Chapter 16. None
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By JOSHUA A. KRISCH Excessive alcohol consumption, including binge drinking, is responsible for 10 percent of deaths among working-age adults in the United States, according to a recent study from the Centers for Disease Control and Prevention. The researchers used an online tool called the Alcohol-Related Disease Impact application to estimate alcohol-related deaths ranging from car crashes and alcohol poisoning to liver and heart disease. They defined binge drinking as at least five consecutive drinks for men and four consecutive drinks for women. One in six adults from 20 to 65 reported binge drinking at least four times a month; the actual number is likely higher because subjects tend to underreport their drinking habits, the researchers said. The number of Americans who binge drink skyrocketed during the 1990s and leveled off in 2001, but the average frequency of binge drinking episodes is still rising. Excessive drinking is the fourth leading cause of preventable death in the United States, after smoking, poor nutrition and physical inactivity. “It’s a huge public health problem any way you slice it,” said Robert D. Brewer, a co-author of the paper and the director of the alcohol program at the C.D.C.“There are things that we can do about it,” like raising the alcohol tax and encouraging doctors to talk to their patients about alcohol abuse, “but a lot of those strategies tend to be underused.” © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19799 - Posted: 07.08.2014
|By Emilie Reas A poor diet can eat away at brain health. Now a study in Neurology helps elucidate why. It suggests that eating a lot of sugar or other carbohydrates can be hazardous to both brain structure and function. Diabetes, which is characterized by chronically high levels of blood glucose, has been linked to an elevated risk of dementia and a smaller hippocampus, a brain region critical for memory. The new study sought to identify whether glucose had an effect on memory even in people without the disease because having it could induce other brain changes that confound the data. In the experiment, researchers at the Charité University Medical Center in Berlin evaluated both short- and long-term glucose markers in 141 healthy, nondiabetic older adults. The participants performed a memory test and underwent imaging to assess the structure of their hippocampus. Higher levels on both glucose measures were associated with worse memory, as well as a smaller hippocampus and compromised hippocampal structure. The researchers also found that the structural changes partially accounted for the statistical link between glucose and memory. According to study co-author Agnes Flöel, a neurologist at Charité, the results “provide further evidence that glucose might directly contribute to hippocampal atrophy,” but she cautions that their data cannot establish a causal relation between sugar and brain health. These findings indicate that even in the absence of diabetes or glucose intolerance, higher blood sugar may harm the brain and disrupt memory function. Future research will need to characterize how glucose exerts these effects and whether dietary or lifestyle interventions might reverse such pathological changes. © 2014 Scientific American
Link ID: 19798 - Posted: 07.08.2014
Priyanka Pulla Not everyone who is obese is unhealthy. So say some researchers, who note that a small fraction of overweight people have normal blood sugar levels and blood pressure, and are thus “healthy obese.” Now, scientists have identified a single protein that seems to determine whether obesity is harmful or benign. The protein is a new player in our understanding of how obesity leads to disease, says Alan Saltiel, a cell biologist at the University of Michigan, Ann Arbor, who was not involved in the study. It is well known that obesity leads to a wide range of health problems, from diabetes to heart disease to cancer. So established is the link between extra pounds and illness that last year the American Medical Association voted to classify obesity itself as a disease. Although some researchers have suggested that a small number of obese people are healthy, that idea remains controversial. Instead, the emerging consensus is that healthy obesity is a transient phase, says Ravi Retnakaran, an endocrinologist at the Leadership Sinai Centre for Diabetes in Toronto, Canada. Sooner or later, he says, these outliers will develop metabolic syndrome, a condition in which glucose, cholesterol, and lipid levels soar, causing diabetes and heart disease. In fact, so-called healthy obese people may already have early signs of disease, which are too muted to show up on routine tests. In a study of more than 14,000 metabolically healthy Korean people last year, scientists found early plaque buildup in the arteries of obese subjects more often than they did in the lean ones. © 2014 American Association for the Advancement of Science
Link ID: 19797 - Posted: 07.04.2014
|By Jessica Wright and SFARI.org CHD8, a gene that regulates the structure of DNA, is the closest thing so far to an ‘autism gene,’ suggests a study published today in Cell. People with mutations in this gene all have the same cluster of symptoms, including a large head, constipation and characteristic facial features; nearly all also have have autism. Autism is notoriously heterogeneous, perhaps involving mutations in any of hundreds of genes. Typically, researchers begin by studying people with similar symptoms and working backward to identify what causes those symptoms. But that approach has not been particularly productive. “We’ve tried for so long to identify subtypes of autism based on behavior alone and we’ve done abysmally at that,” says lead researcher Raphael Bernier, associate professor of psychiatry at the University of Washington in Seattle. The reverse approach — that is, beginning with people who all have mutations in the same gene and characterizing their symptoms — may prove to be more useful for simplifying autism’s complexity. For example, identifying subtypes of autism may help researchers develop drugs tailored to that particular cause, says Evan Eichler, professor of genome sciences at the University of Washington, who spearheaded the genetics side of the study. “I think the most important realization is that not all autisms are created equal,” he says. © 2014 Scientific American,
By GABRIELLE GLASER When their son had to take a medical leave from college, Jack and Wendy knew they — and he — needed help with his binge drinking. Their son’s psychiatrist, along with a few friends, suggested Alcoholics Anonymous. He had a disease, and in order to stay alive, he’d have to attend A.A. meetings and abstain from alcohol for the rest of his life, they said. But the couple, a Manhattan reporter and editor who asked to be identified only by their first names to protect their son’s privacy, resisted that approach. Instead, they turned to a group of psychologists who specialize in treating substance use and other compulsive behaviors at the Center for Motivation and Change. The center, known as the C.M.C., operates out of two floors of a 19th-century building on 30th Street and Fifth Avenue. It is part of a growing wing of addiction treatment that rejects the A.A. model of strict abstinence as the sole form of recovery for alcohol and drug users. Instead, it uses a suite of techniques that provide a hands-on, practical approach to solving emotional and behavioral problems, rather than having abusers forever swear off the substance — a particularly difficult step for young people to take. And unlike programs like Al-Anon, A.A.’s offshoot for family members, the C.M.C.’s approach does not advocate interventions or disengaging from someone who is drinking or using drugs. “The traditional language often sets parents up to feel they have to make extreme choices: Either force them into rehab or detach until they hit rock bottom,” said Carrie Wilkens, a psychologist who helped found the C.M.C. 10 years ago. “Science tells us those formulas don’t work very well.” When parents issue edicts, demanding an immediate end to all substance use, it often lodges the family in a harmful cycle, said Nicole Kosanke, a psychologist at the C.M.C. Tough love might look like an appropriate response, she said, but it often backfires by further damaging the frayed connections to the people to whom the child is closest. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19794 - Posted: 07.04.2014
By Helen Briggs Health editor, BBC News website More than 99% of drug trials for Alzheimer's disease during the past decade have failed, according to a study. There is an urgent need to increase the number of potential therapies being investigated, say US scientists. Only one new medicine has been approved since 2004, they report in the journal Alzheimer's Research & Therapy. The drug failure rate is troubling and higher than for other diseases such as cancer, says Alzheimer's Research UK. Dr Jeffrey Cummings, of the Cleveland Clinic Lou Ruvo Center for Brain Health, in Las Vegas, and colleagues, examined a public website that records clinical trials. Between 2002 and 2012, they found 99.6% of trials of drugs aimed at preventing, curing or improving the symptoms of Alzheimer's had failed or been discontinued. This compares with a failure rate of 81% for cancer drugs. The failure rate was "especially troubling" given the rising numbers of people with dementia, said Dr Simon Ridley, of Alzheimer's Research UK. "The authors of the study highlight a worrying decline in the number of clinical trials for Alzheimer's treatments in more recent years," he said. "There is a danger that the high failure rates of trials in the past will discourage pharmaceutical companies from investing in dementia research. BBC © 2014
Link ID: 19793 - Posted: 07.04.2014
BY Jenny Marder and Rebecca Jacobson Scientists at the NIH are mapping the activity of thousands of individual neurons inside the brain of a zebrafish as the animal hunts for food. In a small, windowless room that houses two powerful electron microscopes, a scientist is searching for the perfect fish brain. As the massive machines hum nearby, two gigantic fish eyes loom large, taking up most of a computer screen. The magnified perspective is misleading. The zebrafish is a larva, a newborn, just one week old, and barely six millimeters long. On the screen, it looks grumpy, like it’s frowning. Chris Harris, a postdoctoral researcher at the lab, is scrolling through the image. As he zooms in, the eyes become even larger and then disappear altogether, replaced by a glimpse of what lies within and behind them in its brain: a jungle of axons and dendrites and cell bodies — all the stuff that makes up individual neurons. He traces the outer edge of one of the cells with a gloved finger. “This layer is the nuclear membrane,” he says. “And just outside of that is the cell body membrane itself.” He points out the mitochondria, the individual axons, which send nerve impulses from one neuron to the next; the branching dendrites, which receive signals; and thick black dots that represent synaptic vesicles — pouches that hold neurotransmitters, or brain chemicals. © 1996 - 2014 MacNeil / Lehrer Productions.
Keyword: Brain imaging
Link ID: 19792 - Posted: 07.04.2014
—By Chris Mooney The United States has a voting problem. In the 2012 presidential election, only about 57 percent of eligible American voters turned out, a far lower participation rate than in comparable democracies. That means about 93 million people who were eligible to vote didn't bother. Clearly, figuring out why people vote (and why they don't) is of premium importance to those who care about the health of democracy, as well as to campaigns that are becoming ever more sophisticated in targeting individual voters. To that end, much research has shown that demographic factors such as age and poverty affect one's likelihood of voting. But are there individual-level biological factors that also influence whether a person votes? The idea has long been heretical in political science, and yet the logic behind it is unavoidable. People vary in all sorts of ways—ranging from personalities to genetics—that affect their behavior. Political participation can be an emotional, and even a stressful activity, and in an era of GOP-led efforts to make voting more difficult, voting in certain locales can be a major hassle. To vote, you need both to be motivated and also not so intimidated you stay away from the polls. So are there biological factors that can shape these perceptions? "Our study is unique in that it is the first to examine whether differences in physiology may be causally related to differences in political activity," says lead study author Jeffrey French. ©2014 Mother Jones
Link ID: 19790 - Posted: 07.04.2014
Hassan DuRant The colorful little guy pictured above puts the eyes of every other animal to shame. Whereas humans receive color information via three color receptors in our eyes, mantis shrimp (Neogonodactylus oerstedii) have 12. Six of these differentiate five discrete wavelengths of ultraviolet light, researchers report online today in Current Biology. The mantis shrimp’s vision is possible by making use of specially tuned, UV-specific optical filters in its color-detecting cone cells. The optical filters are made of mycosporine-like amino acids (MAAs), a substance commonly found in the skin or exoskeleton of marine organisms. Often referred to as nature’s sunscreens, MAAs are usually employed to protect an organism from DNA-damaging UV rays; however, the mantis shrimp has incorporated them into powerful spectral tuning filters. Though the reason for the mantis shrimp’s complex visual perception is poorly understood, one possibility is that the UV detection could help visualize otherwise difficult-to-see prey on coral reefs. Many organisms absorb UV light—these organisms would be easy to spot as black objects in a bright world. © 2014 American Association for the Advancement of Science
Link ID: 19789 - Posted: 07.04.2014
|By Ferris Jabr You know the exit is somewhere along this stretch of highway, but you have never taken it before and do not want to miss it. As you carefully scan the side of the road for the exit sign, numerous distractions intrude on your visual field: billboards, a snazzy convertible, a cell phone buzzing on the dashboard. How does your brain focus on the task at hand? To answer this question, neuroscientists generally study the way the brain strengthens its response to what you are looking for—jolting itself with an especially large electrical pulse when you see it. Another mental trick may be just as important, according to a study published in April in the Journal of Neuroscience: the brain deliberately weakens its reaction to everything else so that the target seems more important in comparison. Cognitive neuroscientists John Gaspar and John McDonald, both at Simon Fraser University in British Columbia, arrived at the conclusion after asking 48 college students to take attention tests on a computer. The volunteers had to quickly spot a lone yellow circle among an array of green circles without being distracted by an even more eye-catching red circle. All the while the researchers monitored electrical activity in the students' brains using a net of electrodes attached to their scalps. The recorded patterns revealed that their brains consistently suppressed reactions to all circles except the one they were looking for—the first direct evidence of this particular neural process in action. © 2014 Scientific American
Link ID: 19788 - Posted: 07.03.2014
by Helen Thomson ONE moment you're conscious, the next you're not. For the first time, researchers have switched off consciousness by electrically stimulating a single brain area. Scientists have been probing individual regions of the brain for over a century, exploring their function by zapping them with electricity and temporarily putting them out of action. Despite this, they have never been able to turn off consciousness – until now. Although only tested in one person, the discovery suggests that a single area – the claustrum – might be integral to combining disparate brain activity into a seamless package of thoughts, sensations and emotions. It takes us a step closer to answering a problem that has confounded scientists and philosophers for millennia – namely how our conscious awareness arises. Many theories abound but most agree that consciousness has to involve the integration of activity from several brain networks, allowing us to perceive our surroundings as one single unifying experience rather than isolated sensory perceptions. One proponent of this idea was Francis Crick, a pioneering neuroscientist who earlier in his career had identified the structure of DNA. Just days before he died in July 2004, Crick was working on a paper that suggested our consciousness needs something akin to an orchestra conductor to bind all of our different external and internal perceptions together. With his colleague Christof Koch, at the Allen Institute for Brain Science in Seattle, he hypothesised that this conductor would need to rapidly integrate information across distinct regions of the brain and bind together information arriving at different times. For example, information about the smell and colour of a rose, its name, and a memory of its relevance, can be bound into one conscious experience of being handed a rose on Valentine's day. © Copyright Reed Business Information Ltd.
Link ID: 19787 - Posted: 07.03.2014
Maggie Fox NBC News Walking is an almost magic elixir, doctors like to say. It can reverse diabetes, lower blood pressure, and help people keep the fat off. Now a study shows it can also help people with Parkinson’s disease. Parkinson’s patients who walked just three times a week felt less tired, less depressed and they found their Parkinson’s symptoms improved, also. “The results of our study suggest that walking may provide a safe and easily accessible way of improving the symptoms of Parkinson’s disease and improve quality of life,” Dr. Ergun Uc of the University of Iowa and the Veterans Affairs Medical Center of Iowa City, who led the study. The findings would only apply to Parkinson’s patients who can still walk easily. Parkinson’s is caused by the loss of brain cells that produce a message carrying-chemical, or neurotransmitter, that is important for movement. Symptoms can start with a barely noticeable trembling but worsen to difficulty walking and talking, depression and other disability. There’s no cure and the drugs used to treat the condition usually stop helping over time. Some people have trouble walking. But for those who don’t, the study found, walking can help their symptoms. And other research suggests that regular exercise can help slow down the progression of Parkinson’s. Various programs show that dancing,cycling, Pilates and even boxing can help. But walking has a big advantage – people can do it anywhere, without special equipment, and on their own schedules.
Link ID: 19786 - Posted: 07.03.2014
By GRETCHEN REYNOLDS Exercise may help to keep the brain robust in people who have an increased risk of developing Alzheimer’s disease, according to an inspiring new study. The findings suggests that even moderate amounts of physical activity may help to slow the progression of one of the most dreaded diseases of aging. For the new study, which was published in May in Frontiers in Aging Neuroscience, researchers at the Cleveland Clinic in Ohio recruited almost 100 older men and women, aged 65 to 89, many of whom had a family history of Alzheimer’s disease. Alzheimer’s disease, characterized by a gradual and then quickening loss of memory and cognitive functioning, can strike anyone. But scientists have discovered in recent years that people who harbor a specific variant of a gene, known as the APOE epsilon4 allele or the e4 gene for short, have a substantially increased risk of developing the disease. Genetic testing among the volunteers in the new study determined that about half of the group carried the e4 gene, although, at the start of the study, none showed signs of memory loss beyond what would be normal for their age. Then the scientists set out to more closely examine their volunteers’ brains. For some time, researchers have suspected that Alzheimer’s disease begins altering the structure and function of the brain years or even decades before the first symptoms appear. In particular, it’s been thought that the disease silently accelerates the atrophy of the hippocampus, a portion of the brain critical for memory processing. Brain scans of people who have Alzheimer’s show that their hippocampi are considerably more shrunken than those of people of the same age without the disease. There’s been less study, though, of possible shrinkage in the brains of cognitively normal people at risk for Alzheimer’s. One reason is that, until recently, few interventions, including drugs, had shown much promise in slowing or preventing the disease’s progression, so researchers – and patients – have been reluctant to identify markers of its potential onset. © 2014 The New York Times Company
Link ID: 19783 - Posted: 07.02.2014
by Laura Sanders At the playground yesterday, Baby V commando-crawled through a tunnel with holes on the side. Every so often, I stuck my face in there with a loud “peekaboo.” She reached up longingly toward the bouncy duck. I picked her up and steadied her as she lurched back and forth. She scrambled up some low stairs and launched down a slide. I lurked near the bottom, ready to assist and yell “yay” when she didn’t face-plant. The one thing I didn’t do was sit back and leave her to her own devices, free from my helicopter-mom tendencies. But since I have the most ridiculous crush on that girl, it’s hard for me to leave her be. As a parent who works outside of the home, I treasure our time together. But as she becomes more capable and independent, I realize that I need to be more thoughtful about letting her carve out some space for herself. A recent research paper emphasized this point. The study, published June 17 in Frontiers in Psychology, finds that children who spend more time in unstructured activities may better master some important life skills. Researchers sorted kids’ activities into structured activities, which included child-initiated activities such as playing alone or with friends, singing, riding bikes and camping, and structured activities, including soccer practice, piano lessons, chores and homework. Six- and seven-year-olds who had more unstructured time scored higher on a measure of executive function, complex cognitive abilities such as seamlessly switching between tasks, resisting impulses and paying attention — all things that help people get along in this world. © Society for Science & the Public 2000 - 2013.
Keyword: Development of the Brain
Link ID: 19780 - Posted: 07.02.2014
James Gorman All moving animals do their best to avoid running into things. And most living things follow a tried and true strategy — Watch where you’re going! Flying and swimming animals both have to cope with some complications that walkers, jumpers and gallopers don’t confront. Not only do they have to navigate in three dimensions, but they also cope with varying air and water flow. Beyond that, they often do so without the same references points and landmarks we have on the ground. Christine Scholtyssek of Lund University in Sweden, and colleagues decided to compare how two species in different mediums, air and water, which pose similar problems, reacted to apparent obstacles as they were moving. What they found, and reported in Biology Letters in May, was that the two species they examined — bumblebees and zebra fish — have very different strategies. It was known that the bees’ navigation depended on optic flow, which is something like the sensation of watching telephone poles speed past from a seat on a moving train. They tend to fly away from apparent obstacles as they approach them. The question was whether fish would do something similar. So, in order to give both animals the same test, Dr. Scholtyssek and her colleagues devised an apparatus that could contain air or water. When one wall had vertical stripes and the other horizontal, the bees, not surprisingly, flew away from the vertical stripes, which would have appeared as one emerging obstacle after another as the bees flew past. Horizontal stripes don’t change as a creature moves past, so they provide no reference for speed or progress. The fish, however, swam closer to the vertical stripes, which wasn’t expected. “It is surprising that although fish and bees have the same challenge, moving with or against streams, they do not use the same mechanisms,” Dr. Scholtyssek said. © 2014 The New York Times Company
Keyword: Animal Migration
Link ID: 19778 - Posted: 07.01.2014
Philip Ball Lead guitarists usually get to play the flashy solos while the bass player gets only to plod to the beat. But this seeming injustice could have been determined by the physiology of hearing. Research published today in the Proceedings of the National Academy of Sciences1 suggests that people’s perception of timing in music is more acute for lower-pitched notes. Psychologist Laurel Trainor of McMaster University in Hamilton, Canada, and her colleagues say that their findings explain why in the music of many cultures the rhythm is carried by low-pitched instruments while the melody tends to be taken by the highest pitched. This is as true for the low-pitched percussive rhythms of Indian classical music and Indonesian gamelan as it is for the walking double bass of a jazz ensemble or the left-hand part of a Mozart piano sonata. Earlier studies2 have shown that people have better pitch discrimination for higher notes — a reason, perhaps, that saxophonists and lead guitarists often have solos at a squealing register. It now seems that rhythm works best at the other end of the scale. Trainor and colleagues used the technique of electroencephalography (EEG) — electrical sensors placed on the scalp — to monitor the brain signals of people listening to streams of two simultaneous piano notes, one high-pitched and the other low-pitched, at equally spaced time intervals. Occasionally, one of the two notes was played slightly earlier, by just 50 milliseconds. The researchers studied the EEG recordings for signs that the listeners had noticed. © 2014 Nature Publishing Group,
Link ID: 19776 - Posted: 07.01.2014
By RICHARD A. FRIEDMAN ADOLESCENCE is practically synonymous in our culture with risk taking, emotional drama and all forms of outlandish behavior. Until very recently, the widely accepted explanation for adolescent angst has been psychological. Developmentally, teenagers face a number of social and emotional challenges, like starting to separate from their parents, getting accepted into a peer group and figuring out who they really are. It doesn’t take a psychoanalyst to realize that these are anxiety-provoking transitions. But there is a darker side to adolescence that, until now, was poorly understood: a surge during teenage years in anxiety and fearfulness. Largely because of a quirk of brain development, adolescents, on average, experience more anxiety and fear and have a harder time learning how not to be afraid than either children or adults. Different regions and circuits of the brain mature at very different rates. It turns out that the brain circuit for processing fear — the amygdala — is precocious and develops way ahead of the prefrontal cortex, the seat of reasoning and executive control. This means that adolescents have a brain that is wired with an enhanced capacity for fear and anxiety, but is relatively underdeveloped when it comes to calm reasoning. You may wonder why, if adolescents have such enhanced capacity for anxiety, they are such novelty seekers and risk takers. It would seem that the two traits are at odds. The answer, in part, is that the brain’s reward center, just like its fear circuit, matures earlier than the prefrontal cortex. That reward center drives much of teenagers’ risky behavior. This behavioral paradox also helps explain why adolescents are particularly prone to injury and trauma. The top three killers of teenagers are accidents, homicide and suicide. The brain-development lag has huge implications for how we think about anxiety and how we treat it. It suggests that anxious adolescents may not be very responsive to psychotherapy that attempts to teach them to be unafraid, like cognitive behavior therapy, which is zealously prescribed for teenagers. © 2014 The New York Times Company
Keyword: Development of the Brain
Link ID: 19775 - Posted: 07.01.2014
by Bethany Brookshire One day when I came in to the office, my air conditioning unit was making a weird rattling sound. At first, I was slightly annoyed, but then I chose to ignore it and get to work. In another 30 minutes, I was completely oblivious to the noise. It wasn’t until my cubicle neighbor Meghan Rosen came in and asked about the racket that I realized the rattle was still there. My brain had habituated to the sound. Habituation, the ability to stop noticing or responding to an irrelevant signal, is one of the simplest forms of learning. But it turns out that at the level of a brain cell, it’s a far more complex process than scientists previously thought. In the June 18 Neuron, Mani Ramaswami of Trinity College Dublin proposes a new framework to describe how habituation might occur in our brains. The paper not only offers a new mechanism to help us understand one of our most basic behaviors, it also demonstrates how taking the time to integrate new findings into a novel framework can help push a field forward. Our ability to ignore the irrelevant and familiar has been a long-known feature of human learning. It’s so simple, even a sea slug can do it. Because the ability to habituate is so simple, scientists hypothesized that the mechanism behind it must also be simple. The previous framework for habituation has been synaptic depression, a decrease in chemical release. When one brain cell sends a signal to another, it releases chemical messengers into a synapse, the small gap between neurons. Receptors on the other side pick up this excitatory signal and send the message onward. But in habituation, neurons would release fewer chemicals, making the signal less likely to hit the other side. Fewer chemicals, fewer signals, and you’ve habituated. Simple. But, as David Glanzman, a neurobiologist at the University of California, Los Angeles points out, there are problems with this idea. © Society for Science & the Public 2000 - 2013
Keyword: Learning & Memory
Link ID: 19772 - Posted: 06.25.2014
|By Lisa Marshall Is Alzheimer's disease an acquired form of Down syndrome? When neurobiologist Huntington Potter first posed the question in 1991, Alzheimer's researchers were skeptical. They were just beginning to explore the causes of the memory-robbing neurological disease. Scientists already knew that by age 40, nearly 100 percent of patients with Down syndrome, who have an extra copy of chromosome 21, had brains full of beta-amyloid peptide—the neuron-strangling plaque that is a hallmark of Alzheimer's. They also knew that the gene that codes for that protein lives on chromosome 21, suggesting that people acquire more plaque because they get an extra dose of the peptide. Potter, though, suggested that if people with Down syndrome develop Alzheimer's because of an extra chromosome 21, healthy people may develop Alzheimer's for the same reason. A quarter of a century later mounting evidence supports the idea. “What we hypothesized in the 1990s and have begun to prove is that people with Alzheimer's begin to make molecular mistakes and generate cells with three copies of chromosome 21,” says Potter, who was recently appointed director of Alzheimer's disease research at the University of Colorado School of Medicine, with the express purpose of studying Alzheimer's through the lens of Down syndrome. He is no longer the only one exploring the link. In recent years dozens of studies have shown Alzheimer's patients possess an inordinate amount of Down syndrome–like cells. One 2009 study by Russian researchers found that up to 15 percent of the neurons in the brains of Alzheimer's patients contained an extra copy of chromosome 21. Others have shown Alzheimer's patients have 1.5 to two times as many skin and blood cells with the extra copy as healthy controls. Potter's own research in mice suggests a vicious cycle: when normal cells are exposed to the beta-amyloid peptide, they tend to make mistakes when dividing, producing more trisomy 21 cells, which, in turn, produce more plaque. In August, Potter and his team published a paper in the journal Neurobiology of Aging describing why those mistakes may occur: the inhibition of a specific enzyme. © 2014 Scientific American
Link ID: 19771 - Posted: 06.25.2014
By Jim Tankersley COLUMBUS, Ohio — First they screwed the end of the gray cord into the metal silo rising out of Ian Burkhart’s skull. Later they laid his right forearm across two foam cylinders, and they wrapped it with thin strips that looked like film from an old home movie camera. They ran him through some practice drills, and then it was time for him to try. If he succeeded at this next task, it would be science fiction come true: His thoughts would bypass his broken spinal cord. With the help of an algorithm and some electrodes, he would move his once-dead limb again — a scientific first. “Ready?” the young engineer, Nick Annetta, asked from the computer to his left. “Three. Two. One.” Burkhart, 23, marshaled every neuron he could muster, and he thought about his hand. 1 of 14 The last time the hand obeyed him, it was 2010 and Burkhart was running into the Atlantic Ocean. The hand had gripped the steering wheel as he drove the van from Ohio University to North Carolina’s Outer Banks, where he and friends were celebrating the end of freshman year. The hand unclenched to drop his towel on the sand. Burkhart splashed into the waves, the hand flying above his head, the ocean warm around his feet, the sun roasting his arms, and he dived. In an instant, he felt nothing. Not his hand. Not his legs. Only the breeze drying the saltwater on his face.
Link ID: 19770 - Posted: 06.25.2014