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Alan Yuhas in Washington DC Scientists working on genetically modified worms have made what they hope are the first steps towards developing a preventative treatment for Alzheimer’s disease. The study, published in the journal Science Advances and presented at the American Association for the Advancement of Science conference, describes how researchers modified nematode worms to develop Alzheimer’s-like symptoms, and then applied the existing anti-cancer drug, bexarotene, at various stages of the disease. “We showed that these worms that were doomed to develop Alzheimer’s disease could be rescued,” said study author Michele Vendruscolo, of the University of Cambridge. “It is a powerful first step,” he said. “It is very exciting, but at the same time we are very aware it the first step and many things can go wrong.” Researchers believe that Alzheimer’s destroys brain function through a catastrophic cascade of events: natural proteins start folding and glomming onto each other in dysfunctional ways, a process that in turn creates the toxic molecules thought to kill brain cells. When the proteins started malfunctioning in the worms, the drug could do nothing to save them. But if administered before symptoms developed, it prevented the first stage of the process. © 2016 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: 21890 - Posted: 02.13.2016

By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company

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: 21887 - Posted: 02.11.2016

By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 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: 21879 - Posted: 02.10.2016

Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016

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: 21871 - Posted: 02.09.2016

Alison Abbott For the second time in four months, researchers have reported autopsy results that suggest Alzheimer’s disease might occasionally be transmitted to people during certain medical treatments — although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly1 on 26 January, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater — the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD. But in addition to the damage caused by the prions, five of the brains displayed some of the pathological signs that are associated with Alzheimer’s disease, researchers from Switzerland and Austria report. Plaques formed from amyloid-β protein were discovered in the grey matter and blood vessels. The individuals, aged between 28 and 63, were unusually young to have developed such plaques. A set of 21 controls, who had not had surgical grafts of dura mater but died of sporadic CJD at similar ages, did not have this amyloid signature. According to the authors, it is possible that the transplanted dura mater was contaminated with small ‘seeds’ of amyloid-β protein — which some scientists think could be a trigger for Alzheimer’s — along with the prion protein that gave the recipients CJD. © 2016 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21822 - Posted: 01.26.2016

By Esther Landhuis Amid gloomy reports of an impending epidemic of Alzheimer’s and other dementias, emerging research offers a promising twist. Recent studies in North America, the U.K. and Europe suggest that dementia risk among seniors in some high-income countries has dropped steadily over the past 25 years. If the trend is driven by midlife factors such as building “brain reserve” and maintaining heart health, as some experts suspect, this could lend credence to staying mentally engaged and taking cholesterol-lowering drugs as preventive measures. At first glance, the overall message seems somewhat confusing. Higher life expectancy and falling birth rates are driving up the global elderly population. “And if there are more 85-year-olds, it’s almost certain there will be more cases of age-related diseases,” says Ken Langa, professor of internal medicine at the University of Michigan. According to the World Alzheimer Report 2015 (pdf), 46.8 million people around the globe suffered from dementia last year, and that number is expected to double every 20 years. Looking more closely, though, new epidemiological studies reveal a surprisingly hopeful trend. Analyses conducted over the last decade in the U.S., Canada, England, the Netherlands, Sweden and Denmark suggest that “a 75- to 85-year-old has a lower risk of having Alzheimer’s today than 15 or 20 years ago,” says Langa, who discussed the research on falling dementia rates in a 2015 Alzheimer’s Research & Therapy commentary (pdf). © 2016 Scientific America

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: 21821 - Posted: 01.26.2016

By David Shultz A rat navigating a maze has to rank somewhere near the top of science tropes. Now, scientists report that they’ve developed an analogous test for humans—one that involves driving through a virtual landscape in a simulated car. The advance, they say, may provide a more sensitive measure for detecting early signs of Alzheimer’s disease. “I think it’s a very well-done study,” says Keith Vossel, a translational neuroscientist at the University of California, San Francisco (UCSF), who was not involved with the work. In the rodent version of the so-called Morris Maze Test, researchers fill a large cylindrical container with water and place a platform just above the waterline. A scientist then places a rat into the tank, and the rodent must swim to the platform to avoid drowning. The experimenter then raises the water level just above the height of the platform and adds a compound to the water to make it opaque. The trial is repeated, but now the rat must find the platform without seeing it, using only its memory of where the safe zone exists relative to the tank’s walls and the surrounding environment. In subsequent trials, researchers place the rat at different starting points along the tank’s edge, but the platform stays put. In essence, the task requires the rat to move to a specific but invisible location within a circular arena from different starting points. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21803 - Posted: 01.20.2016

Blocking the production of new immune cells in the brain could reduce memory problems seen in Alzheimer's disease, a study suggests. University of Southampton researchers said their findings added weight to evidence that inflammation in the brain is what drives the disease. A drug used to block the production of these microglia cells in the brains of mice had a positive effect. Experts said the results were exciting and could lead to new treatments. Up until now, most drugs used to treat dementia have targeted amyloid plaques in the brain which are a characteristic of people with the Alzheimer's disease. But this latest study, published in the journal Brain, suggests that in fact targeting inflammation in the brain, caused by a build-up of immune cells called microglia, could halt progression of the disease. Researchers found increased numbers of microglia in the post-mortem brains of people with Alzheimer's disease. Previous studies have also suggested that these cells could play an important role. Dr Diego Gomez-Nicola, lead study author from the university, said: "These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease. "The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans." © 2016 BBC

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: 21762 - Posted: 01.08.2016

By Karen Weintraub Mild cognitive impairment, or M.C.I., is not a disease in itself. Rather, it is a clinical description based on performance on a test of memory and thinking skills. Depending on its cause, mild cognitive impairment is potentially reversible. Poor performance on a cognitive test could be caused by certain medications, sleep apnea, depression or other problems, said Dr. Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School and Beth Israel Deaconess Medical Center. In those cases, when the underlying disease is treated, cognitive abilities can bounce back. But in about half of people with M.C.I. – doctors are not sure of the exact number — memory problems are the first sign of impending Alzheimer’s disease. If M.C.I. progresses to Alzheimer’s, there is no recovery. Alzheimer’s is marked by an inexorable decline that is always fatal, although the path from the first signs of cognitive impairment to death may take three to 15 years, said Dr. David Knopman, a professor of neurology at the Mayo Clinic in Rochester, Minn. As many as 20 percent to 30 percent of those with M.C.I. who score below but near the cutoff for normal can cross back above in a subsequent cognitive test – perhaps because they are having a better day, he said. But someone whose score is borderline is at higher risk of developing Alzheimer’s than someone who scores higher, said Dr. Knopman, also vice chair of the medical and scientific advisory council of the Alzheimer’s Association. Doctors may be hesitant to label someone with early Alzheimer’s, which can be difficult to diagnose in the early stages, so they often call it mild cognitive impairment instead, said Dr. John C. Morris, a professor of neurology and the director of the Knight Alzheimer's Disease Research Center at Washington University School of Medicine in St. Louis. © 2015 The New York Times Company

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: 21728 - Posted: 12.29.2015

A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease, creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of Alzheimer’s may prevent dementia and reduce damage to the brain. “This exciting research advances our understanding of the role of the proteasomes in neurodegeneration and provides a potential way to alleviate symptoms of neurodegenerative disorders,” said Roderick Corriveau, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. The proteasome is a hollow, cylindrical structure which chews up defective proteins into smaller, pieces that can be recycled into new proteins needed by a cell. To understand how neurodegenerative disorders affect proteasomes, Natura Myeku, Ph.D., a postdoctoral fellow working with Karen E. Duff, Ph.D., professor of pathology and cell biology at Columbia University, New York City, focused on tau, a structural protein that accumulates into clumps called tangles in the brain cells of patients with Alzheimer’s disease and several other neurodegenerative disorders known as tauopathies. Using a genetically engineered mouse model of tauopathy, as well as looking at cells in a dish, the scientists discovered that as levels of abnormal tau increased, the proteasome activity slowed down.

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: 21716 - Posted: 12.22.2015

By Gretchen Reynolds Physical fitness may be critical for maintaining a relatively youthful and nimble brain as we age, according to a new study of brain activation patterns in older people. For most of us, our bodies begin to lose flexibility and efficiency as we enter our 40s. Running and other movements slow down and become more awkward, and something similar seems to occur within our heads. As middle age encroaches, our thinking becomes less efficient. We don’t toggle between mental tasks as nimbly as we once did or process new information with the same aplomb and clarity. Recently, neuroscientists have begun to quantify how those cognitive changes play out in our brains, to disquieting effect. In studies comparing brain activation in young people with that of people past 40, they have found notable differences, especially during mental tasks that require attention, problem solving, decision-making and other types of high-level thinking. Such thinking primarily involves activation of the brain’s prefrontal cortex. In young people, activation in the cortex during these cognitive tasks tends to be highly localized. Depending on the type of thinking, young people’s brains light up almost exclusively in either the right or left portion of the prefrontal cortex. But in older people, studies show, brain activity during the same mental tasks requires far more brainpower. They typically display activity in both hemispheres of their prefrontal cortex. In effect, they require more of their brains’ resources to complete the same tasks that young people do with less cognitive effort. Neuroscientists coined an acronym for this phenomenon: Harold, for hemispheric asymmetry reduction in older adults. Most agree that it represents a general reorganization and weakening of the brain’s function with age. © 2015 The New York Times Company

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: 21688 - Posted: 12.10.2015

By Lindzi Wessel Nighttime restlessness is common among people with Alzheimer’s, and many stay awake agitated and pacing long after their family members have gone to sleep. Now, scientists may have figured out why: The disease appears to degrade a special type of eye cell that tells the brain when it’s day or night. If the discovery holds up, it might offer clinicians a new way to monitor the progression of Alzheimer’s and could lead to treatments that restore a good night’s sleep. The cells in question are known as melanopsin retinal ganglion cells. They send signals to the brain center responsible for circadian rhythms, our body’s daily clock. The cells make up 1% to 2% of the eye’s light-responsive sensors, but they play no role in vision, says lead author Chiara La Morgia, a neuroscientist at the University of Bologna in Italy. Rather, they sense light levels around us, telling us when to get sleepy and when to be alert. La Morgia and her colleagues, aware of the profound sleep problems often seen in Alzheimer’s, wondered whether the cells may stop doing their job as the disease progresses. “If you lose them, you should see dysfunction of the circadian rhythms and see disrupted sleep,” says Alfredo Sadun, neuro-opthamologist at the University of California, Los Angeles, and co-author of the study. “That is the exact symptomology we see in Alzheimer’s disease.” To learn more, the researchers used dyes to mark melanopsin cells in the eyes of 30 recently deceased organ donors. They found approximately 24% fewer melanopsin cells in the eyes of people with Alzheimer’s than in the eyes of donors without the disease. © 2015 American Association for the Advancement of Science.

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: 21686 - Posted: 12.09.2015

Ian Sample Science editor Scientists have discovered a chemical that destroys toxic plaques which build up in the brain in the early stages of Alzheimer’s disease. Preliminary tests found that when added to drinking water, the compound cleared amyloid beta plaques from the brains of mice with Alzheimer’s-like symptoms, and restored their cognitive function to normal. The work is at a very early stage, but raises hopes for drugs that can prevent the accumulation of amyloid plaques and potentially halt the progression of the disease. Amyloid plaques are one of the first hallmarks of Alzheimer’s disease and are thought to contribute to neurodegeneration by killing off brain cells. Researchers in Korea discovered the chemical, EPPS, while screening a variety of molecules for their effects on amyloid plaques. In the latest study, they added the substance to the drinking water of mice that had symptoms of Alzheimer’s disease. They found that administering EPPS for a week improved how well mice performed on maze tests, and cleared amyloid plaques from the animals’ brains. “Our findings clearly support the view that aggregated amyloid-beta is the pathological culprit of Alzheimer’s disease,” said YoungSoo Kim, who led the team at the Korea Institute of Science and Technology in Seoul. The study used mice that had amyloid plaques injected into their brains. The animals suffered cognitive impairments as a result, but they did not develop the kind of widespread brain damage seen in Alzheimer’s patients which would not be reversed by removing amyloid plaques. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21685 - Posted: 12.09.2015

By Kelli Whitlock Burton Evolutionarily speaking, we are born to make babies. Our bodies—and brains—don’t fall apart until we come to the end of our child-bearing years. So why are grandmothers, who don’t reproduce and who contribute little to food production, still around and still mentally sound? A new study offers an intriguing genetic explanation. Scientists have proposed several explanations for why our species lives as long and as healthily as it does. One idea is that grandmothers help out with child rearing. A 1998 study found, for example, that a Hadza group of hunter-gatherers in Tanzania had more babies if grandmothers helped feed their newly-weaned young grandchildren. The researchers speculated this kind of care freed up young mothers to reproduce, and ensured that the caregiver grandmother’s genes were passed on to more young. They called their theory the “grandmother hypothesis.” But grandmothers need to have all their wits about them to help out in this way, and the new study may explain how this happens. Physician-scientist Ajit Varki and evolutionary biologist Pascal Gagneux of the University of California, San Diego, arrived at the findings accidentally. The pair was studying a gene that helps control the body’s inflammatory and immune response to injury or infection. Previous studies have linked two forms of the gene—CD33—to Alzheimer’s disease. While one CD33 variant, or allele, predisposes a person to the disease, the other appears to protect against it by preventing the formation of protein clumps in the brain. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21669 - Posted: 12.01.2015

The town of Yarumal in Colombia is famous for all the wrong reasons: it has the world’s largest population of people with Alzheimer’s disease. In Yarumal and the surrounding state of Antioquia, 5000 people carry a gene mutation which causes early-onset Alzheimer’s – half of them will be diagnosed by the age of 45, and the other half will succumb by the time they are 65. Locals call the disease La Bobera, “the foolishness”, and the village bears uncanny parallels with the fictional Macondo in Gabriel Garcia Marquez’s novel One Hundred Years of Solitude, where people suffer memory disorders and hallucinations. But while Yarumal’s “curse” is well known, no one knew how the mutation first appeared. Now researchers have traced the ancestry of the mutation, concluding that it was probably introduced by a Spanish conquistador early in the 17th century. Ken Kosik at the University of California, Santa Barbara, and colleagues collected blood samples from 102 people in Antioquia and sequenced their genomes. The mutation causing this form of early-onset Alzheimer’s is called E280A and is found in a gene on chromosome 14 – 74 people had the mutation. Because Kosik’s team had information on the genome sequence around the mutation, they could use something called identity-by-descent analysis to determine how the people in the study were related. The analysis suggested the mutation arose from a common ancestor around 375 years ago. © 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: 21647 - Posted: 11.20.2015

By Gretchen Reynolds Sturdy legs could mean healthy brains, according to a new study of British twins. As I frequently have written in this column, exercise may cause robust improvements in brain health and slow age-related declines in memory and thinking. Study after study has shown correlations between physical activity, muscular health and mental acuity, even among people who are quite old. But these studies have limitations and one of them is that some people may be luckier than others. They may have been born to have a more robust brain than someone else. Their genes and early home environment might have influenced their brain health as much as or more than their exercise habits. Their genes and early home environment also might have influenced those exercise habits, as well as how their bodies and brains responded to exercise. In other words, genes and environment can seriously confound experimental results. That problem makes twins so valuable for scientific purposes. (Full disclosure, I am a twin, although not an identical one.) Twins typically share the same early home environment and many of the same genes, and if they are identical, all their genes are the same. So if one twin’s body, brain and thinking abilities begin to differ substantially over the years from their twin’s, the cause is less likely to be solely genetic or the early environment, and more likely to be attributable to lifestyle, including exercise habits. It was that possibility that recently prompted Claire Steves, a senior lecturer in twin research at King’s College London, to consider twins and their thighs. © 2015 The New York Times Company

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: 21641 - Posted: 11.18.2015

Laura Sanders In an unexpected twist, two antibodies designed to fight Alzheimer’s disease instead made nerve cells in mice misbehave more. The results, published online November 9 in Nature Neuroscience, highlight how little is known about how these drugs actually work, says study coauthor Marc Aurel Busche of Technical University Munich. “We need to understand what these antibodies do in the brains of patients better,” he says. The treatment approach relies on antibodies that target amyloid-beta, a protein that builds up in the brains of people with Alzheimer’s. One of the antibodies used in the new study, bapineuzumab, failed to show benefits in much-anticipated trials described in the New England Journal of Medicine in 2014. Despite that setback, some researchers say antibodies are still the best option to halt Alzheimer’s. The bapineuzumab trial was flawed, says neurologist Dennis Selkoe of Harvard Medical School and Brigham and Women’s Hospital. And the new results, which come from mice, have little relevance for ongoing tests of other antibodies in people, he says. “A-beta immunotherapy is the most promising approach right now, and nothing in their paper undercuts that,” he says. Several other antibodies have recently shown modest benefits in people with Alzheimer’s, he adds. Representatives from Eli Lilly and Biogen, pharmaceutical companies that are developing antibody treatments, declined to comment on the new study. © Society for Science & the Public 2000 - 2015

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: 21622 - Posted: 11.10.2015

By Michelle Roberts Health editor, BBC News online An increasingly warped sense of humour could be an early warning sign of impending dementia, say UK experts. The University College London study involved patients with frontotemporal dementia, with the results appearing in the Journal of Alzheimer's Disease. Questionnaires from the friends and family of the 48 patients revealed many had noticed a change in humour years before the dementia had been diagnosed. This included laughing inappropriately at tragic events. Experts say more studies are now needed to understand how and when changes in humour could act as a red flag for dementia. There are many different types of dementia and frontotemporal dementia is one of the rarer ones. The area of the brain it affects is involved with personality and behaviour, and people who develop this form of dementia can lose their inhibition, become more impulsive and struggle with social situations. Dr Camilla Clark and colleagues recruited 48 patients from their dementia clinic at University College London. And they asked the friends or relatives of the patients to rate their loved one's liking for different kinds of comedy - slapstick comedy such as Mr Bean, satirical comedy such as Yes, Minister or absurdist comedy such as Monty Python - as well as any examples of inappropriate humour. Nearly all of the respondents said, with hindsight, that they had noticed a shift in the nine years before the dementia had been diagnosed. Many of the patients had developed a dark sense of humour - for example, laughing at tragic events in the news or in their personal lives. The dementia patients also tended to prefer slapstick to satirical humour, when compared with 21 healthy people of a similar age. © 2015 BBC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21617 - Posted: 11.10.2015

By DAVE ITZKOFF and BENEDICT CAREY For the first time in more than a year, the widow of the actor Robin Williams is speaking publicly about the circumstances that preceded Mr. Williams’s death, and sharing details about a disease he had when he died. Stories from Our Advertisers In interviews with People magazine and with ABC News, the widow, Susan Schneider Williams, laid the blame for her husband’s suicide in 2014 not on depression but on diffuse Lewy body dementia. “It was not depression that killed Robin,” Mrs. Williams said in the People magazine interview. “Depression was one of let’s call it 50 symptoms and it was a small one.” She added: “This was a very unique case and I pray to God that it will shed some light on Lewy bodies for the millions of people and their loved ones who are suffering with it. Because we didn’t know. He didn’t know.” Parts of an interview with Mrs. Williams were shown Tuesday on ABC’s “Good Morning America,” with further segments scheduled for that evening on the network’s “World News Tonight” and “Nightline” programs, and Friday on its morning talk show “The View.” Robin Williams was one of the most explosively, exhaustingly, prodigiously verbal comedians who ever lived, says film critic A. O. Scott. And the only thing faster than Williams’s mouth was his mind. By Adam Freelander on Publish Date August 12, 2014. Photo by ABC, via Associated Press. Watch in Times Video » Mr. Williams, the stand-up comic and star of “Mork & Mindy,” “Good Morning, Vietnam,” “Good Will Hunting” (for which he won an Oscar) and “Dead Poets Society,” killed himself on Aug. 11, 2014, in the home he shared with Mrs. Williams in Tiburon, Calif. He was 63. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 21601 - Posted: 11.04.2015

A drug for Alzheimer’s seems to delay the point at which a person with the condition needs to be moved into a nursing home. Donepezil is usually given to people with moderate forms of the disease, but continuing to take the drug once the disease becomes more severe seems to prolong the period of time a person can remain in their own home. Previously, the drug was not thought to benefit people once they had developed more severe forms of Alzheimer’s. But a study that followed 295 people with moderate to severe Alzheimer’s disease found that those who continued to take donepezil were nearly half as likely to end up in a care home within the next year. “It could mean thousands of patients per year not going into care homes,” says Robert Howard of University College London, who led the study. His team found that those who continued to take donepezil had a 20 per cent chance of being moved into a care home within the first year of the trial, compared to 37 per cent in those who stopped taking the drug. However the effect didn’t last. The trial lasted for three years, and after the first year, those who taking donepezil were just as likely to be moved into a home than those who weren’t, suggesting that the drug does not have a longer-term effect on the care needs of those with Alzheimer’s. “For every six patients treated with donepezil for 12 months, you would prevent one moving into a nursing home,” says Howard. “It’s a modest effect, but it’s important if it’s your mother or your wife.” © 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: 21577 - Posted: 10.28.2015