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by Jessica Hamzelou THE next generation may live to see 100, and with old age inevitably comes illness. While older people may be more prone to getting cancer or Alzheimer's, it seems they are unlikely to succumb to both. Understanding this link could offer insights into treating both diseases. The association was first noticed in 2005 when researchers looked at how many people over 65 with cancer later developed Alzheimer's, and vice versa. To further explore the link, Massimo Musicco at the Institute of Biomedical Technology in Milan, Italy, and his colleagues recorded cancer and Alzheimer's diagnoses for over a million people by looking at registries of drug prescriptions and hospital admissions between 2004 and 2009. In each case of cancer or Alzheimer's, they checked for the other disease before the person was treated, as well as in the years after. The group found that people with Alzheimer's were half as likely to develop cancer as their age-matched peers. People with cancer, on the other hand, were 35 per cent less likely to get Alzheimer's. "It's a very convincing demonstration of the links between two pathologies that we often think of as separate," says Richard Faragher of the British Society for Research on Ageing. "The question is: what is going on?" Although both diseases are linked to ageing, they work in very different ways. While cancer results from the uncontrolled growth of cells, Alzheimer's is related to the death of brain cells. © 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: 18365 - Posted: 07.11.2013

By Helen Briggs BBC News Keeping mentally active by reading books or writing letters helps protect the brain in old age, a study suggests. A lifetime of mental challenges leads to slower cognitive decline after factoring out dementia's impact on the brain, US researchers say. The study, published in Neurology, adds weight to the idea that dementia onset can be delayed by lifestyle factors. An Alzheimer's charity said the best way to lower dementia risk was to eat a balanced diet, exercise and stay slim. In a US study, 294 people over the age of 55 were given tests that measured memory and thinking, every year for about six years until their deaths. They also answered a questionnaire about whether they read books, wrote letters and took part in other activities linked to mental stimulation during childhood, adolescence, middle age, and in later life. After death, their brains were examined for evidence of the physical signs of dementia, such as brain lesions and plaques. The study found that after factoring out the impact of those signs, those who had a record of keeping the brain busy had a rate of cognitive decline estimated at 15% slower than those who did not. Dr Robert Wilson, of Rush University Medical Center in Chicago, who led the study, said the research suggested exercising the brain across a lifetime was important for brain health in old age. BBC © 2013

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: 18347 - Posted: 07.04.2013

By Rachel Nuwer Doctors and nutritionists have long associated the Mediterranean diet with human health benefits, including a lower risk of Alzheimer's disease. A recent study of 1,880 elderly people living in New York City, for example, showed that those who strongly adhered to a Mediterranean diet over the study's 14-year span had a 32 to 40 percent lower incidence of Alzheimer's compared with those who did not. Extra virgin olive oil seems to be one of the main factors behind this risk reduction. People adhering to a Mediterranean diet consume up to 50 milliliters (around one fifth of a cup) of the fragrant green liquid a day. Previously, researchers assumed this benefit came from extra virgin olive oil's high concentration of monounsaturated fatty acids. But in 2005 scientists discovered that oleocanthal—the naturally occurring compound that elicits a peppery, burning sensation in the back of the throat—seemed to produce effects strikingly similar to those of ibuprofen, which tamps down inflammation. Since then, investigators have turned their attention to the potential benefits of this particular compound. Some studies have shown that oleocanthal interferes with the formation of characteristic neurofibrillary tangles and beta-amyloid plaques, both of which play principal roles in Alzheimer's neurological devastation. Research published online in ACS Chemical Neuroscience in February offers new details on how the compound works. The study authors applied different concentrations of oleocanthal over three days to mouse brain cell cultures. They also administered oleocanthal to live mice—the first time such an experiment has been done—every day for two weeks. In both trials, levels of two proteins that play major roles in transporting beta-amyloid out of the brain as well as enzymes that degrade beta-amyloid increased significantly after administering oleocanthal. © 2013 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18278 - Posted: 06.15.2013

Robert Bazell NBC News Just two years ago, Barbara Whitmarsh was a woman who seemed to have it all. She was a highly regarded scientist at the National Institutes of Health. Married for 30 years, she’d raised six children with her beloved husband, John. But then John Whitmarsh started to notice some disturbing changes in his wife, now 62. It was as if the woman he’d married and lived with all that time was slowly and inexorably fading away. “Her ability to feel empathy, her personality, it just disappeared over a period of time,” John said. “I would ask her, ‘Is there anything wrong?’ and she would say, ‘No, I love you and everything's fine,’ but she wasn't there. And she said it in that flat way.” A scientist himself, Whitmarsh knew there was, indeed, something wrong. And he was worried. He asked his wife to see a psychiatrist who eventually diagnosed her with frontotemporal dementia or FTD. It’s a dementia that generally strikes at an earlier age than Alzheimer’s disease. And its symptoms are different – at least in the beginning – from Alzheimer’s because it originates in a different part of the brain. It’s also a disease that until very recently doctors thought was rare -- but that view is changing. “We've begun to realize that frontotemporal dementia is actually more common than Alzheimer's disease in people with degenerative disorders under the age of 60,” said Dr. Bruce Miller, director of the Memory and Aging Center at the University of California, San Francisco.

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: 18277 - Posted: 06.15.2013

Helen Shen Bexarotene, a cancer drug touted as a potential treatment for Alzheimer’s disease, may not be the blockbuster remedy scientists were hoping for, according to several analyses published in Science on 24 May1–4. Four independent research groups report that they failed to fully replicate striking results published in the journal last year5 by Gary Landreth, a neuroscientist at Case Western Reserve University School of Medicine in Cleveland, Ohio, and his colleagues. Landreth's team reported that the drug bexarotene could lower brain concentrations of the β-amyloid protein that has long been suspected as a key contributor to Alzheimer’s disease, and could even reverse cognitive impairments in diseased mice. But the study garnered particular attention for its claim that the drug could clear 50% of amyloid plaques — sticky clumps of the protein thought to interfere with brain function — in as little as 72 hours. “That attracted a lot of folks to try to replicate these studies,” says Philip Wong, a neuroscientist at Johns Hopkins University in Baltimore, Maryland. “No drug at the present moment can do things like that.” None of the follow-up studies published this week replicated the effects of bexarotene on plaques. Two groups did, however, confirm Landreth’s finding that the drug reduced levels of a soluble, free-floating form of β-amyloid, which can aggregate in plaques4. Not all of the papers examined memory in mice, but one group led by Radosveta Koldamova, a neuroscientist at the University of Pittsburgh in Pennsylvania, found that bexarotene treatment led to cognitive improvements1. © 2013 Nature Publishing Group

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: 18190 - Posted: 05.25.2013

by Caroline Williams Those at risk of developing Alzheimer's may be able to slow its onset through daily B vitamins. We already know that a high level of the amino acid homocysteine in the blood is a risk factor for Alzheimer's, and that B vitamin supplements help reduce homocysteine levels. But it was unclear whether or not these supplements would slow the progression of mild cognitive impairment (MCI) to Alzheimer's. David Smith and Gwenaëlle Douaud at the University of Oxford led a research effort to find out. They used MRI to track changes in the brains of 200 elderly volunteers with MCI over two years. During this time, half were given high doses of vitamin B12, B6 and folic acid – 300, 20 and 4 times the UK guideline daily amounts, respectively. The rest took a placebo. In 2010, Smith and his colleagues showed that high doses of B vitamins slowed whole-brain shrinkage by up to 53 per cent in patients with above average homocysteine levels. Now Smith and Douaud's team have looked deeper to work out which brain regions are best protected. They found that it was the areas of the brain most seriously affected by Alzheimer's, including the hippocampus and cerebellum, that were protected in volunteers given the vitamins. For instance, in those with high homocysteine, the atrophy rate in these brain regions was 5.2 per cent in the placebo group but just 0.6 per cent in the vitamin group. © 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: 18177 - Posted: 05.21.2013

By Maggie Fox, Senior Writer, NBC News It might seem against all logic, but adding a little olive oil or a handful of nuts to your diet each day may help keep your mind clear, researchers reported on Monday. It’s the same diet that’s also been shown to reduce deaths from heart attacks and strokes. The researchers found that people who ate these healthy fats were less likely to show the early signs of dementia than those who stuck to a more traditional diet. And this was done in Spain -- where people are already eating a so-called Mediterranean diet. “Our findings support increasing evidence on the protective effects of the Mediterranean Diet on cognitive function,” Miguel Martinez-Gonzalez of the University of Navarra in Spain and colleagues reported in the Journal of Neurology, Neurosurgery and Psychiatry. The findings come from a large and well-publicized trial that showed the Mediterranean diet rich in fruits, vegetables, olive oil and a little wine can cut the risk of heart attacks and strokes by 30 percent. Martinez and colleagues took a part data on 500 volunteers from their own study center, who were followed for more than six and a half years after starting the diet. A Mediterranean diet includes lots of salad, fruit, vegetables, nuts, a little fish, a little lean meat, a small amount of cheese and olive oil. Wine is also served at meals. In the main study, 7,400 volunteers got extra counseling, and either a weekly supply of extra-virgin olive oil or mixed nuts -- walnuts, almonds and hazelnuts. © 2013 NBCNews.com

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18176 - Posted: 05.21.2013

By MARILYNN MARCHIONE DEERFIELD, Ill. (AP) — Baxter International Inc. says that a blood product it was testing failed to slow mental decline or to preserve physical function in a major study of 390 patients with mild to moderate Alzheimer’s disease. The company says that people who received 18 months of infusions with its drug, Gammagard, fared no better than others given infusions of a dummy solution. Gammagard is immune globulin, natural antibodies culled from donated blood. Researchers thought these antibodies might help remove amyloid, the sticky plaque that clogs patients’ brains, sapping memory and ability to think. Patients with moderate disease and those with a gene that raises risk of Alzheimer’s who were taking the higher of two doses in the study seemed to benefit, although the study was not big enough to say for sure. ‘‘The study missed its primary endpoints, however we remain interested by the prespecified sub-group analyses’’ in groups that seemed to benefit, Ludwig Hantson, president of Baxter’s BioScience business, said in a statement. Gammagard is already sold to treat some blood disorders, and the results of the Alzheimer’s study do not affect those uses. About 35 million people worldwide have dementia, and Alzheimer’s is the most common type. In the U.S., about 5 million have Alzheimer's. Current medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure. © 2013 NY Times Co.

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: 18131 - Posted: 05.08.2013

By Gisela Telis, I’ve seen friends fret over the purported link between aluminum and Alzheimer’s disease and have often wondered if their fears are founded on fact. Should they give up aluminum pans or aluminum-containing antiperspirants? I’ve always heard that aluminum’s health dangers are just hype. So what’s the real deal? The connection between aluminum and Alzheimer’s disease is less a myth than a longstanding scientific controversy. It began in 1965, when researchers discovered that injecting rabbits’ brains with aluminum caused them to develop neurofibrillary tangles, the twisted proteins found in brain cells of patients with Alzheimer’s disease, a degenerative brain disorder that destroys memory and cognition. The finding spurred a rush of research. Just eight years later, a Canadian group studying brain tissue from deceased Alzheimer’s patients found that certain parts of their brains had two to three times more aluminum than a normal brain. By 1980, Daniel Perl and Arnold Brody had managed to actually peer inside human tangle-bearing brain cells — and found aluminum there, too. “That really changed the whole complexion of the thing,” recalls Perl, now a professor of pathology in the Uniformed Services University of the Health Sciences in Bethesda. “I was getting called all the time, because there was so much public interest.” Despite the rise in interest, no one could figure out what this meant for human health. Part of the problem was that scientific techniques were — and still are — too imperfect to provide an answer. Whether they were studying brain cells or conducting population-wide epidemiological studies that tracked aluminum exposure and Alzheimer’s risk, researchers lacked the tools to get very precise or conclusive results. © 1996-2013 The Washington Post

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: 18125 - Posted: 05.07.2013

A rat with some human genes could provide a better way to test Alzheimer's drugs. The genetically modified rat is the first rodent model to exhibit the full range of brain changes found in Alzheimer's, researchers in The Journal of Neuroscience. "It's a big step forward" for drug development, says , a program director at the National Institute of Neurological Disorders and Stroke, or NINDS, which helped fund the work. "The closer the model is to the human condition in representing the disease, the more likely the drug will behave and cure the way it would in humans." In recent years, drug companies have developed several Alzheimer's drugs that seemed to work in animals, but with the disease. A lack of good animal models for Alzheimer's may be one reason for those failures, researchers say. For the past couple of decades, Alzheimer's researchers have relied primarily on mice that carry human gene mutations that cause people to get the disease in their 40s or 50s. Like people, these mice develop so-called amyloid plaques in their brains. But that's where the similarity ends. In people with Alzheimer's, after plaques appear, huge numbers of brain cells die. That's never happened in mice, despite lots of genetic tinkering, Corriveau says. So researchers began to consider a different rodent model: the rat. "Rats are 4 [million] to 5 million years closer evolutionarily to humans," Corriveau says, which means their brains are more like ours. ©2013 NPR

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18016 - Posted: 04.11.2013

By PAULA SPAN The long list of roles Margaret Thatcher played during her 87 years — potent politician, free-market evangelist, labor antagonist, dominant global leader — includes the one she never publicly discussed: person with dementia. The stroke that killed her on Monday was not her first. Mrs. Thatcher suffered several small strokes more than a decade earlier, canceled all her speaking engagements in 2003 and largely withdrew from public life. Even before the strokes, her daughter, Carol, wrote in a 2008 memoir, she was losing cognitive ground, repeating questions and showing other signs of confusion. Heartbreakingly, she often forgot that her beloved husband, Denis, had died of cancer in 2003. “I had to keep giving her the bad news over and over again,” her daughter wrote. “Every time it finally sank in that she had lost her husband of more than 50 years, she’d look at me sadly and say, ‘Oh’, as I struggled to compose myself. ‘Were we all there?’ she’d ask softly.” At the time, members of her mother’s political circle and other British commentators denounced Carol Thatcher for invading her mother’s privacy and, supposedly, diminishing her dignity. The criticism arose again in some quarters last year, when Meryl Streep won an Oscar for her portrayal of Mrs. Thatcher’s dementia in “The Iron Lady.” © 2013 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: 18012 - Posted: 04.10.2013

By Janice Lynch Schuster, My grandmother, who is 92, recently reported that she’d seen three giraffes in her Midwest back yard. She is otherwise sharp (and also kind and funny), but the giraffe episode was further evidence of the mild cognitive impairment that has been slowly creeping into her life. The question for my family has become: How should we respond? One of my sisters tried humor. (“Grandmom, I didn’t know you drank in the middle of the day!”) My father suggested that they were deer (to which she replied, “I’m 92 years old, and I know a giraffe when I see one.”) I tried to learn more about what, exactly, the giraffes were doing out there. (She didn’t seem to know, saying only that “the light shimmered.”) Communicating with a family member who has cognitive impairment can be frustrating and disheartening, even downright depressing for patient and caregiver alike. And it’s a problem faced by a growing number of Americans. According to a report published last week, about 4.1 million Americans have dementia. Alzheimer’s, one of the many forms of dementia, is the most expensive disease in the United States, costing $157 billion to $215 billion a year — more than heart disease and cancer, according to the study, which was sponsored by the National Institute on Aging. As baby boomers reach old age, these numbers are expected to increase dramatically. A number of techniques can not only reduce the frustration but also create new ways of connecting. Among the most effective and popular among experts is the “validation method,” a practice pioneered by geriatric social worker and researcher Naomi Feil in the 1980s. © 1996-2013 The Washington Post

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: 18011 - Posted: 04.10.2013

by Dr. Tyeese Gaines African-Americans with a particular gene are twice as likely to develop Alzheimer’s disease in old age as those without it, says a new study published in the Journal of the American Medical Association. This finding is a result of the largest database search for Alzheimer’s genes among African-Americans. “Until now, data on the genetics of Alzheimer’s in this patient population have been extremely limited,” said Dr. Richard Mayeux, chair of neurology at Columbia University Medical Center and senior author of the study. Alzheimer’s disease is the most common cause of dementia — a brain disease that affects memory, personality and the ability to reason. At age 65, only one percent of people have Alzheimer’s, yet over 80 years of age, it increases to 30 percent. A gene called APOE is associated with one in every five cases of Alzheimer’s – known to be a major genetic risk factor for whites and blacks. Yet, in this new research, Mayeux and his team identified an additional gene variant linked to a doubled risk in African-Americans alone, called ABCA7. “ABCA7 is the first major gene implicated in late-onset Alzheimer’s among African-Americans,” said Dr. Christine Reitz, assistant professor of neurology and lead author of the study. To reach this conclusion, researchers examined samples from nearly 6,000 African-American men and women collected between 1989 and 2011 – 2,000 had a diagnosis of probable Alzheimer’s disease and the other 4,000 had no cognitive difficulty. “Although this is a very significant finding, it does not change much for the everyday African-American male or female,” says Rick Kittles, PhD, a human genetics expert who has traced the ancestry of more than 100,000 African-Americans. “There is still much work to do [to] determine how exactly this gene plays a role in Alzheimer’s disease.” ©2013 NBCUniversal

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: 18010 - Posted: 04.10.2013

By Nathan Seppa Tiny components of amyloid plaques, the notorious protein clumps found littering the brains of people with Alzheimer’s disease, might fight inflammation. Researchers report that several of these sticky protein fragments, or peptides, glom onto inflammatory compounds and reverse paralysis in mice that have a condition similar to multiple sclerosis. A fragment of tau protein, which shows up in other brain deposits in Alzheimer’s patients, has a similar effect. When tested on blood taken from three MS patients, the tau peptide weeded out some inflammatory culprits there, too, researchers report in the April 3 Science Translational Medicine. “This is a seriously good study. It opens up more questions than it answers,” says Jian-Guo Geng, a cell biologist at the University of Michigan in Ann Arbor who wasn’t part of the research team. “But I don’t think we’re anywhere close to using these peptides for treatments.” Amyloid is a broad term for clusters of protein in the brain, including those arising with the aid of misfolded versions of tau or another protein implicated in brain disease called a prion. Viewing amyloid-forming peptides as good guys runs against the scientific thinking, since amyloid plaques are a hallmark of Alzheimer’s disease. But study coauthor Lawrence Steinman, a neurologist at Stanford University, points out that the actual role of amyloid plaques in the disease is unclear. He suggests the tiny peptides holding the plaques together might have an alternative, useful role in the body. © Society for Science & the Public 2000 - 2013

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: 17993 - Posted: 04.05.2013

Genetic markers that could help highlight who is at risk of developing Alzheimer's disease have been identified by US scientists. The research in Neuron identifies mutations that affect the build-up of certain proteins in the brain. High levels of these tau proteins increase the chance of having the disease. UK experts said the study could help understand the changes that occur in the brains of Alzheimer's patients. Tangles of a kind of tau called phosphorylated tau (ptau) are a hallmark of the disease. One of the new gene variants identified by the Washington University School of Medicine team was also shown to be linked to a small increased risk of developing Alzheimer's and a greater risk of cognitive decline. The team used genetic information from more than 1,200 people, significantly larger than previous studies in this area. Dr Alison Goate, who led the study, said: "We anticipate that knowledge about the role of these genes in Alzheimer's disease may lead to the identification of new targets from therapies or new animal or cellular models of the disease. Lifestyle 'plays a role' UK experts said the study adds to the number of genetic markers that have been linked to the development of Alzheimer's disease. BBC © 2013

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: 17992 - Posted: 04.05.2013

By JUDITH GRAHAM Three years ago, Kennard Lehmann walked out of a neurologist’s office in Sacramento, Calif., newly diagnosed with early-stage Alzheimer’s disease, a prescription in hand and absolutely no idea where to turn for help. The doctor hadn’t given him a list of resources or discussed how Mr. Lehmann might go about finding them. Knowing nothing about Alzheimer’s, his wife swiped a magazine she had been reading in the doctor’s office to take home and read. Kennard Courtesy of Mary Margaret Lehmann. Kennard “Ken”Lehmann, with his wife, Mary Margaret Lehmann, said monthly get-togethers with other people who also have early-stage Alzheimer’s are “joyful events.” Thus began a journey all too familiar to people with Alzheimer’s — one that Mr. Lehmann, 75, describes as “being put in a box.” “They tell you, you can’t drive, you’re going to get lost,” he told me in a telephone conversation. “Don’t go out at night, you might have sundown syndrome. Don’t try to balance your checkbook, it could be too hard. All these negative things, all these things you’re told you can’t do now that you have Alzheimer’s.” But Mr. Lehmann was lucky. When he and his wife moved to Minneapolis to be near their daughter, they found a group of people like him with early-stage Alzheimer’s who met monthly to socialize and “challenge ourselves so we can continue to grow,” as he put it. The focus was on what people with early-stage dementia can do — dance, write poetry, yoga, visit museums, go to concerts, draw, enjoy one another’s company — not what is no longer within their reach. “These are joyful events,” Mr. Lehmann said, describing how his attitude toward having Alzheimer’s changed after joining the group. “There’s a lot of laughter, a lot of communication. Because we’re all in the same boat, you don’t have that feeling, ‘What is he going to think?’ Everyone there knows you have challenges. There’s no judgment.” © 2013 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: 17972 - Posted: 04.01.2013

By Emily Burns Lots of people set themselves goals – like things to do by the time you’re 30. Maybe it’s to find your dream job, meet the love of your life, or travel the world! For sufferers of Cystic Fibrosis, it’s living to see your 30th birthday. Even with all of the advances in medicine and technology, the average life expectancy of someone with Cystic Fibrosis is 33 years. Cystic Fibrosis is an inherited disease that mostly affects the lungs, but also the pancreas, liver and intestines. The body fluids we need – like the mucus in our lungs and intestines – are much thicker than normal, making it extremely difficult to breathe and digest food. Constant physiotherapy, breathing exercises, diet supplements and antibiotics are needed just to get on with daily life. And all of this suffering is caused by one tiny change in our DNA, which then messes up how one single protein folds into the right shape. It’s otherwise known as a protein misfolding disease. There are over 2 million proteins in the human body, carrying out their individual tasks to keep us breathing, thinking – enabling us to live. But their production isn’t easy. It’s an incredibly intricate and specialised process that is constantly going on inside us. If it goes wrong, there are serious consequences to our health, with Cystic Fibrosis being a prime example.... While the primary causes Alzheimer’s and Parkinson’s is still not known, one of the theories suggests that cellular and ER stress results in the cell death that we see. They are known as amyloid diseases, as they’re caused by the accumulation of amyloids in cells. We usually think of amyloids as being associated with Alzheimer’s, so you might think that they were a particular type of protein, but that’s not quite it. Instead, amyloids are protein delinquents: any protein that can form a beta sheet can become an amyloid. When a mutated protein misfolds, the side chains of amino acids (that dictate the specific fold) are no longer so important: the main chain of the polypeptide now causes these amyloid fibres to stick together. These amyloid fibres are formed regardless of the original folded protein structure (meaning that they form the same fibrous shape for every protein) and can penetrate the cells, causing cell stress and death. © 2013 Scientific American

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: 17964 - Posted: 03.28.2013

A staggering 1 in 3 seniors dies with Alzheimer's disease or other types of dementia, says a new U.S. report that highlights the impact the mind-destroying disease is having on the rapidly aging population. Dying with Alzheimer's is not the same as dying from it. But even when dementia isn't the direct cause of death, it can be the final blow — speeding someone's decline by interfering with their care for heart disease, cancer or other serious illnesses. That's the assessment of the report released Tuesday by the Alzheimer's Association, which advocates for more research and support for families afflicted by it. "Exacerbated aging," is how Dr. Maria Carrillo, an association vice president, terms the Alzheimer's effect. "It changes any health care situation for a family." In fact, only 30 per cent of 70-year-olds who don't have Alzheimer's are expected to die before their 80th birthday. But if they do have dementia, 61 per cent are expected to die, the report found. Already, 5.2 million Americans have Alzheimer's or some other form of dementia. Those numbers will jump to 13.8 million by 2050, Tuesday's report predicts. That's slightly lower than some previous estimates. Count just the deaths directly attributed to dementia, and they're growing fast. Nearly 85,000 people died from Alzheimer's in 2011, the U.S. Centers for Disease Control and Prevention estimated in a separate report Tuesday. Those are people who had Alzheimer's listed as an underlying cause on a death certificate, perhaps because the dementia led to respiratory failure. Those numbers make Alzheimer's the sixth leading cause of death. © CBC 2013

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: 17927 - Posted: 03.20.2013

By GINA KOLATA The Food and Drug Administration plans to loosen the rules for approving new treatments for Alzheimer’s disease. Drugs in clinical trial would qualify for approval if people at very early stages of the disease subtly improved their performance on memory or reasoning tests, even before they developed any obvious impairments. Companies would not have to show that the drugs improved daily, real-world functioning. For more than a decade, the only way to get Alzheimer’s drugs to market was with studies showing that they improved the ability of patients not only to think and remember, but also to function day to day at activities like feeding, dressing or bathing themselves. The proposal, published online Wednesday in The New England Journal of Medicine, could help millions of people at risk of developing the disease by speeding the development and approval of drugs that might slow or prevent it. The proposed policy could also be a boon for the pharmaceutical industry and researchers. They have often felt stymied by regulations that left them uncertain of how to get drugs tested and approved for marketing to people early in the course of Alzheimer’s, when the medications are most likely to be useful. Several studies are being planned for people at high risk of developing Alzheimer’s, and the proposed regulations should lead to even more clinical trials, said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher and professor of psychiatry at Duke University School of Medicine. © 2013 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: 17904 - Posted: 03.15.2013

British researchers have developed a test to detect Alzheimer's disease in its earliest stages. It works by looking for a combination of "markers" in the blood which are different in healthy people and those with the disease. Delegates at the Alzheimer's Research UK Conference heard that the University of Nottingham is now developing a quick and easy test to do in clinics. It could mean much earlier diagnosis and better treatments, they said. The test uses some proteins that have been strongly linked with Alzheimer's disease, such as amyloid and APOE. But through careful analysis of blood from people with the disease, as well as those with early-stage memory problems, the researchers detected some other markers that were suggestive of the disease. Most notably, some proteins related to inflammation seem to have been added to increase the power of the test. Prof Kevin Morgan from the University of Nottingham said they still had to validate the test and it could be a decade before it was used in patients. But he added that the combination of markers they had found was looking very promising. BBC © 2013

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: 17889 - Posted: 03.11.2013