundup of some of the possibilities being studied: Scientists have already found a strong potential link between pesticides and Parkinson’s disease. Now, a preliminary study released in January suggests that the pesticide DDT, which degrades so slowly that it continues to linger in the environment more than 40 years after the U.S. Environmental Protection Agency banned its use in the U.S., may also contribute to Alzheimer’s. © 2014 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: 19236 - Posted: 02.11.2014

|By Geoffrey Giller Working memory—our ability to store pieces of information temporarily—is crucial both for everyday activities like dialing a phone number as well as for more taxing tasks like arithmetic and accurate note-taking. The strength of working memory is often measured with cognitive tests, such as repeating lists of numbers in reverse order or recalling sequences of dots on a screen. For children, performance on working memory assessments is considered a strong predictor for future academic performance. Yet cognitive tests can fail to identify children whose brain development is lagging in subtle ways that may lead to future deficits in working memory and, thus, in learning. Doctors give the tests periodically and plot the results along a development curve, much like a child’s height and weight. By the time these tests reveal that a child’s working memory is below average, however, it may be too late to do much about it. But in a new study, published January 29 in The Journal of Neuroscience, scientists demonstrated that they could predict the future working memory of children and adolescents by examining brain scans from two different types of magnetic resonance imaging (MRI), instead of looking only at cognitive tests. Henrik Ullman, a PhD student at the Karolinska Institute in Stockholm and the lead author on the paper, says that this was the first study attempting to use MRI scans to predict future working memory capacity. “We were pretty surprised when we found what we actually found,” Ullman says. © 2014 Scientific American,

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: 19209 - Posted: 02.05.2014

One thing marijuana isn’t known to do is improve your memory. But there’s another reason why scientists believe it could fight Alzheimer’s disease. Gary Wenk, PhD, professor of neuroscience, immunology and medical genetics at Ohio State University, has studied how to combat brain inflammation for over 25 years. His research has led him to a class of compounds known as cannabinoids, which includes many of the common ingredients in marijuana. He says, throughout all of his research, cannabinoids have been the only class of drugs he’s found to work. What’s more, he believes early intervention may be the best way of fighting Alzheimer’s. Dr. Wenk doesn’t see cannabinoids – or anything else – as a cure. But he took the time to discuss with us how marijuana might prevent the disorder from developing. Q: What’s so important about brain inflammation? Over the past few years, there’s been a focus on inflammation in the brain as causing a lot more than Alzheimer’s. We now know it plays a role in ALS, Parkinson’s disease, AIDS, dementia, multiple sclerosis, autism, schizophrenia, etc. We’re beginning to see that inflammation in the brain, if it lasts too long, can be quite detrimental. And if you do anything, such as smoke a bunch of marijuana in your 20s and 30s, you may wipe out all of the inflammation in your brain and then things start over again. And you simply die of old age before inflammation becomes an issue for you. © 2013-2014 All rights reserved

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19207 - Posted: 02.05.2014

By Ariana Eunjung Cha, The National Institutes of Health is undertaking an ambitious collaboration with private industry in an attempt to speed up the search for treatments for some of the world’s most devastating diseases — Alzheimer’s, type 2 diabetes, rheumatoid arthritis and lupus. The pilot projects announced Tuesday will involve the sharing of not only scientists but also of data, blood samples and tissue specimens among 10 rival companies, the federal government and several nonprofit groups and research foundations. The companies that have signed up to participate include most of the large drug makers, which in the past had resisted calls to share detailed data and samples from experiments, preferring to instead use the information to gain lucrative patents. The agreement with NIH represents a major break from how they used to do business. The competing pharmaceutical companies have said they will hold off launching commercial ventures based on discoveries from the partnership until after the data has been made publicly available. The idea behind the collaboration is similar to that of the “open source” movement among some computer scientists who believe that sharing their code with anyone who wants it is the best way to innovate. The first group of projects, which will last three to five years, will involve an investment of more than $230 million from industry participants including Bristol-Myers Squibb, GlaxoSmithKline, Johnson & Johnson, Eli Lilly, Merck, Pfizer, Sanofi and Takeda, as well as a few smaller biotech companies. © 1996-2014 The Washington Post

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: 19206 - Posted: 02.05.2014

By James Gallagher Health and science reporter, BBC News Exposure to a once widely used pesticide, DDT, may increase the chances of developing Alzheimer's disease, suggest US researchers. A study, published in JAMA Neurology, showed patients with Alzheimer's had four times the levels of DDT lingering in the body than healthy people. Some countries still use the pesticide to control malaria. Alzheimer's Research UK said more evidence was needed to prove DDT had a role in dementia. DDT was a massively successful pesticide, initially used to control malaria at the end of World War Two and then to protect crops in commercial agriculture. However, there were questions about its impact on human health and wider environmental concerns, particularly for predators. It was banned in the US in 1972 and in many other countries. But the World Health Organization still recommends using DDT to keep malaria in check. Not clear DDT also lingers in the human body where it is broken down into DDE. The team at Rutgers University and Emory University tested levels of DDE in the blood of 86 people with Alzheimer's disease and compared the results with 79 healthy people of a similar age and background. The results showed those with Alzheimer's had 3.8 times the level of DDE. However, the picture is not clear-cut. Some healthy people had high levels of DDE while some with Alzheimer's had low levels. Alzheimer's also predates the use of DDT. The researchers believe the chemical is increasing the chance of Alzheimer's and may be involved in the development of amyloid plaques in the brain, a hallmark of the disease, which contribute to the death of brain cells. BBC © 2014

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: 19177 - Posted: 01.28.2014

A new website that helps determine whether someone might have Alzheimer's disease or dementia is so popular that the site crashed temporarily. Ohio State University's website says its Self-Administered Gerocognitive Exam (SAGE) is a test that can be done in your own home with a paper and pencil. When researchers visited 45 community events where they asked people to take the simple test, they found that of the 1, 047 who did it, 28 per cent were identified with cognitive impairment, test developer Dr. Douglas Scharre of Ohio State and his team reported Monday in The Journal of Neuropsychiatry and Clinical Neurosciences. Alzheimer's test Researchers in Ohio say the SAGE test has been shown to be effective in spotting the early signs of cognitive decline. (Ohio State University Wexner Medical Center) Participants were told the test represented their baseline level, which doctors could use for future comparisons during re-screening. "What we found was that this SAGE self-administered test correlated very well with detailed cognitive testing," Scharre said in a release. "If we catch this cognitive change really early, then we can start potential treatments much earlier than without having this test." The Alzheimer Society of Canada says early diagnosis can help with planning, care and support. © CBC 2014

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: 19137 - Posted: 01.16.2014

Training to improve cognitive abilities in older people lasted to some degree 10 years after the training program was completed, according to results of a randomized clinical trial supported by the National Institutes of Health. The findings showed training gains for aspects of cognition involved in the ability to think and learn, but researchers said memory training did not have an effect after 10 years. The report, from the Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study, appears in the January 2014 issue of the Journal of the American Geriatrics Society. The project was funded by the National Institute on Aging (NIA) and the National Institute of Nursing Research (NINR), components of the NIH. “Previous data from this clinical trial demonstrated that the effects of the training lasted for five years,” said NIA Director Richard J. Hodes, M.D. “Now, these longer term results indicate that particular types of cognitive training can provide a lasting benefit a decade later. They suggest that we should continue to pursue cognitive training as an intervention that might help maintain the mental abilities of older people so that they may remain independent and in the community.” “ACTIVE is an important example of intervention research aimed at enabling older people to maintain their cognitive abilities as they age,” said NINR Director Patricia Grady, Ph.D. “The average age of the individuals who have been followed over the last 10 years is now 82. Given our nation’s aging population, this type of research is an increasingly high priority.”

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: 19126 - Posted: 01.14.2014

By Gary Stix The blood-brain barrier is the Berlin Wall of human anatomy and physiology Its closely packed cells shield neurons and the like from toxins and pathogens, while letting pass glucose and other essential chemicals for brain metabolism (caffeine?). For years, pharmaceutical companies and academic researchers have engaged in halting efforts to traverse this imposing blockade in order to deliver some of the big molecules that might potentially help slow the progression of devastating neurological diseases. Like would-be refugees from the former East Germany, many medications get snagged by border guards during the crossing—a molecular security force that either impedes or digests any invader. There have been many attempts to secure safe passage—deploying chemicals that make brain-barrier “endothelial” cells shrivel up, or wielding tiny catheters or minute bubbles that slip through minuscule breaches. Success has been mixed at best—none of these molecular cargo carriers have made their way as far as human trials. Roche, the Swiss-based drugmaker, reported in the Jan. 8 Neuron a bit of progress toward overcoming the lingering technical impediments. The study described a new technique that tricks one of the BBB’s natural checkpoints to let through an elaborately engineered drug that attacks the amyloid-beta protein fragments that may be the primary culprit inflicting the damage wrought by Alzheimer’s. The subterfuge involves the transferrin receptor, a docking site used to transport iron into the brain. Roche took a fragment of an antibody that binds the transferrin receptor and latched it onto another antibody that, once on the other side of the BBB, attaches to and then removes amyloid. © 2014 Scientific American

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: 19121 - Posted: 01.13.2014

By PAM BELLUCK Does vitamin E help people with Alzheimer’s disease? For years, scientists have been trying to find out, guessing that the vitamin’s antioxidant properties might be beneficial. But the results from clinical trials have been mixed and — following a report that high doses of vitamin E may increase the risk of death — cautionary. Now a study suggests that vitamin E supplements may be good for some Alzheimer’s patients after all. The benefit was not huge, but for a devastating disease that has proved almost impervious to treatment, it was notable. The study, published in Wednesday’s issue of JAMA, The Journal of the American Medical Association, found that over a little more than two years, high-dose vitamin E slowed the decline of people with mild to moderate Alzheimer’s by about six months on average. Vitamin E did not delay cognitive or memory deterioration, however. Instead, it seemed to temporarily protect something many patients consider especially valuable: their ability to perform daily activities like putting on clothes and feeding themselves. Compared with other study participants, people who took vitamin E also required about two fewer hours of help from caregivers per day, the researchers said. “Is it really going to dramatically alter the lives of Alzheimer’s patients? That’s unclear,” said Dr. Scott Small, director of Columbia University’s Alzheimer’s Disease Research Center, who was not involved in the study. “But it might improve patients’ ability to bathe themselves and dress themselves.” © 2014 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: 19086 - Posted: 01.02.2014

By Regina Harrell and Pulse, I am a primary-care doctor who makes house calls in and around Tuscaloosa, Ala. Today my rounds start at a house located down a dirt road a few miles outside town. Gingerly, I cross the front walk; Mrs. Edgars told me that she killed a rattlesnake in her flowerbed last year. She is at the door, expecting my visit. Mr. Edgars sits on the couch, unable to recall that I am his doctor, or even that I am a doctor, but happy to see me nonetheless. We chat about the spring garden and the rain, then we move on to Mr. Edgars’s arthritis. Earlier on in his dementia, he wandered the woods, and his wife was afraid he would get lost and die, although the entire family agreed that this was how he would want it. Now, in a strange twist, his knee arthritis has worsened enough that it has curtailed his wanderings. I suspect that Mrs. Edgars is undertreating the pain to decrease the chance that he’ll wander off again. We talk about how anxious he grows whenever she’s out of his sight and how one of his children comes to sit with him so that she can run errands. She shows me a quilt remnant found in a log cabin on their property; it likely belonged to her husband’s grandfather, making the rough-edged fabric about a century old. I leave carrying a parting gift from her — a jar of homegrown pickled okra. When I get back to the office, I turn on the computer to write a progress note in Mr. Edgars’s electronic health record, or EHR. In addition to recording the details of our visit, I must try to meet the new federal criteria for “meaningful use,” criteria that have been adopted by my office with threats that I won’t get paid for my work if I don’t. © 1996-2013 The Washington Post

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: 19067 - Posted: 12.24.2013

A study in mice shows how a breakdown of the brain’s blood vessels may amplify or cause problems associated with Alzheimer’s disease. The results published in Nature Communications suggest that blood vessel cells called pericytes may provide novel targets for treatments and diagnoses. “This study helps show how the brain’s vascular system may contribute to the development of Alzheimer’s disease,” said study leader Berislav V. Zlokovic, M.D. Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of the University of Southern California, Los Angeles. The study was co-funded by the National Institute of Neurological Diseases and Stroke (NINDS) and the National Institute on Aging (NIA), parts of the National Institutes of Health. Alzheimer’s disease is the leading cause of dementia. It is an age-related disease that gradually erodes a person’s memory, thinking, and ability to perform everyday tasks. Brains from Alzheimer’s patients typically have abnormally high levels of plaques made up of accumulations of beta-amyloid protein next to brain cells, tau protein that clumps together to form neurofibrillary tangles inside neurons, and extensive neuron loss. Vascular dementias, the second leading cause of dementia, are a diverse group of brain disorders caused by a range of blood vessel problems. Brains from Alzheimer’s patients often show evidence of vascular disease, including ischemic stroke, small hemorrhages, and diffuse white matter disease, plus a buildup of beta-amyloid protein in vessel walls. Furthermore, previous studies suggest that APOE4, a genetic risk factor for Alzheimer’s disease, is linked to brain blood vessel health and integrity.

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: 19033 - Posted: 12.14.2013

Taking some heartburn medications for more than two years is linked to a higher risk of vitamin B12 deficiency in adults, a U.S. study suggests. Left untreated, vitamin B12 deficiency can lead to dementia, neurological damage, anemia, and other complications. Knowing that stomach acid aids in vitamin B12 absorption, researchers set out to test whether suppressing the acids can lead to vitamin deficiency. The drugs in question are known as proton pump inhibitors and they include such well known brands as Losec, Nexium, Prabacid and Pariet. Doses of more than 1.5 pills per day were more strongly associated with vitamin D deficiency than doses of less than 0.75 pills per day, Dr. Douglas Corley, a gastroenterologist and research scientist with the Kaiser Permanente Division of Research in Broadway, Calif. and his co-authors said in Wednesday's issue of the Journal of the American Medical Association. "This research raises the question of whether people who are taking acid-depressing medications long term should be screened for vitamin B12 deficiency," Corley said in a release. "It's a relatively simple blood test, and vitamin supplements are an effective way of managing the vitamin deficiency, if it is found." For the study, researchers looked at electronic health records of 25,956 adults diagnosed with vitamin B12 deficiency in Northern California between January 1997 and June 2011, and compared them with 184,199 patients without B12 deficiency during the same time period. Among the 25,956 patients who had vitamin B12 deficiency, 12 per cent used proton pump inhibitors for at least two years, compared with 7.2 per cent of those in the control group. © CBC 2013

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: 19019 - Posted: 12.11.2013

By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American

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: 19018 - Posted: 12.11.2013