Links for Keyword: Alzheimers

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Hannah Devlin Science correspondent Two licensed drugs have been shown to halt brain degeneration in mice, raising the prospect of a rapid acceleration in the search for a medicine to beat Alzheimer’s disease. The results, presented on Tuesday at the Alzheimer’s Society annual research conference in Manchester, have been hailed as “hugely promising” because they involve medicines that are already known to be safe and well-tolerated in people – potentially cutting years from the timeline for drugs to reach patients. Speaking ahead of her presentation, Giovanna Mallucci, professor of clinical neuroscience at the University of Cambridge, said: “It’s really exciting. They’re licensed drugs. This means you’d do a straightforward basic clinical trial on a small group of patients because these are not new compounds, they’re known drugs.” The scientists have chosen not to name the two drugs, which are currently used for conditions unrelated to dementia, to avoid the possibility of patients seeking to use them ahead of any clinical trial to prove their efficacy. The findings build on a landmark study two years ago, showing that brain cell death could be halted in mice by switching off a faulty signal in the brain that stops new proteins being produced. However, the breakthrough relied on a compound that had severe physical side-effects including weight loss and diabetes, making it unsuitable for use in humans. The two drugs were identified after Mallucci’s team screened hundreds of licensed compounds in search for something safe that had the same protective effects on the brain. Clare Walton, research manager at the Alzheimer’s Society, said: “The new results are hugely promising because the drugs are already given to people and we know they’re safe.” © 2015 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: 21114 - Posted: 07.01.2015

By Ariana Eunjung Cha One of the most heartbreaking things about Alzheimer's is that it has been impossible for doctors to predict who will get it before symptoms begin. And without early detection, researchers say, a treatment or cure may be impossible. Governments, drug companies and private foundations have poured huge amounts of money into trying to come up with novel ways to detect risk through cutting-edge technologies ranging from brain imaging, protein analysis of cerebrospinal fluid and DNA profiling. Now a new study, published in the journal Neurology, shows that perhaps something more old-fashioned could be the answer: a memory test. The researchers tracked 2,125 participants in four Chicago neighborhoods for 18 years, giving them tests of memory and thinking every three years. They found that those who scored lowest on the tests during the first year were 10 times more likely to be diagnosed with Alzheimer's down the road -- indicating that cognitive impairment may be affecting the brain "substantially earlier than previously established," the researchers wrote.

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: 21109 - Posted: 06.30.2015

Amy Standen A doctor I interviewed for this story told me something that stuck with me. He said for every person with dementia he treats, he finds himself caring for two patients. That's how hard it can be to be a caregiver for someone with dementia. The doctor is Bruce Miller. He directs the Memory and Aging Center at the University of California, San Francisco. According to Miller, 50 percent of caregivers develop a major depressive illness because of the caregiving. "The caregiver is so overburdened that they don't know what to do next," he says. "This adds a huge burden to the medical system." This burden is going increase dramatically in the coming decade. By 2025, 7 million Americans will have Alzheimer's disease, according to one recent estimate. Millions more will suffer from other types of dementia. Together these diseases may become the most expensive segment of the so-called "silver tsunami" — 80 million baby boomers who are getting older and needing more medical care. The cost of caring for Alzheimer's patients alone is expected to triple by 2050, to more than $1 trillion a year. So UCSF, along with the University of Nebraska Medical Center, is beginning a $10 million study funded by the federal Centers for Medicare & Medicaid Innovation. Researchers plan to develop a dementia "ecosystem," which aims to reduce the cost of caring for the growing number of dementia patients and to ease the strain on caregivers. © 2015 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: 21104 - Posted: 06.29.2015

By James Gallagher Health editor, BBC News website Scientists have discovered a chemical in blood that indicates whether people will have declining brain function. Looking for the earliest signs of Alzheimer's disease, they analysed levels of 1,129 proteins circulating in the blood of more than 200 twins. These were compared with data from cognitive-function tests over the next decade, in Translational Psychiatry. And levels of one protein, MAPKAPK5, tended to be lower in those people whose brains declined. MAPKAPK5 is involved in relaying chemical messages within the body, although its connection with cognitive decline is unclear. Dementia cases are expected to treble globally by 2050, but there is no cure or treatment. It can take more than a decade from the first changes in the brain to culminate in symptoms such as memory loss, confusion and personality change. And drug companies believe they need to treat patients years before symptoms appear in order to protect the brain. Dr Steven Kiddle, a Medical Research Council scientist at King's College London, told the BBC News website: "People think it may be hard to reverse 20 years of potential damage to your brain. "But if you could start much earlier in that process, then you might be able to find something that works." He said a blood test could help identify people for clinical trials. But he added: "A test you could go in to your doctor to say, 'Do I have Alzheimer's disease or not?' I think that's a long way off." © 2015 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: 21064 - Posted: 06.17.2015

Rebecca Hersher Greg O'Brien sees things that he knows aren't there, and these visual disturbances are becoming more frequent. That's not uncommon; up to 50 percent of people who have Alzheimer's disease experience hallucinations, delusions or psychotic symptoms, recent research suggests. At first, he just saw spider-like forms floating in his peripheral vision, O'Brien says. "They move in platoons." But in the last year or so, the hallucinations have been more varied, and often more disturbing. A lion. A bird. Sprays of blood among the spiders. Over the past five months, O'Brien has turned on an audio recorder when the hallucinations start, in hopes of giving NPR listeners insight into what Alzheimer's feels like. For now, he says, "I'm able to function. But I fear the day, which I know will come, when I can't." Interview Highlights [It's] St. Patrick's Day, about 9 o'clock in the morning in my office, and they're coming again. Those hallucinations. Those things that just come into the mind when the mind plays games. And then I see the bird flying in tighter and tighter and tighter circles. And all of a sudden, the bird — beak first — it darted almost in a suicide mission, exploding into my heart. Today I'm just seeing this thing in front of me. It looks like a lion, almost looks like something you'd see in The Lion King, and there are birds above it. It's floating, and it disintegrates ... it disintegrates ... it disintegrates.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 21003 - Posted: 06.01.2015

Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 21000 - Posted: 05.30.2015

Nala Rogers Alzheimer’s disease may have evolved alongside human intelligence, researchers report in a paper posted this month on BioRxiv1. The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development. This may have helped to increase the connectivity of neurons, making modern humans smarter as they evolved from their hominin ancestors. But that new intellectual capacity was not without cost: the same genes are implicated in Alzheimer's disease. Kun Tang, a population geneticist at the Shanghai Institutes for Biological Sciences in China who led the research, speculates that the memory disorder developed as ageing brains struggled with new metabolic demands imposed by increasing intelligence. Humans are the only species known to develop Alzheimer's; the disease is absent even in closely related primate species such as chimpanzees. Tang and his colleagues searched modern human DNA for evidence of this ancient evolution. They examined the genomes of 90 people with African, Asian or European ancestry, looking for patterns of variation driven by changes in population size and natural selection. Marked by selection The analysis was tricky, because the two effects can mimic each other. To control for the effects of population changes ― thereby isolating the signatures of natural selection — the researchers estimated how population sizes changed over time. Then they identified genome segments that did not match up with the population history, revealing the DNA stretches that were most likely shaped by selection. © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 20971 - Posted: 05.23.2015

by Clare Wilson Does this qualify as irony? Our bodies need iron to be healthy – but too much could harm our brains by bringing on Alzheimer's disease. If that's the case, measuring people's brain iron levels could help identify those at risk of developing the disease. And since we already have drugs that lower iron, we may be able to put the brakes on. Despite intense efforts, the mechanisms behind this form of dementia are still poorly understood. For a long time the main suspect has been a protein called beta-amyloid, which forms distinctive plaques in the brain, but drugs that dissolve it don't result in people improving. Not so good ferrous Studies have suggested that people with Alzheimer's also have higher iron levels in their brains. Now it seems that high iron may hasten the disease's onset. Researchers at the University of Melbourne in Australia followed 144 older people who had mild cognitive impairment for seven years. To gauge how much iron was in their brains, they measured ferritin, a protein that binds to the metal, in their cerebrospinal fluid. For every nanogram per millilitre people had at the start of the study, they were diagnosed with Alzheimer's on average three months earlier. The team also found that the biggest risk gene for Alzheimer's, ApoE4, was strongly linked with higher iron, suggesting this is why carrying the gene makes you more vulnerable. Iron is highly reactive, so it probably subjects neurons to chemical stress, says team member Scott Ayton. © 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: 20957 - Posted: 05.20.2015

By PAM BELLUCKM The largest analysis to date of amyloid plaques in people’s brains confirms that the presence of the substance can help predict who will develop Alzheimer’s and determine who has the disease. Two linked studies, published Tuesday in JAMA, also support the central early role in Alzheimer’s of beta amyloid, the protein that creates plaques. Data from nearly 9,500 people on five continents shows that amyloid can appear 20 to 30 years before symptoms of dementia, that the vast majority of Alzheimer’s patients have amyloid and that the ApoE4 gene, known to increase Alzheimer’s risk, greatly accelerates amyloid accumulation. The findings also confirm that amyloid screening, by PET scan or cerebral spinal fluid test, can help identify people for clinical trials of drugs to prevent Alzheimer’s. Such screening is increasingly used in research. Experts say previous trials of anti-amyloid drugs on people with dementia failed because their brains were already too damaged or because some patients, not screened for amyloid, may not have had Alzheimer’s. “The papers indicate that amyloid imaging is important to be sure that the drugs are being tested on people who have amyloid,” said Dr. Roger Rosenberg, the director of the Alzheimer’s Disease Center at the University of Texas Southwestern Medical Center at Dallas, who wrote an editorial about the studies. Dr. Samuel Gandy, an Alzheimer’s researcher at Mount Sinai Hospital, who was not involved in the research, said doctors “can feel fairly confident that amyloid is due to Alzheimer’s.” But he and others cautioned against screening most people without dementia because there is not yet a drug that prevents or treats Alzheimer’s, and amyloid scans are expensive and typically not covered by insurance. © 2015 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: 20956 - Posted: 05.20.2015

By Aleksandra Sagan, CBC News In a Dutch town about 20 kilometres outside of Amsterdam, a small community lives in what at first glance seems like a real-life version of The Truman Show. Hogewey has a grocery store, a theatre and a barber shop. The only twist is that many of its 152 residents live unaware that their orderly community is actually a nursing home for people with severe dementia. "We protect our residents from the unsafe world. They do not understand the world outside this because the outside world doesn't understand them," says Yvonne van Amerongen, an employee at Hogewey who also helped develop the concept. Hogewey was officially opened in 2007, but the idea has now caught the attention of health-care professionals in Ontario and Alberta. ​Rhonda Desroches, who helped create a smaller-scale Hogewey in Penetanguishene, Ont., says relatives of the residents are pleased with how happy their family members seem to be in the new facility. Dementia is a growing problem. According to the Alzheimer Society Canada, one out of 20 Canadians over 65 has Alzheimer's Disease, and that figure jumps to one in four for Canadians over 85. In 2012, the World Health Organization declared dementia a public health priority. Many dementia patients move into nursing homes, where they are monitored in a safe setting. But some medical professionals want to shift patients away from unfamiliar, clinical settings and into spaces that resemble more typical surroundings. Hogewey creates a familiar, "normal" environment that dementia patients understand, says van Amerongen. The citizens of Hogewey share a house with about six others, and are classified according to one of seven lifestyles. ©2015 CBC/Radio-Canada

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: 20875 - Posted: 05.04.2015

A study using mice has uncovered a possible cause of Alzheimer’s disease, and suggests that a drug currently being investigated in human clinical trials to treat cancer could prevent the illness. The research has been heralded as offering hope of finding new treatments for dementia, an illness that affects 850,000 people in the UK. The findings, by Duke University in America and published in the Journal of Neuroscience, are surprising, according to one of the authors, as they contradict current thinking on the disease. The research suggests that in mice with Alzheimer’s disease certain immune cells that normally protect the brain begin abnormally to consume an important nutrient called arginine. By blocking this process using the drug difluoromethylornithine (DFMO), memory loss and a buildup of sticky proteins known as brain plaques were prevented. The study used a type of mouse in which a number of important genes had been swapped to make the animal’s immune system more similar to a human’s. Senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences, said: “If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease.” It was previously thought the brain releases molecules that ramp up the immune system, apparently damaging the brain, but the study found a heightened expression of genes associated with the suppression of the immune system. Author Matthew Kan said: “It’s surprising because [suppression of the immune system is] not what the field has been thinking is happening in AD [Alzheimer’s disease].” © 2015 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: 20802 - Posted: 04.15.2015

By LAWRENCE K. ALTMAN, M.D WASHINGTON — Even before Ronald Reagan became the oldest elected president, his mental state was a political issue. His adversaries often suggested his penchant for contradictory statements, forgetting names and seeming absent-mindedness could be linked to dementia. In 1980, Mr. Reagan told me that he would resign the presidency if White House doctors found him mentally unfit. Years later, those doctors and key aides told me they had not detected any changes in his mental abilities while in office. Now a clever new analysis has found that during his two terms in office, subtle changes in Mr. Reagan’s speaking patterns linked to the onset of dementia were apparent years before doctors diagnosed his Alzheimer’s disease in 1994. The findings, published in The Journal of Alzheimer’s Disease by researchers at Arizona State University, do not prove that Mr. Reagan exhibited signs of dementia that would have adversely affected his judgment and ability to make decisions in office. But the research does suggest that alterations in speech one day might be used to predict development of Alzheimer’s and other neurological conditions years before symptoms are clinically perceptible. Detection of dementia at the earliest stages has become a high priority. Many experts now believe that yet-to-be-developed treatments are likely to be effective at preventing or slowing progression of dementia only if it is found before it significantly damages the brain. The “highly innovative” methods used by the researchers may eventually help “to further clarify the extent to which spoken-word changes are associated with normal aging or predictive of subsequent progression to the clinical stages of Alzheimer’s disease,” said Dr. Eric Reiman, the director of the Banner Alzheimer’s Institute in Phoenix, who was not involved in the new study. © 2015 The New York Times Company

Related chapters from BP7e: 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: 20743 - Posted: 04.01.2015

Scientists have found that a compound originally developed as a cancer therapy potentially could be used to treat Alzheimer’s disease. The team demonstrated that the drug, saracatinib, restores memory loss and reverses brain problems in mouse models of Alzheimer’s, and now the researchers are testing saracatinib’s effectiveness in humans. The study was funded by the National Institutes of Health as part of an innovative crowdsourcing initiative to repurpose experimental drugs. Researchers from the Yale University School of Medicine, New Haven, Connecticut, conducted the animal study, published for early view on March 21 in the Annals of Neurology External Web Site Policy, with support from the National Center for Advancing Translational Sciences (NCATS) through its Discovering New Therapeutic Uses for Existing Molecules (New Therapeutic Uses) program. Launched in May 2012, this program matches scientists with a selection of pharmaceutical industry assets that have undergone significant research and development by industry, including safety testing in humans, to test potential ideas for new therapeutic uses. Alzheimer’s disease is the most common form of dementia, a group of disorders that cause progressive loss of memory and other mental processes. An estimated 5 million Americans have Alzheimer’s disease, which causes clumps of amyloid beta protein to build up in the brain, and these protein clusters damage and ultimately kill brain cells (neurons). Alzheimer’s disease also leads to loss of synapses, which are the spaces between neurons through which the cells talk to each other and form memories. Current Alzheimer’s drug therapies can only ease symptoms without stopping disease progression. New treatments are needed that can halt the condition by targeting its underlying mechanisms.

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: 20742 - Posted: 04.01.2015

Jon Hamilton Doctors are much more likely to level with patients who have cancer than patients who have Alzheimer's, according to a report released this week by the Alzheimer's Association. The report found that just 45 percent of Medicare patients who'd been diagnosed with Alzheimer's said they were informed of the diagnosis by their doctor. By contrast, more than 90 percent of Medicare patients with cancer said they were told by their doctor. "What we found is really shocking," says Beth Kallmyer, vice president of constituent services for the Alzheimer's Association. "This is reminiscent of what happened in the 1960s and 1970s with cancer," she says. "But that's changed now, and it really needs to change for Alzheimer's as well." For years, the association's help line has been receiving complaints from family members who say that doctors are reluctant to reveal an Alzheimer's diagnosis, Kallmyer says. So the association decided to investigate by studying medical records and survey results from Medicare recipients. To make sure that Alzheimer's patients hadn't simply forgotten what a doctor said, the group also looked at Medicare survey responses from family members and other caregivers. The result wasn't much better: Just 53 percent said a doctor told them of the patient's diagnosis. © 2015 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: 20721 - Posted: 03.25.2015

By ANDREW POLLACK An experimental drug for Alzheimer’s disease sharply slowed the decline in mental function in a small clinical trial, researchers reported Friday, reviving hopes for an approach to therapy that until now has experienced repeated failures. The drug, being developed by Biogen Idec, could achieve sales of billions of dollars a year if the results from the small trial are replicated in larger trials that Biogen said it hoped to begin this year. Experts say that there are no really good drugs now to treat Alzheimer’s. Biogen’s stock has risen about 50 percent since early December, when the company first announced that the drug had slowed cognitive decline in the trial, without saying by how much. Analysts and investors had been eagerly awaiting the detailed results, some of them flying to France to hear Biogen researchers present them at a neurology meeting on Friday. The drug, called aducanumab, met and in some cases greatly exceeded Wall Street expectations in terms of how much the highest dose slowed cognitive decline. However, there was a high incidence of a particular side effect that might make it difficult to use the highest dose. Still, the net impression was positive. “Out-of-the-ballpark efficacy, acceptable safety,” Ravi Mehrotra, an analyst at Credit Suisse, wrote on Friday. Shares of Biogen rose $42.33, or 10 percent, to $475.98. Alzheimer’s specialists were impressed, but they cautioned that it was difficult to read much from a small early-stage, or Phase 1, trial that was designed to look at safety, not the effect on cognition. Also, other Alzheimer’s drugs that had looked promising in early studies ended up not working in larger trials. “It’s certainly encouraging,” said Dr. Samuel Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York, who was not involved in the study. He said the effect of the highest dose was “pretty impressive.” © 2015 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: 20709 - Posted: 03.21.2015

By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.

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: 20685 - Posted: 03.12.2015

Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.

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: 20683 - Posted: 03.12.2015

Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.

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: 20682 - Posted: 03.12.2015

By Nicholas Bakalar Gout, a form of arthritis, is extremely painful and associated with an increased risk for cardiovascular problems. But there is a bright side: It may be linked to a reduced risk for Alzheimer’s disease. Researchers compared 59,204 British men and women with gout to 238,805 without the ailment, with an average age of 65. Patients were matched for sex, B.M.I., smoking, alcohol consumption and other characteristics. The study, in The Annals of the Rheumatic Diseases, followed the patients for five years. They found 309 cases of Alzheimer’s among those with gout and 1,942 among those without. Those with gout, whether they were being treated for the condition or not, had a 24 percent lower risk of Alzheimer’s disease. The reason for the connection is unclear. But gout is caused by excessive levels of uric acid in the blood, and previous studies have suggested that uric acid protects against oxidative stress. This may play a role in limiting neuron degeneration. “This is a dilemma, because uric acid is thought to be bad, associated with heart disease and stroke,” said the senior author, Dr. Hyon K. Choi, a professor of medicine at Harvard. “This is the first piece of data suggesting that uric acid isn’t all bad. Maybe there is some benefit. It has to be confirmed in randomized trials, but that’s the interesting twist in this story.” © 2015 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 20648 - Posted: 03.04.2015

By Roni Caryn Rabin When my mother, Pauline, was 70, she lost her sense of balance. She started walking with an odd shuffling gait, taking short steps and barely lifting her feet off the ground. She often took my hand, holding it and squeezing my fingers. Her decline was precipitous. She fell repeatedly. She stopped driving, and she could no longer ride her bike in a straight line along the C&O Canal. The woman who taught me the sidestroke couldn’t even stand in the shallow end of the pool. “I feel like I’m drowning,” she’d say. A retired psychiatrist, my mother had numerous advantages — education, resources and insurance — but, still, getting the right diagnosis took nearly 10 years. Each expert saw the problem through the narrow prism of a single specialty. Surgeons recommended surgery. Neurologists screened for common incurable conditions. The answer was under their noses, in my mother’s hunches and her family history. But it took a long time before someone connected the dots. My mother was using a walker by the time she was told she had a rare condition that causes gait problems and cognitive loss, and is one of the few treatable forms of dementia. The bad news was that it had taken so long to get the diagnosis that some of the damage might not be reversible. “This should be one of the first things physicians look for in an older person,” my mother said recently. “You can actually do something about it.”

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: 20643 - Posted: 03.03.2015