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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

By ROBERT PEAR WASHINGTON — Federal investigators say they have found evidence of widespread overuse of psychiatric drugs by older Americans with Alzheimer’s disease, and are recommending that Medicare officials take immediate action to reduce unnecessary prescriptions. The findings will be released Monday by the Government Accountability Office, an arm of Congress, and come as the Obama administration has already been working with nursing homes to reduce the inappropriate use of antipsychotic medications like Abilify, Risperdal, Zyprexa and clozapine. But in the study, investigators said officials also needed to focus on overuse of such drugs by people with dementia who live at home or in assisted living facilities. The Department of Health and Human Services “has taken little action” to reduce the use of antipsychotic drugs by older adults living outside nursing homes, the report said. Doctors sometimes prescribe antipsychotic drugs to calm patients with dementia who display disruptive behavior like hitting, yelling or screaming, the report said. Researchers said this was often the case in nursing homes that had inadequate numbers of employees. Dementia is most commonly associated with a decline in memory, but doctors say it can also cause changes in mood or personality and, at times, agitation or aggression. Experts have raised concern about the use of antipsychotic drugs to address behavioral symptoms of Alzheimer’s and other forms of dementia. The Food and Drug Administration says antipsychotic drugs are often associated with an increased risk of death when used to treat older adults with dementia who also have psychosis. © 2015 The New York Times Company

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: 20638 - Posted: 03.02.2015

By Michelle Roberts Health editor, BBC News online Scientists have proposed a new idea for detecting brain conditions including Alzheimer's - a skin test. Their work, which is at an early stage, found the same abnormal proteins that accumulate in the brain in such disorders can also be found in skin. Early diagnosis is key to preventing the loss of brain tissue in dementia, which can go undetected for years. But experts said even more advanced tests, including ones of spinal fluid, were still not ready for clinic. If they were, then doctors could treatment at the earliest stages, before irreversible brain damage or mental decline has taken place. Brain biomarker Investigators have been hunting for suitable biomarkers in the body - molecules in blood or exhaled breath, for example, that can be measured to accurately and reliably signal if a disease or disorder is present. Dr Ildefonso Rodriguez-Leyva and colleagues from the University of San Luis Potosi, Mexico, believe skin is a good candidate for uncovering hidden brain disorders. Skin has the same origin as brain tissue in the developing embryo and might, therefore, be a good window to what's going on in the mind in later life - at least at a molecular level - they reasoned. Post-mortem studies of people with Parkinson's also reveal that the same protein deposits which occur in the brain with this condition also accumulate in the skin. To test if the same was true in life as after death, the researchers recruited 65 volunteers - 12 who were healthy controls and the remaining 53 who had either Parkinson's disease, Alzheimer's or another type of dementia. They took a small skin biopsy from behind the ear of each volunteer to test in their laboratory for any telltale signs of disease. Specifically, they looked for the presence of two proteins - tau and alpha-synuclein. © 2015 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 20612 - Posted: 02.25.2015

|By Esther Landhuis Whereas cholesterol levels measured in a routine blood test can serve as a red flag for heart disease, there’s no simple screen for impending Alzheimer’s. A new Silicon Valley health start-up hopes to change that. A half million Americans die of Alzheimer’s disease each year. Most are diagnosed after a detailed medical workup and extensive neurological and psychological tests that gauge mental function and rule out other causes of dementia. Yet things begin going awry some 10 to 15 years before symptoms show. Spinal fluid analyses and positron emission tomography (PET) scans can detect a key warning sign—buildup of amyloid-beta protein in the brain. Studies suggest that adults with high brain amyloid have elevated risk for Alzheimer’s and stand the best chance of benefiting from treatments should they become available. Getting Alzheimer’s drugs to market requires long and costly clinical studies, which some experts say have failed thus far because experimental drugs were tested too late in the disease process. By the time people show signs of dementia, their brains have lost neurons and no current therapy can revive dead cells. That is why drug trials are looking to recruit seniors with preclinical Alzheimer’s who are on the verge of decline but otherwise look healthy. This poses a tall order. Spinal taps are cumbersome and PET costs $3,000 per scan. “There’s no cheap, fast, noninvasive test that can accurately identify people at risk of Alzheimer’s,” says Brad Dolin, chief technology officer of Neurotrack. The company is developing a computerized visual test that might fit the bill. © 2015 Scientific American

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: 20576 - Posted: 02.13.2015

|By Andrea Anderson and Victoria Stern Blood type may affect brain function as we age, according to a new large, long-term study. People with the rare AB blood type, present in less than 10 percent of the population, have a higher than usual risk of cognitive problems as they age. University of Vermont hematologist Mary Cushman and her colleagues used data from a national study called REGARDS, which has been following 30,239 African-American and Caucasian individuals older than 45 since 2007. The aim of the study is to understand the heavy stroke toll seen in the southeastern U.S., particularly among African-Americans. Cushman's team focused on information collected twice yearly via phone surveys that evaluate cognitive skills such as learning, short-term memory and executive function. The researchers zeroed in on 495 individuals who showed significant declines on at least two of the three phone survey tests. When they compared that cognitively declining group with 587 participants whose mental muster remained robust, researchers found that impairment in thinking was roughly 82 percent more likely in individuals with AB blood type than in those with A, B or O blood types, even after taking their race, sex and geography into account. The finding was published online last September in Neurology. The seemingly surprising result has some precedent: past studies suggest non-O blood types are linked to elevated incidence of heart disease, stroke and blood clots—vascular conditions that could affect brain function. Yet these cardiovascular consequences are believed to be linked to the way non-O blood types coagulate, which did not seem to contribute to the cognitive effects described in the new study. The researchers speculate that other blood-group differences, such as how likely cells are to stick to one another or to blood vessel walls, might affect brain function. © 2015 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: 20552 - Posted: 02.05.2015

|By Esther Landhuis One in nine Americans aged 65 and older has Alzheimer's disease, a fatal brain disorder with no cure or effective treatment. Therapy could come in the form of new drugs, but some experts suspect drug trials have failed so far because compounds were tested too late in the disease's progression. By the time people show signs of dementia, their brains have lost neurons. No therapy can revive dead cells, and little can be done to create new ones. So researchers running trials now seek participants who still pass as cognitively normal but are on the verge of decline. These “preclinical” Alzheimer's patients may represent a window of opportunity for therapeutic intervention. How to identify such individuals before they have symptoms presents a challenge, however. Today most Alzheimer's patients are diagnosed after a detailed medical workup and extensive tests that gauge mental function. Other tests, such as spinal fluid analyses and positron-emission tomography (PET) scans, can detect signs of approaching disease and help pinpoint the preclinical window but are cumbersome or expensive. “There's no cheap, fast, noninvasive test that can identify people at risk of Alzheimer's,” says Brad Dolin, chief technology officer of Neurotrack in Palo Alto, Calif.—a company developing a computerized visual screening test for Alzheimer's. Unlike other cognitive batteries, the Neurotrack test requires no language or motor skills. Participants view images on a monitor while a camera tracks their eye movements. The test draws on research by co-founder Stuart Zola of Emory University, who studies learning and memory in monkeys. When presented with a pair of images—one novel, the other familiar—primates fixate longer on the novel one. But if the hippocampus is damaged, as it is in people with Alzheimer's, the subject does not show a clear preference for the novel images. © 2015 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 20541 - Posted: 02.02.2015

Ian Sample, science editor People who carry a mutated gene linked to longer lifespan have extra tissue in part of the brain that seems to protect them against mental decline in old age. The finding has shed light on a biological pathway that researchers now hope to turn into a therapy that slows the progression of Alzheimer’s disease and other forms of dementia. Brain scans of more than 400 healthy men and women aged 53 and over found that those who carried a single copy of a particular gene variant had a larger brain region that deals with planning and decision making. Further tests on the group found that those with an enlarged right dorsolateral prefrontal cortex (rDLPFC), as the brain region is known, fared better on a series of mental tasks. About one in five people inherits a single copy of the gene variant, or allele, known as KL-VS, which improves heart and kidney function, and on average adds about three years to human lifespan, according to Dena Dubal, a neurologist at University of California, San Francisco. Her latest work suggests that the same genetic mutation has broader effects on the brain. While having a larger rDLPFC accounted for only 12% of the improvement in people’s mental test scores, Dubal suspects the gene alters the brain in other ways, perhaps by improving the connections that form between neurons.

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: 20526 - Posted: 01.28.2015

Over-the-counter sleeping aids and hayfever treatments can increase the risk of Alzheimer’s disease, a study has found. The sleeping medication Nytol and anti-allergy pills Benadryl and Piriton all belong to a class of drug highlighted in a warning from researchers. Each of these drugs has “anticholinergic” blocking effects on the nervous system that are said – at higher doses – to raise the likelihood of developing Alzheimer’s and other forms of dementia significantly over several years. Other drugs on the risk list include older “tricyclic” antidepressants such as doxepin, and the bladder control treatment Ditropan (oxybutynin). Many of these medicines are taken by vulnerable older people, according to the scientists, who say their findings have public health implications. Anticholinergic drugs block a nervous system chemical transmitter called acetylcholine, which can lead to side-effects including drowsiness, blurred vision and poor memory. People with Alzheimer’s disease are known to lack acetylcholine. The leader of the US study, Professor Shelly Gray, director of the geriatric pharmacy programme at the University of Washington School of Pharmacy, said: “Older adults should be aware that many medications – including some available without a prescription, such as over-the-counter sleep aids – have strong anticholinergic effects. And they should tell their healthcare providers. “Of course, no one should stop taking any therapy without consulting their healthcare provider. Healthcare providers should regularly review their older patients’ drug regimens – including over-the-counter medications – to look for chances to use fewer anticholinergic medications at lower doses.”

Related chapters from BP7e: 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: 20519 - Posted: 01.27.2015