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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

Older people who have a severe vitamin D deficiency have an increased risk of developing dementia, a study has suggested. UK researchers, writing in Neurology, looked at about 1,650 people aged over 65. This is not the first study to suggest a link - but its authors say it is the largest and most robust. However, experts say it is still too early to say elderly people should take vitamin D as a preventative treatment. There are 800,000 people with dementia in the UK with numbers set to rise to more than one million by 2021. Vitamin D comes from foods - such as oily fish, supplements and exposing skin to sunlight. However older people's skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. The international team of researchers, led by Dr David Llewellyn at the University of Exeter Medical School, followed people for six years. All were free from dementia, cardiovascular disease and stroke at the start of the study. At the end of the study they found the 1,169 with good levels of vitamin D had a one in 10 chance of developing dementia. Seventy were severely deficient - and they had around a one in five risk of dementia. 'Delay or even prevent' Dr Llewellyn said: "We expected to find an association between low vitamin D levels and the risk of dementia and Alzheimer's disease, but the results were surprising - we actually found that the association was twice as strong as we anticipated." He said further research was needed to establish if eating vitamin D rich foods such as oily fish - or taking vitamin D supplements - could "delay or even prevent" the onset of Alzheimer's disease and dementia. But Dr Llewellyn added: "We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. BBC © 2014

Related chapters from BP7e: 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: 19923 - Posted: 08.07.2014

By Fredrick Kunkle The way older people walk may provide a reliable clue about how well their brain is aging and could eventually allow doctors to determine whether they are at risk of Alzheimer’s, researchers have found. The study, involving thousands of older people in several countries, suggests that those whose walking pace begins to slow and who also have cognitive complaints are more than twice as likely to develop dementia within 12 years. The findings are among the latest attempts to find and develop affordable, inexpensive diagnostic tools to determine whether a person is at risk for dementia. Last month, researchers attending the Alzheimer’s Association International Conference in Copenhagen presented several studies focused on locating biomarkers of dementia in its earliest stages. Among other things, scientists reported a connection between dementia and sense of smell that suggested a common scratch-and-sniff test could be used to help identify onset of dementia, while other researchers suggested that eye scans could also be useful someday be able to detect Alzheimer’s. Different studies found a new abnormal protein linked to Alzheimer’s and a possible link between sleep disorders and the onset of dementia. Now, researchers at the Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center say that a simple test to measure a patient’s cognitive abilities and walking speed could provide a new diagnostic tool to identify people at risk for dementia. It could be especially important tool in low- and middle-income countries with less access to sophisticated and costly technology, the scientists said.

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: 19910 - Posted: 08.02.2014

Tania Browne As a teenager, I lost my grandfather. But he wasn't dead. He still had his favourite music, he still loved to walk in the woods and name the flowers and plants, and he loved his soap operas. He was alive, but gone. A dignified man, a former aircraft engineer and oil company salesman, reduced to the status of a bewildered toddler lost in a shopping centre. When he died, our family felt an odd mix of relief, then guilt at the relief. The man we loved had left his body years before the body gave out. This was 30 years ago. But while a cure is still far away, two new techniques may at least be able to forewarn us of dementia, and allow us to plan treatment for ourselves or loved ones before any outward symptoms are apparent. According to Alzheimer's Research UK, my experience is currently shared by 24m relatives and close friends of the 800 000 diagnosed dementia sufferers in the UK. In December last year, a G8 summit was told by Alzheimer's Disease International that the worldwide figure was 44m and set to treble by 2050, as the life expectancy of people in middle and lower income countries soars – precisely the countries who have either depleted or non-existent healthcare systems. Dementia is a serious time bomb. “Dementia” covers about 100 conditions, all resulting from large scale brain cell death. People often think that when they're diagnosed they're in the early stages. Yet cell death can be occurring for 10-15 years or more before any outward symptoms occur, and by the time they're diagnosed many dementia patients have already lost one fifth of their memory cells. © 2014 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: 19856 - Posted: 07.21.2014

Associated Press The rate of Alzheimer's disease and other dementias is falling in the United States and some other rich countries - good news about an epidemic that is still growing simply because more people are living to an old age, new studies show. An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded. Dementia rates also are down in Germany, a study there found. "For an individual, the actual risk of dementia seems to have declined," probably because of more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer's Association International Conference in Copenhagen. The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising. More than 5.4 million Americans and 35 million people worldwide have Alzheimer's, the most common form of dementia. It has no cure, and current drugs only temporarily ease symptoms. A drop in rates is a silver lining in the so-called silver tsunami - the expected wave of age-related health problems from an older population. Alzheimer's will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said. © 2014 Hearst Communications, Inc.

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: 19838 - Posted: 07.16.2014

By PAULA SPAN What we really want, if we’re honest, is a pill or a shot that would allow us to stop worrying about ever sinking into dementia. Instead, what we’re hearing about preventing dementia is, in many ways, the same stuff we hear about preventing other kinds of illnesses. Healthy lifestyles. Behavioral modification. Stress reduction. At the Alzheimer’s Association International Conference in Copenhagen this week, researchers from Montefiore Medical Center and the Albert Einstein College of Medicine were among the scientists presenting findings that had little to do with amyloid in the brain and a lot to do with how people feel and act and cope with life. “A number of people have been interested in modifiable lifestyle factors for years,” said Richard Lipton, a neurologist at the college and director of the Einstein Aging Study, which has tracked cognition in elderly Bronx residents since the 1980s. But interest has increased lately, he said: “It’s at least in part a reflection of disappointing drug trials.” Medications have failed, over and over, to prevent or cure or substantially slow the ravages of dementing diseases. What else might help? Dr. Lipton and his colleagues, who monitor about 600 people aged 70 to 105, have been exploring the impact of stress. More specifically, they have been measuring “perceived stress,” a metric not so much about unpleasant things happening as how people respond to them. They use a scale based on the answers to 13 questions like, “In the past month, how often have you felt confident about your ability to handle your personal problems?” and “In the past month, how often have you felt difficulties were piling up so high you could not overcome them?” © 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: 19837 - Posted: 07.16.2014

|By Maria Burke and ChemistryWorld The world needs to tackle head-on the market failures undermining dementia research and drug development, UK Prime Minister David Cameron told a summit of world health and finance leaders in London in June. He announced an investigation into how to get medicines to patients earlier, extend patents and facilitate research collaborations, to report this autumn. But just how much difference will these sorts of measures make when scientists are still grappling with exactly what causes different types of dementia? Added to these problems is that dementia has become a graveyard for a large number of promising drugs. A recent study looked at how 244 compounds in 413 clinical trials fared for Alzheimer's disease between 2002 and 2012. The researchers findings paint a gloomy picture. Of those 244 compounds, only one was approved. The researchers report that this gives Alzheimer's disease drug candidates one of the highest failures rates of any disease area – 99.6%, compared with 81% for cancer. ‘Dementia is a ticking bomb costing the global economy £350 billion and yet progress with research is achingly slow,’ warned the World Dementia Envoy, Dennis Gillings. Businesses need incentives to invest in research and bring in faster, cheaper clinical trials, or the world won’t meet the ambition to find a cure or disease-modifying therapy by 2025, he added. ‘We need to free up regulation so that we can test ground-breaking new drugs, and examine whether the period for market exclusivity could be extended.’ © 2014 Scientific American

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: 19828 - Posted: 07.15.2014

By Fredrick Kunkle Sleep disturbances such as apnea may increase the risk of Alzheimer’s disease, while moderate exercise in middle age and mentally stimulating games, such as crossword puzzles, may prevent the onset of the dementia-causing disease, according to new research to be presented Monday. The findings — which are to be introduced during the six-day Alzheimer’s Association International Conference in Copenhagen — bolster previous studies that suggest sleep plays a critical role in the aging brain’s health, perhaps by allowing the body to cleanse itself of Alzheimer's-related compounds during down time. The studies also add to a growing body of literature that suggests keeping the brain busy keeps it healthy. The battle against Alzheimer’s disease has become more urgent for the United States and other developing nations as their populations turn increasingly gray. The disease is the leading cause of dementia in older people and afflicts more than 5 million Americans. At its current pace, the number is expected to soar to 16 million people by 2050. In 2012, the United States adopted a national plan to combat the disease and the G-8 nations last year adopted a goal of providing better treatment and prevention by 2025. Erin Heintz, a spokeswoman for the Alzheimer’s Association, said U.S. government funding to combat the disease now stands at about $500 million a year. To reach its 2025 goal, the United States should be spending $2 billion a year, she said.

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: 19825 - Posted: 07.14.2014

One in three cases of Alzheimer's disease worldwide is preventable, according to research from the University of Cambridge. The main risk factors for the disease are a lack of exercise, smoking, depression and poor education, it says. Previous research from 2011 put the estimate at one in two cases, but this new study takes into account overlapping risk factors. Alzheimer's Research UK said age was still the biggest risk factor. Writing in The Lancet Neurology, the Cambridge team analysed population-based data to work out the main seven risk factors for Alzheimer's disease. These are: Diabetes Mid-life hypertension Mid-life obesity Physical inactivity Depression Smoking Low educational attainment They worked out that a third of Alzheimer's cases could be linked to lifestyle factors that could be modified, such as lack of exercise and smoking. The researchers then looked at how reducing these factors could affect the number of future Alzheimer's cases. They found that by reducing each risk factor by 10%, nearly nine million cases of the disease could be prevented by 2050. In the UK, a 10% reduction in risk factors would reduce cases by 8.8%, or 200,000, by 2050, they calculated. 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: 19824 - Posted: 07.14.2014