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An analysis of more than 800,000 people has concluded that people who remain single for life are 42 per cent more likely to get dementia than married couples. The study also found that people who have been widowed are 20 per cent more likely to develop the condition, but that divorcees don’t have an elevated risk. Previous research has suggested that married people may have healthier lifestyles, which may help explain the findings. Another hypothesis is that married people are more socially engaged, and that this may protect against developing the condition. The stress of bereavement might be behind the increased risk in those who have been widowed. But marriage isn’t always good for the health. While men are more likely to survive a heart attack if they are married, single women recover better than those who are married. Journal reference: Journal of Neurology, Neurosurgery, and Psychiatry © Copyright New Scientist Ltd.

Related chapters from BN8e: 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: 24382 - Posted: 12.01.2017

By Shawna Williams Neurodegenerative diseases are tough nuts to crack, not just because of the inherent difficulties of sorting through what has gone awry, and why, but also due to a dearth of biomarkers that could help spot the diseases and track their progression. This inability to easily diagnose many forms of neurodegeneration means that the diseases can’t be treated early in their progression. The lack of biomarkers also hinders the certainty with which researchers running clinical trials can assess whether and how well experimental treatments of the diseases are working. A simple, noninvasive eye scan now being developed for Alzheimer’s disease (AD), however, may help address both shortcomings. AD researchers already utilize amyloid positron emission tomography (PET), in which tracers are injected into patients’ brains to make the disease’s characteristic amyloid plaques detectable by PET imaging. But the scans are very expensive, spurring the continuing hunt for biomarkers. “What we now know is that the disease essentially occurs about 20 years before a patient becomes symptomatic,” says Cedars-Sinai Medical Center neuroscientist and neurosurgeon Keith Black. “And by the time one is symptomatic, they’ve already lost a lot of their brain weight; they’ve already lost a significant number of brain cells; they’ve already lost a significant amount of connectivity.” What’s needed, he says, is a way to detect the disease early so it can be treated—with drugs, lifestyle interventions, or both—before it’s too late. © 1986-2017 The Scientist

Related chapters from BN8e: 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: 24376 - Posted: 11.29.2017

By Linda Searing Benzodiazepines, also known as benzos, are drugs sometimes prescribed to ease the agitation, anxiety and insomnia often experienced by people with Alzheimer’s disease. Might these powerful medications have an effect beyond their sleep-inducing or calming properties? This study Researchers analyzed data on 31,140 adults with Alzheimer’s, most in their early 80s and predominantly women. The group included 10,380 people who started taking benzodiazepines (6,438), benzodiazepine-related “Z-drugs” (3,826) or both (116) after being diagnosed with Alzheimer’s. None of them had taken these drugs for at least a year before their diagnosis. Prescribed benzos included Valium, Librium, Ativan, Xanax, Restoril, Serax and one drug not approved for use in the United States. Prescribed Z-drugs were Ambien and one non-U.S. drug. Within six months of starting to take the medication, 1,225 people had died. Those taking benzos were 41 percent more likely to have died than were people who did not take these drugs, with the strongest mortality risk occurring within four months of starting the medication. No increased risk was linked to Z-drugs. Who may be affected? People with Alzheimer’s, which usually affects those 60 and older. The researchers noted that benzodiazepines and similar drugs have a stronger effect on the central nervous system of older people than of younger ones, and they have been shown to raise older people’s risk for hip fractures, pneumonia and stroke. Because of this, they wrote, “the observed association with an increased risk of death might result from these outcomes.” Today, about 5 million Americans are living with Alzheimer’s — a number that may triple in the next three decades. © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24369 - Posted: 11.28.2017

By NICHOLAS BAKALAR Heart attack survivors have an increased risk for developing dementia, a new study has found. Danish researchers studied 314,911 heart attack patients and compared them with 1,573,193 controls who had not had a heart attack. They excluded anyone who had already been diagnosed with dementia or other memory disorders. The study, in Circulation, adjusted for heart failure, pulmonary disease, head trauma, kidney disease and many other variables. During 35 years of follow-up, there were 3,615 cases of Alzheimer’s disease, 2,034 cases of vascular dementia and 5,627 cases of other dementias among the heart attack patients. There was no association of heart attack with Alzheimer’s disease. But heart attack increased the risk for vascular dementia, the type caused by impaired blood flow to the brain, by 35 percent. There are several possible reasons for the link, including similar underlying causes for dementia and heart attack — among them, hypertension, stroke and having undergone coronary artery bypass surgery. The researchers had no data on smoking, and they acknowledge that there may be other variables they were unable to account for. “Dementia can’t be cured,” said the lead author, Dr. Jens Sundboll, a resident in cardiology at Aarhus University in Denmark. “What’s the solution? Prevention. And for prevention we have to identify risk factors. Here we’ve identified an important one.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24330 - Posted: 11.16.2017

By Anna Cranston, Around 50m people worldwide are thought to have Alzheimer’s disease. And with rapidly ageing populations in many countries, the number of sufferers is steadily rising. We know that Alzheimer’s is caused by problems in the brain. Cells begin to lose their functions and eventually die, leading to memory loss, a decline in thinking abilities and even major personality changes. Specific regions of the brain also shrink, a process known as atrophy, causing a significant loss of brain volume. But what’s actually happening in the brain to cause this? Advertisement The main way the disease works is to disrupt communication between neurons, the specialised cells that process and transmit electrical and chemical signals between regions of the brain. This is what is responsible for the cell death in the brain – and we think its due to a build up of two types of protein, called amyloid and tau. The exact interaction between these two proteins is largely unknown, but amyloid accumulates into sticky clusters known as beta-amyloid “plaques”, while tau builds up inside dying cells as “neurofibrillary tangles”. One of the difficulties of diagnosing Alzheimer’s is that we’ve no reliable and accurate way of measuring this protein build-up during the early stages of the disease. In fact, we can’t definitively diagnose Alzheimer’s until after the patient has died, by examining their actual brain tissue. Another problem we have is that beta-amyloid plaques can also be found in the brains of healthy patients. This suggests the presence of the amyloid and tau proteins may not tell the whole story of the disease. © 2017 Scientific American,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24300 - Posted: 11.07.2017

For the first time, scientists have found a connection between abnormalities in how the brain breaks down glucose and the severity of the signature amyloid plaques and tangles in the brain, as well as the onset of eventual outward symptoms, of Alzheimer’s disease. The study was supported by the National Institute on Aging (NIA), part of the National Institutes of Health, and appears in the Nov. 6, 2017, issue of Alzheimer's & Dementia: the Journal of the Alzheimer's Association. Led by Madhav Thambisetty, M.D., Ph.D., investigator and chief of the Unit of Clinical and Translational Neuroscience in the NIA’s Laboratory of Behavioral Neuroscience, researchers looked at brain tissue samples at autopsy from participants in the Baltimore Longitudinal Study of Aging (BLSA), one of the world’s longest-running scientific studies of human aging. The BLSA tracks neurological, physical and psychological data on participants over several decades. Researchers measured glucose levels in different brain regions, some vulnerable to Alzheimer’s disease pathology, such as the frontal and temporal cortex, and some that are resistant, like the cerebellum. They analyzed three groups of BLSA participants: those with Alzheimer’s symptoms during life and with confirmed Alzheimer’s disease pathology (beta-amyloid protein plaques and neurofibrillary tangles) in the brain at death; healthy controls; and individuals without symptoms during life but with significant levels of Alzheimer’s pathology found in the brain post-mortem. They found distinct abnormalities in glycolysis, the main process by which the brain breaks down glucose, with evidence linking the severity of the abnormalities to the severity of Alzheimer’s pathology. Lower rates of glycolysis and higher brain glucose levels correlated to more severe plaques and tangles found in the brains of people with the disease. More severe reductions in brain glycolysis were also related to the expression of symptoms of Alzheimer’s disease during life, such as problems with memory.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24299 - Posted: 11.07.2017

Laura Sanders An Alzheimer’s-related protein can move from the blood to the brain and accumulate there, experiments on mice show for the first time. The results, published online October 31 in Molecular Psychiatry, suggest that the protein amyloid-beta outside the brain may contribute to the Alzheimer’s disease inside it, says Mathias Jucker, a neurobiologist at the University of Tübingen in Germany. This more expansive view of the disease may lead scientists to develop treatments that target parts of the body that are easier than the brain to access. The experiments don’t suggest that people could contract Alzheimer’s from another person’s blood. “The bottom line is that this study is thought-provoking but shouldn’t cause alarm,” says neurologist John Collinge of University College London. “There really isn’t any evidence that you can transmit Alzheimer’s disease by blood transfusion.” But researchers wondered whether, over time, A-beta might build up in the brain by moving there from the blood, where it’s normally found in small quantities. Earlier animal studies have shown that A-beta can move into the brain if it’s injected into the bloodstream, but scientists didn’t know whether A-beta from the blood can be plentiful enough to form plaques in the brain. To test this, researchers used a form of extreme blood-sharing in the experiment. Six pairs of mice — with one mouse engineered to produce gobs of human A-beta and one normal — were surgically joined for a year, causing blood mingling that’s far more extensive than that of a blood transfusion. After a year, the brains of the mice carrying the mutations were full of A-beta plaques, as expected. But these plaques were also inside the brains of the normal mice in the joined pairs. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24295 - Posted: 11.06.2017

JoNel Aleccia People who abhor the thought of being kept alive with feeding tubes or other types of artificial nutrition and hydration have, for years, had a way out: They could officially document their wishes to halt such interventions using advance directives. Even patients diagnosed with progressive dementia who are able to record crucial end-of-life decisions before the disease robs them of their mental capacity could write advance directives. But caregivers and courts have rarely honored patients' wishes to refuse food and fluids offered by hand. Margot Bentley, 85, of British Columbia, died last year. She was a retired nurse who had cared for dementia patients before being diagnosed with Alzheimer's in 1999. In 1991, she wrote a statement stipulating that she wanted no nourishment or liquids if she developed an incurable illness. However, the nursing home where she was a patient continued to spoon-feed her, despite her family's protests. A court ruling upheld the nursing home's action, saying that food is basic care that cannot be withdrawn. Nora Harris, 64, of Medford, Ore., died on Oct. 11 after an eight-year struggle with early-onset Alzheimer's disease. More than a year earlier, her husband had gone to court to stop caregivers from spoon-feeding Harris, who had an advance directive that called for no artificial nourishment or hydration. A judge declined, siding with officials who said the state was required to feed vulnerable adults. © 2017 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24284 - Posted: 11.03.2017

Alison Abbott The first controlled, but controversial and small, clinical trial of giving young blood to people with dementia has reported that the procedure appears safe. It has also hinted that it may even produce modest improvements in the daily lives of people who have Alzheimer's disease. Researchers who conducted the trial and others caution that the results are based on just 18 people and therefore are only a first step in exploring this type of treatment. “This is a really very small trial and the results should not be over-interpreted,” says Tony Wyss-Coray, a neurologist at Stanford University in California who led the study. The trial was conducted by his start-up company Alkahest, which is based in San Carlos, California. The results suggest the procedure is safe and hint that it could even boost the ability of people with dementia to undertake everyday skills, such as shopping or preparing a meal. The team plans to present the results on 4 November at the 10th Clinical Trials on Alzheimer’s Disease conference in Boston, Massachusetts. Wyss-Coray and his colleagues tested people aged between 54 and 86 with mild to moderate Alzheimer's disease. The team gave the 18 subjects weekly infusions for four weeks. They received either a saline placebo or plasma — blood from which the red cells have been removed — from blood donors aged 18–30. During the study, the team monitored the patients to assess their cognitive skills, mood and general abilities to manage their lives independently. The study detected no serious adverse reactions. It saw no significant effect on cognition, but two different batteries of tests assessing daily living skills both showed significant improvement. © 2017 Macmillan Publishers Limited,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 24279 - Posted: 11.02.2017

By NICHOLAS BAKALAR Chronic inflammation in middle age may be associated with an increased risk for brain shrinkage and Alzheimer’s disease later in life. A new study, published in Neurology, looked at 1,633 people whose average age was 53 in 1987-89, measuring white blood cell count and various blood proteins that indicate inflammation. They followed the participants for 24 years. In 2011-13, when the subjects’ average age was 77, the scientists measured their brain volume using M.R.I. and tested their mental agility with a word-memorization task. They found that the greater the number of elevated inflammatory markers earlier in life, the smaller the volume of several parts of the brain, including those associated with Alzheimer’s disease. Higher levels of inflammation were also associated with poorer performance on the memory test. The authors acknowledge that they had blood tests for only one point in time, and that they are assuming that brain loss occurred in the years after the inflammatory markers were assessed. “It’s important early in life that we prevent diseases like diabetes, heart disease or hypertension that cause systemic inflammation,” said the lead author, Keenan A. Walker, a postdoctoral fellow at Johns Hopkins. “This study shows a temporal relationship between early inflammation and later brain volume loss.” © 2017 The New York Times Company

Related chapters from BN8e: 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: 24277 - Posted: 11.02.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Related chapters from BN8e: 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: 24266 - Posted: 10.31.2017

There is no good evidence that a nutrient drink being sold online in the UK to "help" people with early Alzheimer's actually slows the disease, say experts. Latest trial results in patients who took Souvenaid did not find it preserves memory and thinking. The authors say in Lancet Neurology that bigger studies are needed to show if the product can work as hoped. And consumers should be aware that the £3.49 per bottle drink "is not a cure". Manufacturer Nutricia says its drink should only be taken under the direction of a doctor, specialist nurse or pharmacist. Souvenaid comes in strawberry or vanilla flavour and contains a combination of fatty acids, vitamins and other nutrients. Taken once daily, the idea is that the boost of nutrients it provides will help keep Alzheimer's at bay in people with the earliest signs of this type of dementia. But the latest phase two clinical trial results do not prove this. What the trial found The study involved 311 patients with very early Alzheimer's or mild cognitive impairment. All of them were asked to take a daily drink, but only half were given Souvenaid - the other half received one with no added nutrients. After two years of participating, the patients were reassessed to see if there was any difference between the two groups in terms of dementia progression, measured by various memory and cognitive tests. The treatment did not appear to offer an advantage, although patients in the Souvenaid group did have slightly less brain shrinkage on scans, which the researchers say is promising because shrinkage in brain regions controlling memory is seen with worsening dementia. But experts remain cautious. Prof Tara Spires-Jones, a dementia expert at the University of Edinburgh, said: "Some of the other tests of brain structure and function were promising, but overall this study indicates that a specific change in nutrition is unlikely to make a large difference to people with Alzheimer's, even in the early stages. © 2017 BBC.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24265 - Posted: 10.31.2017

By Michael Ellenbogen Twenty years ago, at age 39, I began having memory and cognitive problems. My primary-care doctor and my neurologists said I was stressed and depressed. I also was diagnosed with mild cognitive impairment, or MCI. Ten years later, I received another diagnosis. Well, really two. One doctor said I had Alzheimer’s disease, and another thought it was semantic dementia. Alzheimer’s is a devastating chronic neurodegenerative disease. It is a progressive mental deterioration that advances to affect bodily functions such as walking and swallowing, and always leads to death. Semantic dementia leads to losses of vocabulary, fluency of speech and meanings of familiar words. It also is progressive. After another year of testing, physicians decided that I had Alzheimer’s. While it was a relief to finally get a diagnosis, I realized that I had been given a death sentence. There is no prevention or cure for Alzheimer’s, and no survivors. Overwhelmed, I decided to help the search for a cure by advocating for Alzheimer’s and dementia. I got involved with clinical trials and advocacy. My huge network on LinkedIn allowed me to connect with advocates and information. It gave me access to many tests, including gene tests, free. Two contacts — health-care professionals — even read my medical records and scans and gave me their opinions. Alzheimer’s is a complex disease to diagnose. The science is just not there yet. Sixty to 80 percent of dementia cases are said to be due to Alzheimer’s. But postmortem tests of elderly patients have found that dementia has several causes. s. © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24260 - Posted: 10.30.2017

By Esther Landhuis Among hundreds of genes that might nudge your risk of Alzheimer's up or down, Apolipoprotein E (APOE) has the strongest effect. Scientists discovered a quarter century ago that people with the APOE ε4 version of this gene are four to 15 times more likely to develop Alzheimer’s, a deadly brain disorder that afflicts more than five million Americans. Yet how APOE actually sets off dementia has been somewhat of a mystery—and efforts to use it as a drug target have floundered. The field’s attention has focused on another “A” word—amyloid beta (Aβ). This protein can unwittingly accrue in the brain for years, disrupting nerve connections essential for thinking and memory. APOE has been thought of as a co-conspirator in this process, but finding ways to undermine its collusion have proved challenging. Anti-amyloid drugs have consumed the labors of pharmaceutical companies. If a drug could break those insidious clumps of protein or keep them from forming, drug developers reasoned, it could in theory halt the progression of the disease. But billions of dollars have poured into large-scale clinical trials of amyloid-lowering therapies that so far have failed. Advertisement APOE has hovered on the periphery as far as drug development, but this could soon change. Connections have emerged between the functioning of APOE and Aβ. In 2012 Boston scientists studying autopsy tissue from Alzheimer’s patients found APOE ε4 individuals had unusually high levels of brain Aβ. And they noticed Aβ clumped more readily in test tubes if mixed with ApoE proteins, especially ApoE4. Mouse data from teams at Washington University in Saint Louis and the University of California, San Francisco—suggested a similar relationship. Each lab worked with existing Alzheimer’s mouse models and further modified their genomes to make different types and amounts of ApoE proteins. In both studies animals with less ApoE had fewer Aβ plaques in their brains. © 2017 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24176 - Posted: 10.12.2017

By NICHOLAS BAKALAR Women with high blood pressure in their 40s are at increased risk for dementia in later years, researchers report. But the finding does not hold for men. Beginning in 1964, investigators collected health and lifestyle information on 5,646 men and women when they were 30 to 35 years old, and again when they were in their 40s. From 1996 to 2015, 532 of them were found to have Alzheimer’s or other forms of dementia. The study is in Neurology. Hypertension in women in their 30s was not associated with dementia. But women who were hypertensive at an average age of 44 had a 68 percent higher risk for dementia than those who had normal blood pressure at that age, even after adjusting for B.M.I., smoking and other risk factors. High blood pressure in men in their 30s or 40s was not associated with later dementia, but the study’s senior author, Rachel A. Whitmer, said that studies have tied hypertension in men in their 50s to later dementia. Dr. Whitmer, a senior research scientist at Kaiser Permanente in Oakland, Calif., added that hypertension is more common in men, and the hypertensive men in the study tended to die at a younger age than the women. “The big picture here is that brain health is a lifelong issue,” she said. “What you do in young adulthood matters for your brain in old age.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24175 - Posted: 10.12.2017

Jon Hamilton Fresh evidence that the body's immune system interacts directly with the brain could lead to a new understanding of diseases from multiple sclerosis to Alzheimer's. A study of human and monkey brains found lymphatic vessels — a key part of the body's immune system — in a membrane that surrounds the brain and nervous system, a team reported Tuesday in the online journal eLife. Lymphatic vessels are a part of the lymphatic system, which extends throughout the body much like our network of veins and arteries. Instead of carrying blood, though, these vessels carry a clear fluid called lymph, which contains both immune cells and waste products. The new finding bolsters recent evidence in rodents that the brain interacts with the body's lymphatic system to help fend off diseases and remove waste. Until a few years ago, scientists believed that the brain's immune and waste removal systems operated independently. The discovery of lymphatic vessels near the surface of the brain could lead to a better understanding of multiple sclerosis, which seems to be triggered by a glitch in the immune system, says Dr. Daniel Reich, an author of the study and a senior investigator at the National Institute of Neurological Disorders and Stroke. © 2017 npr

Related chapters from BN8e: 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: 24146 - Posted: 10.04.2017

Tina Hesman Saey A genetic risk factor for Alzheimer’s disease is a double, make that triple, whammy. In addition to speeding up the development of brain plaques associated with Alzheimer’s, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature. APOE4 protein also ramps up brain inflammation that kills brain cells, neuroscientist David Holtzman of Washington University School of Medicine in St. Louis and colleagues have discovered. “This paper is a tour de force,” says Robert Vassar, a neuroscientist at Northwestern University Feinberg School of Medicine in Chicago. “It’s a seminal study that’s going to be a landmark in the field” of Alzheimer’s research, Vassar predicts. For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood. But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24103 - Posted: 09.23.2017

By Anil Ananthaswamy Artificial intelligence can identify changes in the brains of people likely to get Alzheimer’s disease almost a decade before doctors can diagnose the disease from symptoms alone. The technique uses non-invasive MRI scans to identify alterations in how regions of the brain are connected. Alzheimer’s is a neurodegenerative disease that is the leading cause of dementia for the elderly, eventually leading to loss of memory and cognitive functions. The race is on to diagnose the disease as early as possible. Although there is no cure, drugs in development are likely to work better the earlier they are given. An early diagnosis can also allow people to start making lifestyle changes to help slow the progression of the disease. When will we cure Alzheimer’s? Learn more at New Scientist Live In an effort to enable earlier diagnosis, Nicola Amoroso and Marianna La Rocca at the University of Bari in Italy and their colleagues developed a machine-learning algorithm to discern structural changes in the brain caused by Alzheimer’s disease. First, they trained the algorithm using 67 MRI scans, 38 of which were from people who had Alzheimer’s and 29 from healthy controls. The scans came from the Alzheimer’s Disease Neuroimaging Initiative database at the University of Southern California in Los Angeles. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24067 - Posted: 09.15.2017

By Michael Le Page We are still evolving – very slowly. In the 20th century, people in the UK evolved to be less likely to smoke heavily, but the effect was tiny. So claims a study of 200,000 genomes. A population can be described as evolving when the frequency of gene variants changes over time. Because most people in rich countries now live well beyond reproductive age, some argue that we have stopped evolving because natural selection has been weakened. But several recent studies claim we are still evolving, albeit slowly. Now Joseph Pickrell at Columbia University in New York and his team have analysed human genome sequences to spot gene variants that are becoming rarer. One variant, of a gene called CHRNA3, is associated with heavier smoking in those that smoke, raising their risk of a smoking-related death. Comparing people over the age of 80 with people over the age of 60, Pickrell estimates that the variant has declined by 1 per cent between generations. However, his team was not able to prove this, as they did not have any genomic data from people under the age of 40. A variant of the ApoE4 gene that is known to increase the risk of late-onset Alzheimer’s disease, as well as cardiovascular disease, may also be getting rarer. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24038 - Posted: 09.06.2017

Anna VlasitsAnna Vlasits A sheen is starting to appear on Rocky Blumhagen’s forehead, just below his gray hair. He’s marching in place in a starkly lit room decked out with two large flatscreens. On both of the TVs, a volcano lets off steam through wide cracks glowing with lava, their roar muffling the Andean percussion and flutes on the soundtrack. Golden coins slide across the screen. Rocky reaches out his left hand, as if to grasp a coin from midair, and one of them disappears with a brrring. “I don’t know if I can do it,” he says to a guy named Josh sitting nearby in a felt-covered lounge chair. He looks up from his iPad, watching Rocky, age 66, grab, jog, kick, and reach his way through the videogame. “Keep it up,” Josh says as the heart monitor in the corner of the screen reads 129. Rocky and research assistant Josh Volponi are technically in a lab clinic at the University of California, San Francisco, but aside from the mannequin heads studded with electrodes, the room looks more like a man cave. But here, the videogames could halt the mental decay of aging. This is the premise that the university’s new research institute, named Neuroscape, was built to test. This is Rocky’s 18th training session at Neuroscape, founded by neuroscientist Adam Gazzaley. Rocky is fit for his age—he works as a substitute yoga instructor, after retiring from careers producing radio and performing Cole Porter songs—but as he makes it to the end of the level, he looks exhausted. The game cuts to an animation of a jungle, birds chirping and light playing through the canopy as a list of his past scores pops up. This round wasn’t his best. “I haven’t been here for a week,” he says. Volponi asks him to rate his physical exertion level. Rocky gives it a 15 out of 20; Volponi marks it on the iPad. “I feel rusty,” he says, wiping his hands on his orange exercise shorts.

Related chapters from BN8e: 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: 24033 - Posted: 09.04.2017