Links for Keyword: Alzheimers

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Aspirin may 'slow elderly brain decline', study finds

By Anna-Marie Lever Health reporter, BBC News An aspirin a day may slow brain decline in elderly women at high risk of cardiovascular disease, research finds. Around 500 at risk women, between the ages of 70 to 92, were tracked for five years - their mental capacity was tested at the start and end of the study. Those taking aspirin for the entire period saw their test scores fall much less than those who had not. The Swedish study is reported in the journal BMJ Open. Dr Silke Kern, one of paper's authors, said: "Unlike other countries - Sweden is unique, it is not routine to treat women at high risk of heart disease and stroke with aspirin. This meant we had a good group for comparison." The women were tested using a mini mental state exam (MMSE) - this tests intellectual capacity and includes orientation questions like, "what is today's date?", "where are we today?" and visual-spatial tests like drawing two interlinking pentagons. But the report found that while aspirin may slow changes in cognitive ability in women at high risk of a heart attack or stroke, it made no difference to the rate at which the women developed dementia - which was also examined for by a neuropsychiatrist. BBC © 2012

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17332 - Posted: 10.04.2012

Is Alzheimer’s disease akin to ‘type 3 diabetes’?

By Deborah Kotz, Globe Staff Is Alzheimer’s disease really a form of diabetes? Let’s call it type 3, because that’s what a Brown Medical School researcher dubbed it back in 2005 when she autopsied the brains of Alzheimer’s patients and found that they had signs of insulin resistance -- an early indicator of diabetes. Since then, however, we haven’t seen a sea-change in preventive treatments based on this idea. Those who carry the gene for hereditary Alzheimer’s aren’t given diabetes drugs to help stave off dementia. Nor are Alzheimer’s patients given insulin injections. What has been getting attention, however, is whether we should make extra efforts to eat a low glycemic diet -- which is low in processed foods, sugar, and starchy carbohydrates that cause quick spikes in blood sugar -- to help protect our brains from developing those gunky amyloid plaques associated with Alzheimer’s. The September issue of the New Scientist advocates for changing our eating patterns with a frightening image of a cracked chocolate brain on its cover. (Chocolate consumption, though, hasn’t been linked to cognitive decline, much to my relief.) New York Times food columnist Mark Bittman pointed out in a recent post that the latest studies provide some persuasive evidence linking diet to the development of Alzheimer’s. I’ve covered those studies too, including this one that measured a smaller Alzheimer’s risk in people who eat a diet rich in fish, veggies, and fruit compared with those who eat a diet centered on processed foods containing trans fats. © 2012 NY Times Co.

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of Internal States
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 17328 - Posted: 10.03.2012

Ageing cells offer new target for Alzheimer's therapy

by Jessica Hamzelou ALZHEIMER'S disease is more prevalent in older people, but we have never known why. Now it seems that about 80 per cent of our brain cells are vulnerable to a process that can turn them toxic. For the first time, cells in the brains of people with Alzheimer's have been shown to "senesce" - a mechanism that stops them dividing and starts them on a path of destruction. With hundreds of experimental treatments for the disease falling by the wayside, we need a new target and it seems as if we have now found one. The discovery of huge numbers of senescent cells in people with Alzheimer's suggests that they play a key role in the condition. Cells that continually replicate in the body, such as those in the skin, lung and kidney, eventually accumulate DNA damage - typically with age. Not all of these damaged cells die though, instead some senesce. When this happens, biological changes within the cell prevent it from dividing or carrying out its normal functions. Research suggests that senescing cells also start producing proteins that trigger inflammation. "It's pretty clear that cell senescence evolved to protect us against cancer," says Judith Campisi of the Buck Institute for Research on Aging in Novato, California. The idea is that once cells accumulate DNA damage, they senesce to avoid incorrect division that can lead to cancer. The benefit of this mechanism over self-destruction is that it sends out a call to the immune system to destroy nearby cells that might also be affected. © Copyright Reed Business Information Ltd.

Bad sleep may predict Alzheimer's, says study

Problems sleeping may be an early sign of Alzheimer's if a study in mice also applies to people, say researchers. Clumps of protein, called plaques, in the brain are thought to be a key component of the illness. A study, published in the journal Science Translational Medicine, showed that when plaques first developed, the mice started having disrupted sleep. Alzheimer's Research UK argued that if the link was proven it could become a useful tool for doctors. The hunt for early hints that someone is developing Alzheimer's is thought to be crucial for treating the disease. People do not show problems with their memory or clarity of thought until very late on in the disease. At this point, parts of the brain will have been destroyed, meaning treatment will be very difficult or maybe even impossible. It is why researchers want to start early, years before the first symptoms. One large area of research is in plaques of beta amyloid which form on the brain. Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people. However, the protein forms permanent plaques in Alzheimer's disease. BBC © 2012

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 17228 - Posted: 09.07.2012

Glimmer of a Silver Lining in Latest Alzheimer's Trial

by Greg Miller Earlier this summer, Alzheimer's researchers got disappointing—but not entirely unexpected—news from a phase III clinical trial of bapineuzumab, an antibody that targets β amyloid, the protein fragment that forms pathological clumps in the brains of patients. Bapineuzumab failed to improve cognition in two large trials of patients with mild to moderate Alzheimer’s disease. Today, Eli Lilly and Company announced slightly more encouraging results from another closely watched trial, for an anti-amyloid antibody called solanezumab. First the bad news: Solanezumab failed to slow cognitive decline in two trials with more than 2000 people with mild to moderate Alzheimer’s disease. However, the company says in a statement, a secondary analysis of data from the mild Alzheimer's patients enrolled in both trials indicated that the drug did slow cognitive decline in this subgroup. A similar analysis of the moderate Alzheimer’s patients in both trials showed no effect. Lilly says its plans for solanezumab are still undecided, pending discussions with regulators, but it will continue an open-label extension study in which patients from the two recently completed trials can continue to take the drug. "We see hopeful and encouraging information here," says Maria Carrillo, senior director of medical and scientific relations for the Alzheimer's Association. So far, Lilly has released only preliminary findings, but Carrillo says they appear to be the best evidence yet that anti-amyloid therapy can slow cognitive decline in some patients. © 2010 American Association for the Advancement of Science

Brain function remains sharp in rare 'SuperAgers'

By Linda Carroll Scientists have long assumed that fading memories are just a normal part of aging. But a new study suggests that certain 80-somethings can remember every bit as well as people much younger. Researchers from Northwestern University found that these mentally sharp octogenarians, dubbed SuperAgers, also have brains that look very much like those of people in middle-age, according to the study published in the Journal of International Neuropsychological Society. For the new study, researchers used MRIs to look at the thickness of the outer layer of the brain, a region called the cortex, in SuperAgers, normally aging 80-somethings, and healthy 50- to 65-year-olds. What they found was intriguing – the SuperAgers had brains that looked very much like those of the younger people in the study and in some ways looked even healthier. "We were very surprised at that," says study co-author Emily Rogalski, an assistant research professor at the cognitive neurology and Alzheimer's disease center at the Northwestern University Feinberg School of Medicine "When we looked at cortical thickness, we were very shocked to see that even with a 20- to 30-year age gap, there was seemingly no difference in the cortical thickness," she says. "In normally aging 80-year-olds, you see quite a bit of cortical thinning, even among those who are still performing normally for their age." © 2012 NBCNews.com

Despite fears of Alzheimer’s, many would like to know their risk for the disease

By Michelle Andrews, Alzheimer’s disease can’t be prevented or cured, and it ranks second only to cancer among diseases that people fear. Still, in an international study last year from the Harvard School of Public Health, about two-thirds of respondents from the United States said they would want to know if they were destined to get the disease. Although there are no definitive tests that predict whether most people will get the disease, people sometimes want such information for legal and financial planning purposes or to help weigh the need for long-term-care insurance. Current tests to identify the risk of developing Alzheimer’s disease when no symptoms are present provide only limited information, and health insurance generally doesn’t cover them. But that’s not stopping some people from trying to learn more. Most of the 5 million people who have Alzheimer’s developed it after age 60. In these cases, the disease is likely caused by a combination of genetic, lifestyle and environmental factors. About 5 percent of Alzheimer’s patients have inherited an early-onset form that is generally linked to a mutation on one of three chromosomes. Research suggests that the brain may show signs of Alzheimer’s decades before obvious symptoms appear. Scans can identify the presence of beta-amyloid, a protein that is often deposited in the brains of people with the disease, for example. Changes in proteins in the blood or cerebrospinal fluid may also be associated with Alzheimer’s disease. © 1996-2012 The Washington Post

Trials for Alzheimer’s Drug Halted After Poor Results

By KATIE THOMAS Johnson & Johnson and Pfizer announced on Monday that they were halting development of a closely watched Alzheimer’s drug after two clinical trials failed to show that it was effective in patients with mild to moderate forms of the disease. Late last month, results of a large clinical trial of the drug, called bapineuzumab, failed to show that patients — all of whom carried a particular gene that raises the risk of getting Alzheimer’s — improved either cognition or daily functioning compared with a placebo. The companies announced Monday that the results of a second trial, which tested the drug on patients who did not carry the gene, also did not meet its goals. Because the results of the earlier trial were already known, the decision to discontinue the drug was not altogether unexpected. Bapineuzumab, like other Alzheimer’s drugs being developed, targets beta amyloid, a protein that has toxic effects on the brain and is believed to be a cause of the disease. Given the failure of the drug, some have called that theory into question. But Dr. Husseini K. Manji, the global therapeutic area head for neuroscience at Janssen Research and Development, a unit of Johnson & Johnson, said the failed trials did not mean researchers should abandon the beta amyloid theory. “While we are disappointed in the results of the two bapineuzumab IV studies, particularly in light of the urgent need for new advancements in Alzheimer’s disease, we believe that targeting and clearing beta amyloid remains a promising path to potential clinical benefits for people suffering from this disease,” he said in a news release. © 2012 The New York Times Company

Be Well: Can one head injury lead to Alzheimer’s?

By Lara Salahi Can one head injury lead to Alzheimer’s? New research suggests one moderate to severe head injury can disrupt the proteins that regulate an enzyme associated with Alzheimer’s disease. Researchers from Tufts University School of Medicine and Harvard Medical School first measured protein levels in the brains of mice two days after they had incurred moderate to severe head trauma. The researchers found a reduction in the levels of two proteins, GGA1 and GGA3, and an increased level of the enzyme BACE1, which has previously been associated with Alzheimer’s disease. Researchers analyzed Alzheimer’s patients’ brain tissue and found the same protein reduction and enzyme level increase the mice had experienced. The findings suggest that a single brain injury could significantly increase the risk of developing Alzheimer’s disease, according to the researchers. BOTTOM LINE: A moderate to severe head injury can disrupt the proteins that regulate an enzyme associated with Alzheimer’s. CAUTIONS: The study does not look at the long-term effects of enzyme disruption after a traumatic brain injury and whether it leads to the development of Alzheimer’s disease. WHERE TO FIND IT: Journal of Neuroscience, July issue © 2012 NY Times Co.

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Language and Our Divided Brain
Link ID: 17135 - Posted: 08.07.2012

Alzheimer’s Drug Fails Its First Big Clinical Trial

By ANDREW POLLACK The most closely watched experimental treatment for Alzheimer’s disease proved ineffective in its first large clinical trial, dealing a blow to the field, to a theory about the cause of the disease, and to the three companies behind the drug. Pfizer, which is one of those companies, announced late Monday that the drug, bapineuzumab, did not improve either cognition or daily functioning of patients compared to a placebo in the Phase 3 trial. The company did not provide detailed results, saying they would be presented at a medical meeting in September. But one of the principal investigators in the study, Dr. Reisa Sperling, said in an interview that there was no sign of any effect. “There was absolutely no evidence at all of a clinical benefit of treatment on either of the primary measures, one cognitive and one functional,” said Dr. Sperling, director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital in Boston. To be sure, most doctors and Wall Street analysts had been expecting the drug not to succeed, since an earlier phase 2 trial had not shown a statistically significant effect. Moreover, the patients in the new trial — 1,100 Americans with mild to moderate disease — all had a gene called ApoE4, which raises the risk a person will get Alzheimer’s disease and can make the disease worse. Based on the phase 2 data, bapineuzumab has a somewhat better chance of working in patients who do not have that gene. © 2012 The New York Times Company

Alzheimer’s: A Ray of Hope? Just Perhaps Maybe

By Gary Stix The Search for Extraterrestrial Intelligence has always looked for an anomaly in the persistent cosmic background chatter—a change perhaps in the intensity of a signal that can be taken as a sign that a transmission might be a message to us earthlings from other intelligent beings. Each year, medical researchers who gather at the Alzheimer’s Association International Conference search for something similar as they weigh reports of the complex biology of the human brain for some sign that a drug might actually change the relentless course of the disease. Unlike many other major diseases that afflict millions of people, Alzheimer’s lacks a medicine that can send a patient into remission or maybe even effect a cure. On Tuesday, in Vancouver, the pharmaceutical company Baxter International reported to conference attendees on a weak but enticing signal, a drug that, if it works in larger clinical trials now under way, might actually stabilize patients and stop disease progression. Gammagard, or intravenous immunoglobulin, a soup of antibodies extracted from blood donors and already approved for some immune disorders, stopped for three years any decline in cognition and ability to go about the chores of daily living for four patients who received the highest dose. Four patients? True, it may be nothing. Too few patients, for sure, to make any predictions about whether, as so often in the past, the drug may falter and go by the wayside as it makes its way through the clinical trials pipeline . But the results still intrigued some in the research community who are normally circumspect about early reports. ‘‘It’s tantalizing. If you were to pick out four people with Alzheimer’s disease, the likelihood that they would perform the same on standardized tests three years later is very, very tiny,’’ William Thies, the scientific director for the Alzheimer’s Association, told the Associated Press. © 2012 Scientific American

Alzheimer's predictor tested in blood

Having high levels of a fat in the blood may increase someone's risk of developing Alzheimer's disease, a U.S. study suggests. Researchers are searching for better ways to screen, prevent and treat the mind-robbing disease that is projected to increase in prevalence worldwide. Scientists are looking for an accurate blood test to predict risk of Alzheimer's risk.Scientists are looking for an accurate blood test to predict risk of Alzheimer's risk. (Eliseo Fernandez/Reuters) Wednesday's issue of the journal Neurology includes a study on a biomarker in the blood that seems to predict the development of Alzheimer’s over the next decade. In the study, 99 women in the U.S. who were aged 70 to 79 and free of dementia when the study began had their blood tested. Investigators were checking levels of serum ceramides, a fatty compound found throughout the body that is associated with inflammation and cell death. Over the nine year study, 27 women developed dementia and 18 of those were diagnosed with probable Alzheimer's disease. Women who had the highest levels of the biomarker were 10 times more likely to develop Alzheimer's disease than women with the lowest levels, study author Michelle Mielke, an epidemiologist with the Mayo Clinic in Rochester, Minn., and her co-authors found. © CBC 2012

Study to test Alzheimer’s prevention medication awaits decision on funding

By Kay Lazar, Globe Staff If all goes according to plan, 1,000 older people who have no symptoms of Alzheimer’s disease, but who have an abnormal protein in their brains believed to be a hallmark of the illness, will be selected to test whether drugs can hold off the disease in a first of its kind study to be led by Boston scientists. The proposed study, detailed Tuesday at the Alzheimer’s Association International Conference in Vancouver, received a preliminary thumbs up earlier this month from the National Institutes of Health, but the project’s leaders are awaiting a final decision on funding the project, expected in September. “In this tough time of federal funding, we are keeping our fingers very tightly crossed,” lead researcher Dr. Reisa Sperling, an Alzheimer’s specialist at Brigham and Women’s Hospital, said in a phone interview. Recent drug trials aimed at clearing the abnormal amyloid proteins in the brains of Alzheimer’s patients have produced disappointing results, with no apparent easing of symptoms, and researchers think that’s because the drugs were used too late. Scientists believe that more than 50 percent of certain critical brain cells are already lost by the time a patient displays even mild cognitive impairment. There is no known cure for Alzheimer’s disease. Sperling’s study would enroll 1,000 adults over age 70 who have amyloid plaques revealed by brain scans and who are exhibiting very subtle cognitive problems that are typically reported in people years before they are diagnosed with Alzheimer’s. © 2012 NY Times Co.

Small Trial Hints Drug Can Slow Alzheimer’s

By ANDREW POLLACK A drug already on the market that treats immune disorders may help stabilize patients with Alzheimer’s disease for up to three years, according to the results of a tiny study presented at a conference on Tuesday. All four patients who received the optimal dose of the drug, Gammagard from Baxter International, had no decline in several measures of cognition and daily function for three years, researchers said. Dr. Norman Relkin of Weill Cornell Medical College, the lead investigator of the study, said the results were “remarkable” because patients with Alzheimer’s disease typically worsen within 12 months. “If we have a patient who goes 18 months without changing we begin to doubt they have Alzheimer’s,” Dr. Relkin said in a news conference at the Alzheimer’s Association International Conference in Vancouver, British Columbia, where the results were presented. But some experts not involved in the trial said it was premature to conclude that the drug was responsible for the stabilization. “There will be some patients who at three years don’t have a decline” even without an experimental therapy, said Dr. Rachelle S. Doody, director of the Alzheimer’s Disease and Memory Disorders Center at Baylor College of Medicine. She said some patients go six or eight years without worsening. © 2012 The New York Times Company

Footprints to Cognitive Decline and Alzheimer’s Are Seen in Gait

By PAM BELLUCK The way people walk appears to speak volumes about the way they think, so much so that changes in an older person’s gait appear to be an early indicator of cognitive impairment, including Alzheimer’s disease. Five studies presented at the Alzheimer’s Association International Conference in Vancouver this month provide striking evidence that when a person’s walk gets slower or becomes more variable or less controlled, his cognitive function is also suffering. Thinking skills like memory, planning activities or processing information decline almost in parallel with the ability to walk fluidly, these studies show. In other words, the more trouble people have walking, the more trouble they have thinking. “Changes in walking may predate actually observable cognitive changes in people who are on their way to developing dementia,” said Molly Wagster, chief of the National Institute on Aging’s behavioral and systems neuroscience branch. Experts said the studies could lead to developing a relatively simple tool that doctors could use to forecast, if not diagnose, possible Alzheimer’s disease. “You can probably just watch them walk down the hall in your office and look for people who are starting to show deterioration in their gait and have no other explanation for it,” said William Thies, the chief medical and scientific officer for the Alzheimer’s Association. “If gait begins to deteriorate, we begin to have a conversation about how is your memory.” © 2012 The New York Times Company

Related chapters from BP6e: 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: 17053 - Posted: 07.17.2012

Gene mutation defends against Alzheimer’s disease

Ewen Callaway Almost 30 million people live with Alzheimer’s disease worldwide, a staggering health-care burden that is expected to quadruple by 2050. Yet doctors can offer no effective treatment, and scientists have not been able definitively to pin down the underlying mechanism of the disease. Research published this week offers some hope on both counts, by showing that a lucky few people carry a genetic mutation that naturally prevents them from developing the condition1. The discovery not only confirms the principal suspect that is responsible for Alzheimer’s, it also suggests that the disease could be an extreme form of the cognitive decline seen in many older people. The mutation — the first ever found to protect against the disease — lies in a gene that produces amyloid-β precursor protein (APP), which has an unknown role in the brain and has long been suspected to be at the heart of Alzheimer’s. APP was discovered 25 years ago in patients with rare, inherited forms of Alzheimer’s that strike in middle age2–5. In the brain, APP is broken down into a smaller molecule called amyloid-β. Visible clumps, or plaques, of amyloid-β found in the autopsied brains of patients are a hallmark of Alzheimer’s, but scientists have long debated whether the plaques are a cause of the neurodegenerative condition or a consequence of other biochemical changes associated with the disease. The latest finding supports other genetics studies blaming amyloid-β, and it makes the protein “the prime therapeutic target”, says Rudolph Tanzi, a neurologist at the Massachusetts General Hospital in Boston and a member of one of the four teams that discovered APP’s role in the 1980s. © 2012 Nature Publishing Group,

What the Supercool Arctic Ground Squirrel Teaches Us about the Brain's Resilience

By Ferris Jabr Every September arctic ground squirrels in Alaska, Canada and Siberia retreat into burrows more than a meter beneath the tundra, curl up in nests built from grass, lichen and caribou hair, and begin to hibernate. As their lungs and hearts slow, the rivers of blood flowing through their bodies dwindle and their core body temperatures plummet, dipping below the freezing point of water. Electrical signals zipping along crisscrossing neural highways vanish in many areas of the brain. Seven months later the squirrels wake up and return to the surface—famished, eager to mate and perfectly healthy. How hibernating mammals survive for so long at such low temperatures without any food or water beyond what they have stored in their own fat fascinates scientists for many reasons. Hibernation is an amazing biological feat and an opportunity to learn new ways of pushing the human body beyond its ostensible limits, as well as healing it when it breaks down. The arctic ground squirrel's brain, in particular, seems to be incredibly resilient. When ground squirrels hibernate their neurons shrink and many connections between neurons shrivel. But their brains periodically compensate for this loss with massive growth spurts, multiplying neural links beyond what existed before hibernation. Learning how the ground squirrel's brain recuperates could not only help scientists understand the brain's plasticity, but also suggest new ways to reverse or prevent cellular damage in neurodegenerative diseases. In particular, recent research on hibernating brains is changing the way some scientists think about misshapen tau proteins, which are a hallmark of Alzheimer's disease. Most small hibernating mammals—hamsters, hedgehogs, bats—turn down their body's thermostat during hibernation, relinquishing one of the defining features of all mammals: warm blood. Arctic ground squirrels are the most extreme example. In August 1987 Brian Barnes of the University of Alaska Fairbanks (U.A.F.) captured 12 arctic ground squirrels and implanted tiny temperature-sensitive radio transmitters in the animals' abdomens. © 2012 Scientific American

Related chapters from BP6e: Chapter 13: Homeostasis: Active Regulation of Internal States; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 16975 - Posted: 06.27.2012

Like a prion, Alzheimer's protein seeds itself in the brain

By Laura Sanders The Alzheimer’s-related protein amyloid-beta is an infectious instigator in the brain, gradually contorting its harmless brethren into dangerous versions, compelling new evidence shows. The study adds to the argument that A-beta is a prion, a misfolded protein that behaves like the contagious culprits behind Creutzfeldt-Jakob disease in people, scrapie in sheep and mad cow disease. There’s no evidence that Alzheimer’s can spread from person to person, but thinking of Alzheimer’s as a prion disease could change the way researchers approach treatment and prevention strategies. The results also raise troubling implications for people who participated in a clinical trial in which they received a form of A-beta made in the lab, Stanley Prusiner of the University of California, San Francisco and colleagues write online June 18 in the Proceedings of the National Academy of Sciences. In the study, the researchers injected purified A-beta protein to seed one side of mice’s brains and monitored it with a fluorescent molecule that became visible as the protein accumulated. After about 300 days, the A-beta had accumulated throughout the brain, similar to what happens in Alzheimer’s. “It really does spread,” says study coauthor Kurt Giles of UCSF. “We inoculate in one part of the brain but the pathology spreads through the whole brain.” © Society for Science & the Public 2000 - 2012

Related chapters from BP6e: 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: Biological Basis of Behavioral Disorders
Link ID: 16934 - Posted: 06.20.2012

Alzheimer's gene 'diabetes link'

Scientists say they have identified a possible genetic link between diabetes and Alzheimer's disease. It has been known for some time that people with diabetes have a much higher risk of developing Alzheimer's, but not why this is so. Now US researchers writing in Genetics say a study of worms has indicated a known Alzheimer's gene also plays a role in the way insulin is processed. Dementia experts said more work in humans was now needed. Alzheimer's is the most common cause of dementia, which affects 820,000 people in the UK. There are medications which can slow the progress of the disease, but none that can halt its progress. A key indication of Alzheimer's, which can only be seen after death, is the presence of sticky plaques of amyloid protein in decimated portions of patients' brains. Scientists have already found mutations in a gene involved in the processing of amyloid protein in Alzheimer's which run in families. In this study, a team from the City College of New York looked at a similar gene in the nematode worms (C. elegans). These worms are often studied because they, perhaps surprisingly, a useful model for human research. BBC © 2012

Alzheimer's gene found to affect women over men

Erin Allday A gene that's been known for two decades as the largest inheritable risk for developing Alzheimer's disease mostly affects the brains of women, not men, according to a team of researchers from Stanford and UCSF. The gene variant known as APOE4 is the most common genetic risk factor for Alzheimer's - only about 15 percent of people carry the gene, but it's found in more than half of all Alzheimer's patients. The variant was first connected to Alzheimer's in 1993, but doctors and scientists for the most part have been unaware of any gender differences, despite early studies that showed an increased risk for women with the gene. The new research, which is being published Wednesday in the Journal of Neuroscience, looked at two biological indicators - or biomarkers - associated with Alzheimer's disease: decreased activity in a brain network related to memory, and increased levels of the tau protein in spinal fluid. Women with the APOE4 gene were more likely to test positive for both markers than men who had the gene and women who didn't have the gene. The findings will not have any immediate clinical impact - very few people are encouraged to learn their APOE4 status because there is no treatment for Alzheimer's. But the results could open a torrent of new research possibilities, such as studying the relationship between hormones and Alzheimer's, or looking for other gender differences that could be making women with the gene more vulnerable, scientists said. © 2012 Hearst Communications Inc.

Related chapters from BP6e: 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: 16908 - Posted: 06.13.2012

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