Links for Keyword: Alzheimers

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 81 - 100 of 959

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

By NICHOLAS BAKALAR Being physically fit in midlife is associated with a lower risk of dementia in old age, a new study reports. Between 1971 and 2009, 19,458 healthy adults younger than age 65 took a treadmill fitness test as part of a broader health examination. Researchers followed the subjects through their Medicare records for an average of 24 years. After adjusting for age, smoking, diabetes, cholesterol and other health factors, the researchers found that compared with those in the lowest 20 percent for fitness in midlife, those in the highest 20 percent had a 36 percent reduced risk of dementia. The reason for the association is unclear, but it was independent of cardiovascular and cerebrovascular risk factors for dementia, suggesting that both vascular and nonvascular mechanisms may be involved. “Dementia is a disease with no cure and no good therapies,” said the lead author, Dr. Laura F. DeFina, the interim chief scientific officer at the Cooper Institute in Dallas. Physical activity may be “a preventive way to address dementia instead of addressing the costs of a disabled elder.” The study population was largely white and highly educated, and the researchers acknowledge that their findings, published last week in The Annals of Internal Medicine, cannot be generalized to other populations. They emphasize that the study is observational and does not prove causation. Copyright 2013 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: 17790 - Posted: 02.12.2013

By Stephen Ornes Newborns with a certain version of a gene are more likely to have a smaller medial temporal lobe (blue spots). This brain region is also smaller in adults with Alzheimer’s disease. People with the gene version are three times more likely to develop the disorder, which affects memory. Credit: R. Knickmeyer et al Illnesses like the memory disorder known as Alzheimer’s disease are linked to particular changes in the brain. This disease typically doesn’t show up until late in adulthood. But telltale hints that it may be coming can appear much, much earlier. Like at birth. A new study found brain differences linked to Alzheimer’s disease in newborns. These differences appear in a region called the medial temporal lobe. Basically, this part of the brain is smaller in people with Alzheimer’s than in those without the disease. That’s important because this region plays a role in making and keeping memories. The new study scanned the brains of 272 infants. Some of their brains had smaller medial temporal lobes too. Until now, researchers didn’t know when the size differences first show up. Now it’s clear that the key region of the brain can be smaller at birth, reports Rebecca Knickmeyer. She’s a psychiatrist at the University of North Carolina at Chapel Hill. Her team’s new study was published in January. © 2013 Copyright Science News for Kids

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: 17709 - Posted: 01.26.2013

Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com.

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: 17700 - Posted: 01.22.2013

By Consumers Union of United States, More than 5 million people in the United States have Alzheimer’s disease, an insidious disorder that gradually destroys the brain, robbing people of the ability to remember, complete everyday tasks and function on their own. Several drugs are approved to treat it, including donepezil (Aricept and its generic cousins) and memantine (Namenda). But they don’t work well for most people, according to a report from Consumer Reports Best Buy Drugs. In fact, the report concluded that none of the drugs could be recommended as a Best Buy. The decision was based in part on a large-scale analysis by the federal Agency for Healthcare Research and Quality published in April 2010. It found that the drugs didn’t delay the onset of Alzheimer’s or improve or maintain mental function. An earlier review by the American College of Physicians and the American Academy of Family Physicians, published in 2008, reached similar conclusions. Besides not being very effective, Alzheimer’s medication can cause side effects. While most are relatively minor, such as nausea, vomiting, diarrhea, dizziness, muscle cramps and tremors, they could be debilitating in older people with dementia who can’t communicate their discomfort. In rare cases, the drugs can cause a slowed heartbeat, gastrointestinal bleeding and possibly even convulsions or seizures. They’re also expensive: An average monthly prescription can range from $177 to more than $400. © 1996-2013 The Washington Post

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: 17678 - Posted: 01.14.2013

By Laura Sanders At birth, some infants are already saddled with brains that carry features of Alzheimer’s disease and schizophrenia. Newborns who carry certain versions of genes already show brain shrinkage reminiscent of that in adults with brain illnesses, a study of 272 newborn babies reveals. The new results, published online January 2 in Cerebral Cortex, illuminate what happens to the brain in the earliest stages of life, says neuroscientist Jay Giedd of the National Institute of Mental Health in Bethesda, Md., who was not involved in the study. “As we go through life, there are so many uncontrollable factors,” he says. “This is a way to see gene influences before the world steps in.” Until this study, scientists didn’t have a good idea of whether certain brain signatures — such as reduced volume in parts of the brain — were present from birth or whether they accumulated over a lifetime, says study coauthor Rebecca Knickmeyer of the University of North Carolina at Chapel Hill. To test this, Knickmeyer and her colleagues looked for the influence of 10 versions of seven genes on newborns’ brains. The researchers chose genes that affect how the brain grows and develops. These gene variants have also been linked to adult brain diseases, such as the ε4 version of the ApoE gene, which triples the risk of getting Alzheimer’s, and a version of the COMT gene, which has been implicated in schizophrenia. © Society for Science & the Public 2000 - 2013

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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17669 - Posted: 01.12.2013

Elderly people with dementia should be prescribed antipsychotics carefully, say Ontario doctors who found men are at higher risk of hospitalization and death than women when the treatment begins. Researchers focused on new prescriptions of a class of drugs called atypical antipsychotics that are used to manage behaviour problems associated with dementia. "It tells us a little bit more about drug therapy and perhaps what might be affecting women and men differently," said Dr. Paula Rochon, a senior scientist at Toronto's Women College Hospital. In Wednesday's issue of the Journal of the American Geriatric Society, Rochon and her co-authors said of 21,526 older adults with dementia in Ontario who started taking the medications, about seven per cent of the women and nearly 11 per cent of the men died or were hospitalized during the 30 days after the treatment started. Little is known about how drugs may affect men and women differently after the age of 85, says Dr. Paula Rochon. "While younger women may be more likely than younger men to experience an adverse drug event, our results suggest that the incidence of serious events in the elderly is reversed and that older men are more likely than older women to experience a serious event related to atypical antipsychotic initiation," the study's authors concluded. © CBC 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17667 - Posted: 01.10.2013

Taking beta-blocker drugs may cut the risk of dementia, a trial in 774 men suggests. The medication is used to treat high blood pressure, a known risk factor for dementia. In the study, which will be presented at the American Academy of Neurology's annual meeting in March, men on beta-blockers were less likely to have brain changes suggestive of dementia. Experts say it is too early to recommend beta-blockers for dementia. The findings are preliminary and larger studies in men and women from different ethnicities are needed to see what benefit beta-blockers might offer. People with high blood pressure are advised to see their doctor and get their condition under control to prevent associated complications like heart disease, stroke and vascular dementia. Having high blood pressure may damage the small vessels that supply the brain with blood. Blood carries essential oxygen and nourishment to the brain and without it, brain cells can die. Vascular dementia is the second most common cause of dementia after Alzheimer's disease and can occur if blood flow to the brain is reduced. Other research in a much larger sample of men - 800,000 in all - suggests another type of blood pressure drug known as an angiotensin receptor blocker (ARB) may cut dementia risk, including Alzheimer's disease, by as much as 50%. 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: 17661 - Posted: 01.08.2013

Scientists say they have found a way to distinguish between different types of dementia without the need for invasive tests, like a lumbar puncture. US experts could accurately identify Alzheimer's disease and another type of dementia from structural brain patterns on medical scans, Neurology reports. Currently, doctors can struggle to diagnose dementia, meaning the most appropriate treatment may be delayed. More invasive tests can help, but are unpleasant for the patient. Despite being two distinct diseases, Alzheimer's and frontotemporal dementia, share similar clinical features and symptoms and can be hard to tell apart without medical tests. Both cause the person to be confused and forgetful and can affect their personality, emotions and behaviour. Alzheimer's tends to attack the cerebral cortex - the layer of grey matter covering the brain - where as frontotemporal dementia, as the name suggests, tends to affect the temporal and frontal lobes of the brain, which can show up on brain scans, but these are not always diagnostic. A lumbar puncture - a needle in the spine - may also be used to check protein levels in the brain, which tend to be higher in Alzheimer's than with frontotemporal dementia. BBC © 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 17638 - Posted: 12.27.2012

Posted by Monya Baker Plaques and tangles pockmark the brains of people with Alzheimer’s disease. The extracellular protein amyloid-β makes plaques, and the intracellular protein tau makes tangles, but how exactly these might kill neurons is unclear. Work presented at the annual meeting of the American Society for Cell Biology in San Francisco, California, this week starts to connect some of these dots. George Bloom, of the University of Virginia in Charlottesville, and his colleagues began by following up on work that neurons exposed to amyloid-β die not from direct poisoning, but because amyloid-β prompts inappropriate cell behaviour. They re-enter the cell cycle but never divide, and die instead. “The framework of the process has now been defined,” he says. “We think we’ve stumbled upon one of the seminal events in the transition of healthy neurons into Alzheimer neurons.” The work identifies several potential very early biomarkers of Alzheimer’s disease and suggests new ideas to treat it. Within 24 hours of exposing neurons to amyloid-β, Bloom and his students could see that the neurons had begun to duplicate DNA — an early preparation for division. When they repeated the experiment with neurons that lacked tau, however, the neurons did not respond this way. Guessing that a cell-signaling cascade could explain these observations, Bloom’s then-student Matt Seward began listing potential protein mediators. He identified enzymes called kinases that had been implicated in Alzheimer’s disease, cell-cycle regulation or tau modification. © 2012 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: 17626 - Posted: 12.21.2012

Daniel Cressey The search for a drug to treat Alzheimer’s disease could be being undermined by flaws in a test used in clinical trials to assess patients. And though few experts would blame the test for the recent failures of potential new drugs, a major push is now on to produce more sensitive ways of measuring the progress of the disease. During the past few years, a number of clinical trials have produced disappointing results for high-profile drugs, and some pharmaceutical companies have abandoned Alzheimer’s disease altogether, frustrated by the high costs and difficulty of producing a drug with a measurable effect. Jeremy Hobart, a neurologist at the Plymouth University Peninsula Schools of Medicine and Dentistry, UK, says that flaws in the ADAS-Cog test could be partly responsible. In many trials branded ‘failures’, the ADAS-Cog (Alzheimer’s Disease Assessment Scale — Cognitive Behaviour section) has been used as the key test of whether a drug is working. The test scores patients on 11 components using a variety of tasks relating to memory, language and praxis (the planning of movement to achieve a purpose), such as word recognition and remembering instructions. Lower scores indicate better cognitive performance and so less severe disease. There is, says Hobart, an argument that any study that has used ADAS-Cog may have underestimated changes in and differences between patients given the drug and controls. In two papers in Alzheimer’s & Dementia, Hobart and his colleagues detail flaws in the test that undermine its utility. © 2012 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: 17620 - Posted: 12.19.2012

By KATIE THOMAS The drug maker Eli Lilly & Company said on Wednesday that it planned an additional study of an experimental Alzheimer’s drug that failed to improve the condition of people with the disease, saying that it remained hopeful about the drug’s prospects. The newest study is expected to get under way in the third quarter of 2013 and will focus on patients with mild Alzheimer’s disease. Lilly released results of two clinical trials in August that showed the drug, called solanezumab, did not significantly improve either the cognition or the daily functioning of people with mild and moderate forms of the disease. But despite that failure, the results also gave some reason for hope: when patients with mild Alzheimer’s were separated out, the drug was shown to significantly slow their decline in cognition. In a statement on Wednesday, the company said it decided not to pursue approval of the drug based on existing study results after it met with officials from the Food and Drug Administration. A Lilly executive said, however, that the company was still optimistic. “We remain encouraged and excited by the solanezumab data,” David Ricks, a senior vice president at Lilly and president of Lilly Bio-Medicines, said in the statement. “We are committed to working with the F.D.A. and other regulatory authorities to bring solanezumab to the millions of patients and caregivers suffering from this devastating disease who urgently need this potential treatment.” The Lilly drug is the second Alzheimer’s treatment to fail in clinical trials this year. Pfizer and Johnson & Johnson stopped development of a similar treatment, bapineuzumab, after it, too, was not shown to work. Both drugs target beta amyloid, a protein in the brain that is found in people with Alzheimer’s disease. © 2012 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: 17598 - Posted: 12.13.2012