Chapter 7. Life-Span Development of the Brain and Behavior
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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
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
by Dennis Normile Puberty has always been a time of stress and emotional turmoil for adolescents and for their parents. And scientists have long recognized that kids who start puberty ahead of their peers are particularly likely to have trouble getting along with other children and with adults. New research suggests that those difficulties can be traced back to even earlier ages, indicating that early puberty may not be the root cause. Australian researchers drew on data for 3491 children, roughly half boys and half girls, who were recruited at ages 4 or 5 and then followed until they reached ages 10 or 11. Every 2 years, a researcher visited each subject's home, evaluated the child, and interviewed the primary caregiver, which in most cases was a parent, who later completed and returned a questionnaire about their child's behavior. The primary caregiver was also asked to judge the child's pubertal status, based on indicators for an early phase of puberty such as breast growth in girls, adult-type body odor, and body hair; and growth spurts, deepening voices in boys, and menstruation in girls for a later stage. Girls typically enter puberty at age 10 or 11 and boys at 11 or 12. The researchers found that 16% of the girls and 6% of the boys in the study had entered puberty early, at age 8 or 9. Previously, researchers thought that any negative effects of early puberty showed up only after puberty's onset. But by tracking a cohort of children from age 4 to 5 to age 10 to 11, they found that problems thought restricted to postpuberty children actually appeared well before puberty. Retrospectively, they were able to show that children who later had early onset puberty had difficulty playing with other children and participating in normal school activities, even when they were 4 or 5 years old. Boys, though not girls, in this group had also showed behavior problems, such as being overactive, losing their tempers, and preferring to play alone from a young age. © 2010 American Association for the Advancement of Science.
By Kathryn Doyle Despite concerns that antidepressant use during pregnancy might affect infants’ growth and development, a small new study finds no size differences in the first year of life between babies exposed and not exposed to the drugs. The medications — known as selective serotonin reuptake inhibitors, or SSRIs, which include fluoxetine (marketed as Prozac) and citalopram (Celexa) — have been tied to premature births and lower birth weight. But their effect on growth during infancy had not been studied. The agency will lift a requirement that the products carry a strict limit on how long they can be used. “It’s a reassuring finding in that when you have an illness during pregnancy, you want to know what is the impact of the illness and what is the impact of the medication,” Katherine Wisner, the study’s lead author, said. Untreated depression also didn’t seem to influence infant growth, according to Wisner, the director of Northwestern University’s Asher Center for the Study and Treatment of Depressive Disorders. That’s important because a baby’s most rapid growth happens in the first year, which sets the stage for growth patterns for the whole life span, she added. Wisner and her colleagues tracked 97 pregnant women without depression, 46 on antidepressants and 31 with depression that was not treated with medication. Their babies were measured and weighed four times over the first year of life. © 1996-2013 The Washington Post
By Bruce Bower Babies take a critical step toward learning to speak before they can say a word or even babble. By 3 months of age, infants flexibly use three types of sounds — squeals, growls and vowel-like utterances — to express a range of emotions, from positive to neutral to negative, researchers say. Attaching sounds freely to different emotions represents a basic building block of spoken language, say psycholinguist D. Kimbrough Oller of the University of Memphis in Tennessee and his colleagues. Any word or phrase can signal any mental state, depending on context and pronunciation. Infants’ flexible manipulation of sounds to signal how they feel lays the groundwork for word learning, the scientists conclude April 1 in the Proceedings of the National Academy of Sciences. Language evolution took off once this ability emerged in human babies, Oller proposes. Ape and monkey researchers have mainly studied vocalizations that have one meaning, such as distress calls. “At this point, the conservative conclusion is that the human infant at 3 months is already vocally freer than has been demonstrated for any other primate at any age,” Oller says. Oller’s group videotaped infants playing and interacting with their parents in a lab room equipped with toys and furniture. Acoustic analyses identified nearly 7,000 utterances made by infants up to 1 year of age that qualified as laughs, cries, squeals, growls or vowel-like sounds. © Society for Science & the Public 2000 - 2013
By DAVID W. DUNLAP Words of comfort, encouragement and empathy had been available to Nancy Lanza and her son, Adam, within a pair of books that were found by the police during a search of their home in Newtown, Conn., after Mr. Lanza’s murderous rampage on Dec. 14. “It’s the most widely read book about Asperger’s out there,” said Mr. Robison of his memoir. It is all but impossible to know if mother or son were helped by the books, “Look Me in the Eye: My Life With Asperger’s” and “Born on a Blue Day: Inside the Extraordinary Mind of an Autistic Savant,” or whether either opened, or even had use for, them. While those familiar with Mr. Lanza and his family have said he had an autism variant known as Asperger’s syndrome, investigators have not confirmed the diagnosis. “Look Me in the Eye” (2007), by John Elder Robison, and “Born on a Blue Day” (2006), by Daniel Tammet, are both memoirs that chronicle the painful chasm of misunderstanding that separates people with Asperger’s from the world around them. Both accounts turn hopeful as their writers grow comfortable in their own skins and more successful in communicating with others. That is why Mr. Robison, 55, said it might be expected that his book would have been found among the Lanzas’ belongings. “It’s the most widely read book about Asperger’s out there,” Mr. Robison said by telephone from his home in Amherst, Mass. “Hundreds, if not thousands, of parents have come to me in the years since that book was published to say, ‘Your stories have given me a window into the mind of my son or daughter.’ It’s not a surprise to see that book in the home of any family touched by autism.” The discovery is not entirely welcome, however, if it reinforces an imagined link between autism and violent crime — a link for which experts say there is no evidence. Americans have struggled for three and a half months to understand why Mr. Lanza killed first his mother, then 20 first graders and 6 educators at Sandy Hook Elementary School, before taking his own life. © 2013 The New York Times Company
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
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
By Melissa Healy, Listening in on the electrical currents of teenagers’ brains during sleep, scientists have begun to hear the sound of growing maturity. It happens most intensively between the ages of 12 and 161 / 2: After years of frenzied fluctuation, the brain’s electrical output during the deepest phase of sleep — the delta, or slow-wave phase, when a child’s brain is undergoing its most restorative rest — becomes practically steady. That reduced fluctuation in electroencephalogram signals appears to coincide with what neuroscientists have described as major architectural changes in the brain that pave the way for cognitive maturity. While babies, toddlers and young children are taking in and making sense of the world, their brain cells are wiring themselves together willy-nilly, creating super-dense networks of interwoven neurons. But as we reach and progress through adolescence, neuroscientists have observed, a period of intensive “synaptic pruning” occurs in which those networks are thinned and the strongest and most evolutionarily useful remain. In a study published last week, scientists from the University of California at Davis say they believe the slowed fluctuations observed during the delta phase of teens’ sleep may be evidence of that pruning process at work. And since major mental illnesses such as schizophrenia appear to take root during adolescence, the authors of the study say the changing architecture of sleep may offer clues as to how and when mental illness sets in. © 1996-2013 The Washington Post
By Bruce Bower Children with autism may understand more about how other people think than they’re usually given credit for. The trick to exposing this awareness, a new study finds, is to motivate these youngsters to show what they know. In a lab game that requires a child to compete with two adults for a prize, many kids with autism demonstrate insight into how other people’s thoughts shape their behavior, say psychologist Candida Peterson of the University of Queensland in Brisbane, Australia, and her colleagues. The finding suggests that previous research testing this ability, called theory of mind, underestimates how well youngsters with autism can interpret other people’s actions, Peterson’s team reports March 19 in Developmental Science. Studies published since 1985 have found that most high-functioning individuals with autism — those who have serious social and language problems but average or better IQs — fail a standard theory of mind test at least through adolescence. Kids without autism usually pass the test by age 5. In the standard test, called the Sally-Anne test, children watch an experimenter play with a doll named Sally, who has a covered basket, and a doll named Anne, who has a box. Sally puts a marble in her basket and leaves. Anne moves Sally’s marble to the box. Kids with autism usually indicate that, when Sally returns, she will look for her marble in the box, failing to recognize that Sally falsely believes the marble remains in her basket. © Society for Science & the Public 2000 - 2013
Link ID: 17960 - Posted: 03.28.2013
A lack of a protein in Down's syndrome brains could be the cause of learning and memory problems, says a US study. Writing in Nature Medicine, Californian researchers found that the extra copy of chromosome 21 in people with the condition triggered the protein loss. Their study found restoring the protein in Down's syndrome mice improved cognitive function and behaviour. The Down's Syndrome Association said the study was interesting but the causes of Down's were very complex. Prof Huaxi Xu, senior author of the study from the Sanford-Burnham Medical Research Institute, said that in experiments on mice they discovered that the SNX27 protein was important for brain function and memory formation. Mice with less SNX27 had fewer active glutamate receptors and therefore had impaired learning and memory. The SNX27-deficient mice shared some characteristics with Down's syndrome, so the researchers looked at human brains with the condition. This confirmed their findings in the lab - that people with Down's syndrome also have significantly lower levels of SNX27. BBC © 2013
By Tina Hesman Saey Like many women with parents of the Mad Men generation, Susan Murphy grew up in a household full of cigarette smoke. Both dad and mom smoked heavily, even while Murphy was still in her mother’s womb. “That explains a lot,” Murphy quips, poking fun at herself. But Murphy isn’t worried about her own health. She’s fine. Her children aren’t, though. One boy died of cancer as a toddler. Another has autism. And her daughter has attention deficit disorder. Murphy knows the scientific evidence isn’t in yet, but she still can’t help wondering whether their fates might have been affected by her exposure to tobacco smoke before she was born. Murphy, a researcher at Duke University, studies links between a mother’s diet and chemical exposures during pregnancy with the child’s later health. She and others have established that the womb is the antithesis of Las Vegas; what happens there not only doesn’t stay there, it can influence a child’s health for life. Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring. Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down. © Society for Science & the Public 2000 - 2013
By Smitha Mundasad Health reporter, BBC News The risk of developing autism may be passed on through - and not just to - future generations, researchers say. The international study suggests older fathers are more likely to have grandchildren with autism than their younger counterparts. The mechanism is unclear but it is thought they may transmit "silent mutations" to their grandchildren. But experts have urged caution, stressing autism is the result of many different factors. The study, looking at almost 6,000 people with the condition, is published in the journal Jama Psychiatry. According to the National Autistic Society, more than one in every 100 people in the UK have the condition. Previous studies suggested older fathers may be at greater risk of having children with autism than younger dads. But the team of UK, Swedish and Australian researchers say this is one of the first pieces of evidence to show the risk can be passed on through - rather than just straight to - future generations. The "silent mutations" - changes in genetic material - are likely to have no obvious impact on older fathers' own children, but they may build up through subsequent generations, or interact with other genes and environmental factors, to increase the chance of their grandchildren developing the condition, the researchers say. BBC © 2013
by Peter Aldhous Women abused in childhood are more likely to have children with autism, a new epidemiological study suggests. The finding adds a disturbing new dimension to the heated debate over the condition's underlying causes. Andrea Roberts of the Harvard School of Public Health suspected that there might be a link between childhood abuse and having an autistic child: women abused early in life are more likely to smoke, suffer from gestational diabetes and have premature babies – all factors that may affect fetal brain development. To investigate, Roberts and her colleagues turned to the Nurses' Health Study II, which includes almost 55,000 women who had indicated if they had a child with autism spectrum disorder and also answered a questionnaire about their experience of abuse as a child. This allowed the researchers to develop a scale rating all the women for the intensity of abuse in their childhood. There was a clear link between the "dose" of abuse received and the risk of having an autistic child. "The associations get stronger as the level of abuse increases," Roberts says. After accounting for demographic factors such as age and socioeconomic status, the 2 per cent of women who reported the most serious childhood abuse – who were frequently hit and also sexually abused – were about 3.5 times as likely to have a child with autism as those who reported no abuse at all. "I think it's a really interesting, innovative and well-conducted study," says Hannah Gardener at the University of Miami in Florida. "There aren't a lot of risk factors with that magnitude." © Copyright Reed Business Information Ltd.
At 7 months of age, children who are later diagnosed with autism take a split second longer to shift their gaze during a task measuring eye movements and visual attention than do typically developing infants of the same age, according to researchers supported by the National Institutes of Health. The difference between the groups’ test results was 25 to 50 milliseconds on average, the researchers found, too brief to be detected in social interactions with an infant. However, they showed that this measurable delay could be accounted for by differences in the structure and organization of actively developing neurological circuits of a child’s brain. Image of brain structure known as the splenium of the corpus callosum When they were infants, children who were later diagnosed with autism took longer to shift their gaze during a measure of eye movements than did infants who were not diagnosed with autism. The researchers believe that brain circuits involved with a brain structure known as the splenium of the corpus callosum (shown in this scan) may account for the differences in gaze shifting between the two groups. Image courtesy of Jason Wolff, Ph.D., University of North Carolina at Chapel Hill. Efficiently shifting attention early in infancy is thought to be important for later social and cognitive development. Split-second delays, the researchers suggested, could be a precursor to such well known symptoms of autism as difficulty making eye contact or following a parent’s pointing finger, problems that generally emerge after a child turns 1. Typically, autism spectrum disorder (ASD) is not diagnosed until after 3 or 4 years of age. The study appears in the American Journal of Psychiatry.
By Bruce Bower Malnutrition in the first year life, even when followed by a good diet and restored physical health, predisposes people to a troubled personality at age 40, new research suggests. The study of 77 formerly malnourished people represents the first evidence linking malnutrition shortly after birth to adult personality traits. The traits in some cases may foretell psychiatric problems, says a team led by psychiatrist Janina Galler of Harvard Medical School in Boston and psychologist Paul Costa of Duke University Medical Center in Durham. Compared with peers who were well-fed throughout their lives, formerly malnourished men and women reported markedly more anxiety, vulnerability to stress, hostility, mistrust of others, anger and depression, Galler’s team reports March 12 in the Journal of Child Psychology and Psychiatry. Survivors of early malnutrition also cited relatively little intellectual curiosity, social warmth, cooperativeness and willingness to try new experiences and to work hard at achieving goals. Previous studies of people exposed prenatally to famine have reported increased rates of certain personality disorders and schizophrenia. Another investigation found that malnutrition at age 3 predisposed youngsters on the Indian Ocean island of Mauritius to delinquent and aggressive behavior at ages 8, 11 and 17. As is true in the new study, distrust of others, anxiety and depression often accompany high levels of anger, says psychologist Adrian Raine of the University of Pennsylvania in Philadelphia, who directed the Mauritius research. “Poor nutrition early in life seems to predispose individuals to a suspicious personality, which may then fuel a hostile attitude toward others,” Raine proposes. © Society for Science & the Public 2000 - 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
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
Link ID: 17904 - Posted: 03.15.2013
By Jan Brogan Paula Driscoll had a hard time sitting still as a kid, doodled a lot, and often wrestled with the feeling that she should be accomplishing more. But she made it through high school and college and became an elementary school teacher. With three small children at home, she did not feel she had trouble managing her life. But when her youngest child went to school, she found herself with what felt like too much time on her hands. “I couldn’t get anything done,” she said. “I had one room I started to paint, another I was going to reorganize, and I could never complete a task. I couldn’t stay in the house. I went out on one errand after the next.” Driscoll was 45 when she was diagnosed with attention deficit hyperactivity disorder, or ADHD. ADHD, a neurobiological disorder that makes it difficult to focus and can also include hyperactivity and impulsivity, has historically been viewed as a childhood disease. Over the last couple decades, research has shown that many of those afflicted carry symptoms into adulthood. The latest study, led by a Boston Children’s Hospital researcher and published Monday in the journal Pediatrics, suggests that nearly 30 percent of those with childhood ADHD still have the condition as adults — often after discontinuing treatment. The researchers followed hundreds of children with ADHD into adulthood and reported that the majority had mental health problems such as alcohol or drug dependence, anxiety, depression, or a personality disorder. © 2012 NY Times Co.
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
Link ID: 17889 - Posted: 03.11.2013