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By Michelle Roberts Health editor, BBC News online The brain has a weak spot for Alzheimer's disease and schizophrenia, according to UK scientists who have pinpointed the region using scans. The brain area involved develops late in adolescence and degenerates early during ageing. At the moment, it is difficult for doctors to predict which people might develop either condition. The findings, in the journal PNAS, hint at a potential way to diagnose those at risk earlier, experts say. Although they caution that "much more research is needed into how to bring these exciting discoveries into the clinic". The Medical Research Council team who carried out the study did MRI brain scans on 484 healthy volunteers aged between eight and 85 years. The researchers, led by Dr Gwenaëlle Douaud of Oxford University, looked at how the brain naturally changes as people age. The images revealed a common pattern - the parts of the brain that were the last to develop were also the first to show signs of age-related decline. These brain regions - a network of nerve cells or grey matter - co-ordinate "high order" information coming from the different senses, such as sight and sound. When the researchers looked at scans of patients with Alzheimer's disease and scans of patients with schizophrenia they found the same brain regions were affected. The findings fit with what other experts have suspected - that although distinct, Alzheimer's and schizophrenia are linked. Prof Hugh Perry of the MRC said: "Early doctors called schizophrenia 'premature dementia' but until now we had no clear evidence that the same parts of the brain might be associated with two such different diseases. This large-scale and detailed study provides an important, and previously missing, link between development, ageing and disease processes in the brain. BBC © 2014

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: 20354 - Posted: 11.25.2014

By Emma Wilkinson Health reporter, BBC News Taking vitamin B12 and folic acid supplements does not seem to cut the risk of developing dementia in healthy people, say Dutch researchers. In one of the largest studies to date, there was no difference in memory test scores between those who had taken the supplements for two years and those who were given a placebo. The research was published in the journal Neurology. Alzheimer's Research UK said longer trials were needed to be sure. B vitamins have been linked to Alzheimer's for some years, and scientists know that higher levels of a body chemical called homocysteine can raise the risk of both strokes and dementia. Vitamin B12 and folic acid are both known to lower levels of homocysteine. That, along with studies linking low vitamin B12 and folic acid intake with poor memory, had prompted scientists to view the supplements as a way to ward off dementia. Yet in the study of almost 3,000 people - with an average age of 74 - who took 400 micrograms of folic acid and 500 micrograms of vitamin B12 or a placebo every day, researchers found no evidence of a protective effect. All those taking part in the trial had high blood levels of homocysteine, which did drop more in those taking the supplements. But on four different tests of memory and thinking skills taken at the start and end of the study, there was no beneficial effect of the supplements on performance. The researchers did note that the supplements might slightly slow the rate of decline but concluded the small difference they detected could just have been down to chance. Study leader Dr Rosalie Dhonukshe-Rutten, from Wageningen University in the Netherlands, said: "Since homocysteine levels can be lowered with folic acid and vitamin B12 supplements, the hope has been that taking these vitamins could also reduce the risk of memory loss and Alzheimer's disease. BBC © 2014

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 20313 - Posted: 11.15.2014

Sara Reardon Delivering medications to the brain could become easier, thanks to molecules that can escort drugs through the notoriously impervious sheath that separates blood vessels from neurons. In a proof-of-concept study in monkeys, biologists used the system to reduce levels of the protein amyloid-β, which accumulates in the brain plaques associated with Alzheimer's disease1. The blood–brain barrier is a layer of cells lining the inner surface of the capillaries that feed the central nervous system. It is nature's way of protecting the delicate brain from infectious agents and toxic compounds, while letting nutrients and oxygen in and waste products out. Because the barrier strictly regulates the passage of larger molecules and often prevents drug molecules from entering the brain, it has long posed one of the most difficult challenges in developing treatments for brain disorders. Several approaches to bypassing the barrier are being tested, including nanoparticles that are small enough to pass through the barrier's cellular membranes and deliver their payload; catheters that carry a drug directly into the brain; and ultrasound pulses that push microbubbles through the barrier. But no approach has yet found broad therapeutic application. Neurobiologist Ryan Watts and his colleagues at the biotechnology company Genentech in South San Francisco have sought to break through the barrier by exploiting transferrin, a protein that sits on the surface of blood vessels and carries iron into the brain. The team created an antibody with two ends. One end binds loosely to transferrin and uses the protein to transport itself into the brain. And once the antibody is inside, its other end targets an enzyme called β-secretase 1 (BACE1), which produces amyloid-β. Crucially, the antibody binds more tightly to BACE1 than to transferrin, and this pulls it off the blood vessel and into the brain. It locks BACE1 shut and prevents it from making amyloid-β. © 2014 Nature Publishing Group,

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: 20286 - Posted: 11.06.2014

By CLIVE THOMPSON “You just crashed a little bit,” Adam Gazzaley said. It was true: I’d slammed my rocket-powered surfboard into an icy riverbank. This was at Gazzaley’s San Francisco lab, in a nook cluttered with multicolored skullcaps and wires that hooked up to an E.E.G. machine. The video game I was playing wasn’t the sort typically pitched at kids or even middle-aged, Gen X gamers. Indeed, its intended users include people over 60 — because the game might just help fend off the mental decline that accompanies aging. It was awfully hard to play, even for my Call of Duty-toughened brain. Project: Evo, as the game is called, was designed to tax several mental abilities at once. As I maneuvered the surfboard down winding river pathways, I was supposed to avoid hitting the sides, which required what Gazzaley said was “visual-motor tracking.” But I also had to watch out for targets: I was tasked with tapping the screen whenever a red fish jumped out of the water. The game increased in difficulty as I improved, making the river twistier and obliging me to remember turns I’d taken. (These were “working-memory challenges.”) Soon the targets became more confusing — I was trying to tap blue birds and green fish, but the game faked me out by mixing in green birds and blue fish. This was testing my “selective attention,” or how quickly I could assess a situation and react to it. The company behind Project: Evo is now seeking approval from the Food and Drug Administration for the game. If it gets that government stamp, it might become a sort of cognitive Lipitor or Viagra, a game that your doctor can prescribe for your aging mind. After only two minutes of play, I was making all manner of mistakes, stabbing frantically at the wrong fish as the game sped up. “It’s hard,” Gazzaley said, smiling broadly as he took back the iPad I was playing on. “It’s meant to really push it.” “Brain training” games like Project: Evo have become big business, with Americans spending an estimated $1.3 billion a year on them. They are also a source of controversy. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 20238 - Posted: 10.23.2014

By Emily Underwood Aging baby boomers and seniors would be better off going for a hike than sitting down in front of one of the many video games designed to aid the brain, a group of nearly 70 researchers asserted this week in a critique of some of the claims made by the brain-training industry. With yearly subscriptions running as much as $120, an expanding panoply of commercial brain games promises to improve memory, processing speed, and problem-solving, and even, in some cases, to stave off Alzheimer’s disease. Many companies, such as Lumosity and Cogmed, describe their games as backed by solid scientific evidence and prominently note that neuroscientists at top universities and research centers helped design the programs. But the cited research is often “only tangentially related to the scientific claims of the company, and to the games they sell,” according to the statement released Monday by the Stanford Center on Longevity in Palo Alto, California, and the Max Planck Institute for Human Development in Berlin. Although the letter, whose signatories include many researchers outside those two organizations, doesn’t point to specific bad actors, it concludes that there is “little evidence that playing brain games improves underlying broad cognitive abilities, or that it enables one to better navigate a complex realm of everyday life.” A similar statement of concern was published in 2008 with a smaller number of signatories, says Ulman Lindenberger of the Max Planck Institute for Human Development, who helped organize both letters. Although Lindenberger says there was no particular trigger for the current statement, he calls it the “expression of a growing collective concern among a large number of cognitive psychologists and neuroscientists who study human cognitive aging.” © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 20237 - Posted: 10.23.2014

By Paula Span Maybe it’s something else. That’s what you tell yourself, isn’t it, when an older person begins to lose her memory, repeat herself, see things that aren’t there, lose her way on streets she’s traveled for decades? Maybe it’s not dementia. And sometimes, thankfully, it is indeed some other problem, something that mimics the cognitive destruction of Alzheimer’s disease or another dementia — but, unlike them, is fixable. “It probably happens more often than people realize,” said Dr. P. Murali Doraiswamy, a neuroscientist at Duke University Medical Center. But, he added, it doesn’t happen nearly as often as family members hope. Several confounding cases have appeared at Duke: A woman who appeared to have Alzheimer’s actually was suffering the effects of alcoholism. Another patient’s symptoms resulted not from dementia but from chronic depression. Dr. Doraiswamy estimates that when doctors suspect Alzheimer’s, they’re right 50 to 60 percent of the time. (The accuracy of Alzheimer’s diagnoses, even in specialized medical centers, is more haphazard than you would hope.) Perhaps another 25 percent of patients actually have other types of dementia, like Lewy body or frontotemporal — scarcely happy news, but because these diseases have different trajectories and can be exacerbated by the wrong drugs, the distinction matters. The remaining 15 to 25 percent “usually have conditions that can be reversed or at least improved,” Dr. Doraiswamy said. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 20227 - Posted: 10.22.2014

By GINA KOLATA For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease. In doing so, they resolved a longstanding problem of how to study Alzheimer’s and search for drugs to treat it; the best they had until now were mice that developed an imperfect form of the disease. The key to their success, said the lead researcher, Rudolph E. Tanzi of Massachusetts General Hospital in Boston, was a suggestion by his colleague Doo Yeon Kim to grow human brain cells in a gel, where they formed networks as in an actual brain. They gave the neurons genes for Alzheimer’s disease. Within weeks they saw the hard Brillo-like clumps known as plaques and then the twisted spaghetti-like coils known as tangles — the defining features of Alzheimer’s disease. The work, which also offers strong support for an old idea about how the disease progresses, was published in Nature on Sunday. Leading researchers said it should have a big effect. “It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.” Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 20203 - Posted: 10.13.2014

By Fredrick Kunkle Years ago, many scientists assumed that a woman’s heart worked pretty much the same as a man’s. But as more women entered the male-dominated field of cardiology, many such assumptions vanished, opening the way for new approaches to research and treatment. A similar shift is underway in the study of Alzheimer’s disease. It has long been known that more women than men get the deadly neurodegenerative disease, and an emerging body of research is challenging the common wisdom as to why. Although the question is by no means settled, recent findings suggest that biological, genetic and even cultural influences may play heavy roles. Of the more than 5 million people in the United States who have been diagnosed with Alzheimer’s, the leading cause of dementia, two-thirds are women. Because advancing age is considered the biggest risk factor for the disease, researchers largely have attributed that disparity to women’s longer life spans. The average life expectancy for women is 81 years, compared with 76 for men. Yet “even after taking age into account, women are more at risk,” said Richard Lipton, a physician who heads the Einstein Aging Study at Albert Einstein College of Medicine in New York. With the number of Alzheimer’s cases in the United States expected to more than triple by 2050, some researchers are urging a greater focus on understanding the underlying reasons women are more prone to the disease and on developing gender-specific treatments. .

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 20155 - Posted: 10.04.2014

By Fredrick Kunkle Here’s something to worry about: A recent study suggests that middle-age women whose personalities tend toward the neurotic run a higher risk of developing Alzheimer’s disease later in life. The study by researchers at the University of Gothenburg in Sweden followed a group of women in their 40s, whose disposition made them prone to anxiety, moodiness and psychological distress, to see how many developed dementia over the next 38 years. In line with other research, the study suggested that women who were the most easily upset by stress — as determined by a commonly used personality test — were two times more likely to develop Alzheimer’s disease than women who were least prone to neuroticism. In other words, personality really is — in some ways — destiny. “Most Alzheimer’s research has been devoted to factors such as education, heart and blood risk factors, head trauma, family history and genetics,” study author Lena Johansson said in a written statement. “Personality may influence the individual’s risk for dementia through its effect on behavior, lifestyle or reactions to stress.” The researchers cautioned that the results cannot be extrapolated to men because they were not included in the study and that further work is needed to determine possible causes for the link. The study, which appeared Wednesday in the American Academy of Neurology’s journal, Neurology, examined 800 women whose average age in 1968 was 46 years to see whether neuroticism — which involves being easily distressed and subject to excessive worry, jealousy or moodiness — might have a bearing on the risk of dementia.

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: 20148 - Posted: 10.02.2014

By Gary Stix If it’s good for the heart, it could also be good for the neurons, astrocytes and oligodendrocytes, cells that make up the main items on the brain’s parts list. The heart-brain adage comes from epidemiological studies that show that people with cardiovascular risk factors such as high-blood pressure and elevated cholesterol levels, may be more at risk for Alzheimer’s and other dementias. This connection between heart and brain has also led to some disappointments: clinical trials of lipid-lowering statins have not helped patients diagnosed with Alzheimer’s, although epidemiological studies suggest that long-term use of the drugs may help prevent Alzheimer’s and other dementias. The link between head and heart is still being pursued because new Alzheimer’s drugs have failed time and again. One approach that is now drawing some interest looks at the set of proteins that carry around fats in the brain. These lipoproteins could potentially act as molecular sponges that mop up the amyloid-beta peptide that clogs up connections among brain cells in Alzheimer’s. One of these proteins—Apolipoprotein J, also known as clusterin—intrigues researchers because of the way it interacts with amyloid-beta and the status of its gene as a risk factor for Alzheimer’s. A researcher from the University of Minnesota, Ling Li, recently presented preliminary work at the Alzheimer’s Disease Drug Discovery Foundation annual meeting that showed that, at least in a lab dish, a molecule made up of a group of amino acids from APOJ is capable of protecting against the toxicity of the amyloid-beta peptide. It also quelled inflammation and promoted the health of synapses—the junctions where one brain cell encounters another. Earlier work by another group showed that the peptide prevented the development of lesions in the blood vessels of animals.

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: 20135 - Posted: 09.30.2014

By Smitha Mundasad Health reporter, BBC News A spice commonly found in curries may boost the brain's ability to heal itself, according to a report in the journal Stem Cell Research and Therapy. The German study suggests a compound found in turmeric could encourage the growth of nerve cells thought to be part of the brain's repair kit. Scientists say this work, based in rats, may pave the way for future drugs for strokes and Alzheimer's disease. But they say more trials are needed to see whether this applies to humans. Researchers from the Institute of Neuroscience and Medicine in Julich, Germany, studied the effects of aromatic-turmerone - a compound found naturally in turmeric. Rats were injected with the compound and their brains were then scanned. Particular parts of the brain, known to be involved in nerve cell growth, were seen to be more active after the aromatic-turmerone infusion. Scientists say the compound may encourage a proliferation of brain cells. In a separate part of the trial, researchers bathed rodent neural stem cells (NSCs) in different concentrations of aromatic-tumerone extract. NSCs have the ability to transform into any type of brain cell and scientists suggest they could have a role in repair after damage or disease. Dr Maria Adele Rueger, who was part of the research team, said: "In humans and higher developed animals their abilities do not seem to be sufficient to repair the brain but in fish and smaller animals they seem to work well." Picture of the spice turmeric Turmeric belongs to the same plant family as ginger BBC © 2014

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: 20119 - Posted: 09.27.2014

By Linda Searing THE QUESTION Benzodiazepines such as Valium, Xanax and Ativan, widely prescribed to relieve anxiety and alleviate insomnia, are known to affect memory and cognition in the short term. Might they also have a more serious, longer-term effect on the brain? THIS STUDY analyzed data on 8,990 adults older than 66, including 1,796 with Alzheimer’s disease. In a five-to-10-year span before the start of the study, 3,767 of the participants (52 percent) had taken benzodiazepines. Overall, those who had taken the drugs were 51 percent more likely to have Alzheimer’s than were those who had never taken benzodiazepines. The longer people took the drugs, the greater their risk for Alzheimer’s. Those who took the drugs for less than 90 days had essentially the same risk as those who never took them. But risk nearly doubled for people who took them for longer than six months. Risk also was greater for longer-acting vs. shorter-acting benzodiazepines. WHO MAY BE AFFECTED? Adults, especially older people, who take benzodiazepines. The drugs have a calming effect on the body and work quickly, unlike antidepressants, which can take weeks to have an effect. The American Geriatrics Society lists benzodiazepines as inappropriate for treating older people for insomnia or agitation because of their negative effect on cognition seen in that age group and an increased likelihood of falls and accidents. However, some recent estimates note that roughly half of older adults take benzodiazepines. CAVEATS Some study participants may have been prescribed benzodiazepines to treat early symptoms of unrecognized dementia, which can include depression, anxiety and sleep disorders; the study authors noted that use of the drugs “might be an early marker of a condition associated with an increased risk of dementia and not the cause.”

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: 20079 - Posted: 09.16.2014

By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20078 - Posted: 09.16.2014

by Michael Slezak It's one of the biggest mysteries of Alzheimer's. The disease is associated with the formation of protein plaques in the brain, but why is it that some people with plaques seem not to have the disease? Research suggests that some people's brains are able to reorganise during the early stages of Alzheimer's, delaying the appearance of initial symptoms. The plaques in question are small mounds of a protein called beta-amyloid, and are found in the brains of people with Alzheimer's disease. Whether these plaques are a cause of the disease has been hotly debated. One reason for doubt is the appearance of plaques in many older people who have no symptoms Movie Cameraof dementia at all. Using fMRI to measure changes in blood flow around the brain, William Jagust from the University of California in Berkley and colleagues compared brain function in three groups of people without symptoms of dementia: 22 young people, 16 older people with beta-amyloid plaques and 33 older people without the plaques. He asked each of them to memorise a photographed scene while inside the machine. Jagust found that older people with plaques had increased blood flow – which means stronger activation of that brain area – in the regions of the brain that are usually activated during memory formation, compared with the older people who did not have plaques. The team then analysed whether this extra brain activation might be helping to compensate for the plaques. © Copyright Reed Business Information Ltd.

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: 20075 - Posted: 09.15.2014

By Helen Briggs Health editor, BBC News website There may be a link between a rare blood type and memory loss in later life, American research suggests. People with AB blood, found in 4% of the population, appear more likely to develop thinking and memory problems than those with other blood groups. The study, published in Neurology, builds on previous research showing blood type may influence heart risk. A charity said the best way to keep the brain healthy was a balanced diet, regular exercise and not smoking. A US team led by Dr Mary Cushman, of the University of Vermont College of Medicine, Burlington, analysed data from about 30,000 US citizens aged 45 and above. It identified 495 participants who had developed thinking and memory problems, or cognitive impairment, during the three-year study. They were compared to 587 people with no cognitive problems. People with AB blood type made up 6% of the group who developed cognitive impairment, which is higher than the 4% found in the general population. They were 82% more likely to have difficulties with day-to-day memory, language and attention, which can signal the onset of dementia. However, the study did not look at the risk of dementia. The study supported the idea that having a certain blood group, such as O, may give a lower risk for cardiovascular disease, which in turn protected the brain, the researchers said. "Our study looks at blood type and risk of cognitive impairment, but several studies have shown that factors such as high blood pressure, high cholesterol and diabetes increase the risk of cognitive impairment and dementia," said Dr Cushman. BBC © 2014

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: 20062 - Posted: 09.11.2014

By Helen Briggs Health editor, BBC News website Long-term use of pills for anxiety and sleep problems may be linked to Alzheimer's, research suggests. A study of older Canadian adults found that past benzodiazepine use for three months or more was linked to an increased risk (up to 51%) of dementia. NHS guidelines say the drugs should be used for eight to 12 weeks at most. The French-Canadian team says while the link is not definitive, it is another warning that treatments should not exceed three months. "Benzodiazepine use is associated with an increased risk of Alzheimer's disease," lead researcher, Sophie Billioti de Gage of the University of Bordeaux, France, and colleagues wrote in the BMJ. "Unwarranted long-term use of these drugs should be considered as a public health concern." The study involved about 2,000 cases of Alzheimer's disease in adults aged over 66 living in Quebec. All had been prescribed benzodiazepines. They were compared with about 7,000 healthy people of the same age living in the same community. While an increased risk was found in those on benzodiazepines, the nature of the link was unclear. Dr Eric Karran, director of research at Alzheimer's Research UK, said: "This study shows an apparent link between the use of benzodiazepines and Alzheimer's disease although it's hard to know the underlying reason behind the link. BBC © 2014

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: 20057 - Posted: 09.10.2014

By C. CLAIBORNE RAY Q. Is there a difference between alcoholic dementia and “regular” dementia in the elderly? A. Dementia refers to the general category of diseases that cause acquired cognitive loss, usually in later life, said Dr. Mark S. Lachs, director of geriatrics for the NewYork-Presbyterian Healthcare System. Such loss has scores of possible causes, he said, but Alzheimer’s disease is the culprit in a vast majority of cases in the developed world. Alzheimer’s and what doctors call alcohol-related dementia affect parts of the brain cortex that control memory, language and the ability to follow motor commands. Because Alzheimer’s and excessive drinking are relatively common in the older population and can occur at the same time, and because many of their clinical features overlap and affect similar parts of the brain, “it is more accurate to say that each condition potentially exacerbates the other,” Dr. Lachs said. Abstinence is the treatment of choice in alcohol-related dementia, with or without concurrent Alzheimer’s disease or another form of dementia. Even in patients with “pure” Alzheimer’s disease or another kind of dementia, Dr. Lachs said, most experts recommend greatly moderating alcohol consumption or eliminating it, as even occasional drinking “can serve as a brain stress test for a patient with impaired cognition from any cause.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20048 - Posted: 09.09.2014

By Fredrick Kunkle Years ago, many scientists assumed that a woman’s heart worked pretty much the same as a man’s. But as more women entered the male-dominated field of cardiology, many such assumptions vanished, opening the way for new approaches to research and treatment. A similar shift is underway in the study of Alzheimer’s disease. It has long been known that more women than men get the deadly neurodegenerative disease, and an emerging body of research is challenging the common wisdom as to why. Although the question is by no means settled, recent findings suggest that biological, genetic and even cultural influences may play heavy roles. Of the more than 5 million people in the United States who have been diagnosed with Alzheimer’s, the leading cause of dementia, two-thirds are women. Because advancing age is considered the biggest risk factor for the disease, researchers largely have attributed that disparity to women’s longer life spans. The average life expectancy for women is 81 years, compared with 76 for men. Yet “even after taking age into account, women are more at risk,” said Richard Lipton, a physician who heads the Einstein Aging Study at Albert Einstein College of Medicine in New York. With the number of Alzheimer’s cases in the United States expected to more than triple by 2050, some researchers are urging a greater focus on understanding the underlying reasons women are more prone to the disease and on developing gender-specific treatments. The area of inquiry has been growing in part because of a push by female Alzheimer’s researchers, who have formed a group to advocate for a larger leadership role in the field and more gender-specific research.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 20034 - Posted: 09.04.2014

by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © 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: 19969 - Posted: 08.18.2014

By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19943 - Posted: 08.12.2014