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By GRETCHEN REYNOLDS Sleep is essential for good health, as we all know. But a new study hints that there may be an easy but unrealized way to augment its virtues: lower the thermostat. Cooler bedrooms could subtly transform a person’s stores of brown fat — what has lately come to be thought of as “good fat” — and consequently alter energy expenditure and metabolic health, even into daylight hours. Until recently, most scientists thought that adults had no brown fat. But in the past few years, scanty deposits — teaspoonfuls, really — of the tissue have been detected in the necks and upper backs in many adults. This is important because brown fat, unlike the more common white stuff, is metabolically active. Experiments with mice have shown that it takes sugar out of the bloodstream to burn calories and maintain core temperature. A similar process seems to take place in humans. For the new study, published in June in Diabetes, researchers affiliated with the National Institutes of Health persuaded five healthy young male volunteers to sleep in climate-controlled chambers at the N.I.H. for four months. The men went about their normal lives during the days, then returned at 8 every evening. All meals, including lunch, were provided, to keep their caloric intakes constant. They slept in hospital scrubs under light sheets. For the first month, the researchers kept the bedrooms at 75 degrees, considered a neutral temperature that would not prompt moderating responses from the body. The next month, the bedrooms were cooled to 66 degrees, a temperature that the researchers expected might stimulate brown-fat activity (but not shivering, which usually begins at more frigid temperatures). The following month, the bedrooms were reset to 75 degrees, to undo any effects from the chillier room, and for the last month, the sleeping temperature was a balmy 81 degrees. Throughout, the subjects’ blood-sugar and insulin levels and daily caloric expenditures were tracked; after each month, the amount of brown fat was measured. © 2014 The New York Times Company
Link ID: 19844 - Posted: 07.17.2014
By Lizzie Wade This week, a team from the National Institute on Drug Abuse (NIDA) reported that heavy marijuana use may damage the brain's pleasure center. Meanwhile, researchers in the United Kingdom say they’ve figured out why pot makes you paranoid. But does focusing research on cannabis’s “bad side” give the drug short shrift? Science talked to Ian Mitchell, an emergency physician at the University of British Columbia’s Southern Medical Program in Kamloops, Canada, and author of the blog Clinical Cannabis in Context, who says that politics influences research in this controversial field. As a doctor who recommends medical cannabis to patients, he follows research on the drug and often critiques studies he believes are based on outdated information or were performed with an anticannabis bias. This interview has been edited for clarity and brevity. Q: What do you think of the NIDA study? A: They said they gave marijuana abusers Ritalin and nothing happened. One of the ways you could interpret that is, OK, these pleasure centers are damaged. But you could also say, perhaps marijuana decreases the effects of [Ritalin] on people. That would be equally as right an interpretation. Q: Why do we hear more about studies that show negative effects of marijuana? A: NIDA is at the center of cannabis research in America. And their mandate, very plainly, is to study drug abuse. So they overwhelmingly fund studies that look at abuse. In America, if you wanted to run a study that showed a benefit of cannabis, you weren’t allowed to do that because NIDA couldn’t give you samples to use. So there were no trials [on potential medical benefits] being done. For example, there hasn’t been a good trial yet to study marijuana’s potential for treating posttraumatic stress disorder. They couldn’t get it done, due to all these political roadblocks. © 2014 American Association for the Advancement of Science
by Richard Frackowiak "A GRASS roots effort is under way to stop the project... 'Mediocre science, terrible science policy,' begins the spirited letter..." The year was 1990 and the journal Science was reporting on what it called a "backlash" against the Human Genome Project. Given the furore this past week you could be forgiven for thinking these words were written about another big science initiative: the Human Brain Project (HBP). Less than a year into its planned 10-year lifetime, the project was publicly criticised in an open letter posted online on 7 July, signed by more than 150 scientists. At the time of writing a further 400 individuals have added their names. The Human Genome Project weathered its criticisms and reached its goal in 2003, birthing the entire field of genomics and opening new medical, scientific and commercial avenues along the way. The Human Brain Project will similarly overcome its own teething troubles and catalyse a methodological paradigm shift towards unified brain research that weaves together neuroscience, computing and medicine. The goal of the HBP is a comprehensive understanding of brain structure and function through the development and use of computing tools. This is popularly deemed a "simulation of the whole human brain" but we prefer the analogy "CERN for the brain" (after Europe's premier particle physics lab): a large facility for diverse experiments and sharing of knowledge with a common goal of unlocking the most complex structure in the known universe. This brings me to two of the criticisms in the open letter: the apparent lack of experimental neuroscience and data generation in the HBP, and the emphasis on information and communications technologies (ICT) in what is billed as a neuroscience project. I will address a third criticism regarding funding later on. © Copyright Reed Business Information Ltd.
Keyword: Brain imaging
Link ID: 19842 - Posted: 07.17.2014
By Jonathan Webb Science reporter, BBC News After leaders of the billion-euro Human Brain Project hit back at critics, six top neuroscientists have expressed "dismay" at their public response. Last week an open message, signed by over 600 researchers, said the HBP was "not on course", demanding a review. An official reply said HBP members were "saddened" by the protest but Prof Henry Markram, the project's chair, has labelled it a personal crusade. In a letter to Nature, the six authors call for a more "open-minded attitude". They did not sign the original protest letter, but are disappointed by the publicly reported stance of the HBP leadership. "Instead of acknowledging that there is a problem and genuinely seeking to address scientists' concerns, the project leaders seem to be of the opinion that the letter's 580 signatories [now over 600] are misguided," wrote Prof Richard Morris, an eminent neuroscientist from the University of Edinburgh, and five colleagues. The six correspondents describe themselves as "neuroscientists in Europe who care about the success of research projects large and small in our field". Prof Richard Frackowiak, a co-executive director of the HBP, told the BBC he "strongly objects" to the idea that the project leaders were dismissive. "We've taken this extremely seriously," he said. The HBP is one of two flagship technology projects (the other being graphene research) announced in January 2013 by the European Commission (EC). BBC © 2014
Keyword: Brain imaging
Link ID: 19841 - Posted: 07.17.2014
|By Nidhi Subbaraman and SFARI.org A team at Duke University in Durham, North Carolina, is set to launch a $40 million clinical trial to explore stem cells from umbilical cord blood as a treatment for autism. But experts caution that the trial is premature. A $15 million grant from the Marcus Foundation, a philanthropic funding organization based in Atlanta, will bankroll the first two years of the five-year trial, which also plans to test stem cell therapy for stroke and cerebral palsy. The autism arm of the trial aims to enroll 390 children and adults. Joanne Kurtzberg, the trial’s lead investigator, has extensive experience studying the effectiveness of cord blood transplants for treating various disorders, such as leukemia and sickle cell anemia. Most recently, she showed that cord blood transplants can improve the odds of survival for babies deprived of oxygen at birth. A randomized trial of the approach for this condition is underway. “To really sort out if [stem] cells can treat these children, we need to do randomized, controlled trials that are well designed and well controlled, and that’s what we intend to do,” says Kurtzberg, professor of pediatrics and pathology at Duke. “We firmly believe we should be moving ahead in the clinic.” Early animal studies have shown that stem cells isolated from umbilical cord blood can stimulate cells in the spinal cord to regrow their myelin layers, and in doing so help restore connections with surrounding cells. Autism is thought to result from impaired connectivity in the brain. Because of this, some groups of children with the disorder may benefit from a stem cell transplant, Kurtzberg says. © 2014 Scientific American
By NICHOLAS BAKALAR The incidence of stroke in the United States has declined significantly over the past two decades, a new analysis has found. The decreases were apparent in people older than 65, the most common age group for stroke, and were similar in men and women and in blacks and whites. There were decreases in stroke deaths as well, but they were concentrated in younger research participants. The report appeared in JAMA. Researchers followed 14,357 people, ages 45 to 64 at the start of the study, from 1987 to 2011. After accounting for coronary heart disease, hypertension, diabetes, smoking, statin use and other factors, they found that the incidence of stroke decreased by about 50 percent over the period of the study, and stroke deaths by about 40 percent. Smoking cessation and better treatment of hypertension and high cholesterol accounted for part of the decrease, according to the senior author, Dr. Josef Coresh, a professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, and improved medical care and more rigorous control of risk factors probably helped as well. Increased diabetes prevalence, on the other hand, contributed to higher risk. “The decrease in stroke also suggests that there’s a decrease in smaller strokes that we may not detect,” he said, “and that would bode well for overall brain health and the potential for decreasing the risk of dementia with aging.” © 2014 The New York Times Company
Link ID: 19839 - Posted: 07.16.2014
Associated Press The rate of Alzheimer's disease and other dementias is falling in the United States and some other rich countries - good news about an epidemic that is still growing simply because more people are living to an old age, new studies show. An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded. Dementia rates also are down in Germany, a study there found. "For an individual, the actual risk of dementia seems to have declined," probably because of more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer's Association International Conference in Copenhagen. The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising. More than 5.4 million Americans and 35 million people worldwide have Alzheimer's, the most common form of dementia. It has no cure, and current drugs only temporarily ease symptoms. A drop in rates is a silver lining in the so-called silver tsunami - the expected wave of age-related health problems from an older population. Alzheimer's will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said. © 2014 Hearst Communications, Inc.
Link ID: 19838 - Posted: 07.16.2014
By PAULA SPAN What we really want, if we’re honest, is a pill or a shot that would allow us to stop worrying about ever sinking into dementia. Instead, what we’re hearing about preventing dementia is, in many ways, the same stuff we hear about preventing other kinds of illnesses. Healthy lifestyles. Behavioral modification. Stress reduction. At the Alzheimer’s Association International Conference in Copenhagen this week, researchers from Montefiore Medical Center and the Albert Einstein College of Medicine were among the scientists presenting findings that had little to do with amyloid in the brain and a lot to do with how people feel and act and cope with life. “A number of people have been interested in modifiable lifestyle factors for years,” said Richard Lipton, a neurologist at the college and director of the Einstein Aging Study, which has tracked cognition in elderly Bronx residents since the 1980s. But interest has increased lately, he said: “It’s at least in part a reflection of disappointing drug trials.” Medications have failed, over and over, to prevent or cure or substantially slow the ravages of dementing diseases. What else might help? Dr. Lipton and his colleagues, who monitor about 600 people aged 70 to 105, have been exploring the impact of stress. More specifically, they have been measuring “perceived stress,” a metric not so much about unpleasant things happening as how people respond to them. They use a scale based on the answers to 13 questions like, “In the past month, how often have you felt confident about your ability to handle your personal problems?” and “In the past month, how often have you felt difficulties were piling up so high you could not overcome them?” © 2014 The New York Times Company
Link ID: 19837 - Posted: 07.16.2014
Claudia M. Gold At the recent gubernatorial candidates forum on mental health, Martha Coakley repeated the oft-heard phrase that depression is like diabetes. Her motivation was good, the idea being to reduce the stigma of mental illness, and to offer "parity" or equal insurance coverage, for mental and physical illness. However, I am concerned that this phrase, and its companion, "ADHD is like diabetes," will, in fact, have the exact opposite effect. A recent New York Times op ed, The Trouble with Brain Science, helped me to put my finger on what is troubling about these statements. Psychologist Gary Marcus identifies the need for a bridge between neuroscience and psychology that does not currently exist. Diabetes is a disorder of insulin metabolism. Insulin is produced in the pancreas. The above analogies disregard the intimate intertwining of brain and mind. For the pancreas, there is no corresponding "mind" that exists in the realm of feelings and relationships. While there is some emerging evidence of the brain structures involved in the collection of symptoms named by the DSM (Diagnostic and Statistical Manual of Mental Disorders,) there are no known biological processes corresponding to depression, ADHD or any other diagnosis in the DSM. There is, however, a wealth of new evidence showing how brain structure and function changes in relationships. ©2014 Boston Globe Media Partners, LLC
Link ID: 19836 - Posted: 07.16.2014
By BENEDICT CAREY The 8-year-old juggling a soccer ball and the 48-year-old jogging by, with Japanese lessons ringing from her earbuds, have something fundamental in common: At some level, both are wondering whether their investment of time and effort is worth it. How good can I get? How much time will it take? Is it possible I’m a natural at this (for once)? What’s the percentage in this, exactly? Scientists have long argued over the relative contributions of practice and native talent to the development of elite performance. This debate swings back and forth every century, it seems, but a paper in the current issue of the journal Psychological Science illustrates where the discussion now stands and hints — more tantalizingly, for people who just want to do their best — at where the research will go next. The value-of-practice debate has reached a stalemate. In a landmark 1993 study of musicians, a research team led by K. Anders Ericsson, a psychologist now at Florida State University, found that practice time explained almost all the difference (about 80 percent) between elite performers and committed amateurs. The finding rippled quickly through the popular culture, perhaps most visibly as the apparent inspiration for the “10,000-hour rule” in Malcolm Gladwell’s best-selling “Outliers” — a rough average of the amount of practice time required for expert performance. Scientists begin to shed light on the placenta, an important organ that we rarely think of; virtual reality companies work out the kinks in their immersive worlds; research shows that practice may not be as important as once thought. The new paper, the most comprehensive review of relevant research to date, comes to a different conclusion. Compiling results from 88 studies across a wide range of skills, it estimates that practice time explains about 20 percent to 25 percent of the difference in performance in music, sports and games like chess. In academics, the number is much lower — 4 percent — in part because it’s hard to assess the effect of previous knowledge, the authors wrote. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 19835 - Posted: 07.15.2014
By Gary Stix Popular neuroscience books have made much in recent years of the possibility that the adult brain is capable of restoring lost function or even enhancing cognition through sustained mental or physical activities. One piece of evidence often cited is a 14-year-old study that that shows that London taxi drivers have enlarged hippocampi, brain areas that store a mental map of one’s surroundings. Taxi drivers, it is assumed, have better spatial memory because they must constantly distinguish the streets and landmarks of Shepherd’s Bush from those of Brixton. A mini-industry now peddles books with titles like The Brain that Changes Itself or Rewire Your Brain: Think Your Way to a Better Life. Along with self-help guides, the value of games intended to enhance what is known as neuroplasticity are still a topic of heated debate because no one knows for sure whether or not they improve intelligence, memory, reaction times or any other facet of cognition. Beyond the controversy, however, scientists have taken a number of steps in recent years to start to answer the basic biological questions that may ultimately lead to a deeper understanding of neuroplasticity. This type of research does not look at whether psychological tests used to assess cognitive deficits can be refashioned with cartoonlike graphics and marketed as games intended to improve mental skills. Rather, these studies attempt to provide a simple definition of how mutable the brain really is at all life stages, from infancy onward into adulthood. One ongoing question that preoccupies the basic scientists pursuing this line of research is how routine everyday activities—sleep, wakefulness, even any sort of movement—may affect the ability to perceive things in the surrounding environment. One of the leaders in these efforts is Michael Stryker, who researches neuroplasticity at the University of California San Francisco. Stryker headed a group that in 2010 published a study on what happened when mice run on top of a Styrofoam ball floating on air. They found that neurons in a brain region that processes visual signals—the visual cortex—nearly doubled their firing rate when the mice ran on the ball. © 2014 Scientific American
By Joel Achenbach Friends often look alike. The tendency of people to forge friendships with people of a similar appearance has been noted since the time of Plato. But now there is research suggesting that, to a striking degree, we tend to pick friends who are genetically similar to us in ways that go beyond superficial features. For example, you and your friends are likely to share certain genes associated with the sense of smell. Our friends are as similar to us genetically as you’d expect fourth cousins to be, according to the study published Monday in the Proceedings of the National Academy of Sciences. This means that the number of genetic markers shared by two friends is akin to what would be expected if they had the same great-great-great-grandparents. “Your friends don’t just resemble you superficially, they resemble you genetically,” said Nicholas A. Christakis, a physician and social scientist at Yale University and a co-author of the study. The resemblance is slight, just about 1 percent of the genetic markers, but that has huge implications for evolutionary theory, said James Fowler, a professor of medical genetics and political science at the University of California at San Diego. “We can do better than chance at predicting if two people are going to be friends if all we have is their genetic data,” Fowler said. This is a data-driven study that covers hundreds of friendship pairs and stranger pairs, plus hundreds of thousands of genetic markers. There’s no single “friendship” gene driving people together. There’s no way to say that a person befriended someone else because of any one genetic trait.
By Lizzie Wade It probably won’t come as a surprise that smoking a joint now and then will leave you feeling … pretty good, man. But smoking a lot of marijuana over a long time might do just the opposite. Scientists have found that the brains of pot abusers react less strongly to the chemical dopamine, which is responsible for creating feelings of pleasure and reward. Their blunted dopamine responses could leave heavy marijuana users living in a fog—and not the good kind. After high-profile legalizations in Colorado, Washington, and Uruguay, marijuana is becoming more and more available in many parts of the world. Still, scientific research on the drug has lagged. Pot contains lots of different chemicals, and scientists don’t fully understand how those components interact to produce the unique effects of different strains. Its illicit status in most of the world has also thrown up barriers to research. In the United States, for example, any study involving marijuana requires approval from four different federal agencies, including the Drug Enforcement Administration. One of the unanswered questions about the drug is what, exactly, it does to our brains, both during the high and afterward. Of particular interest to scientists is marijuana’s effect on dopamine, a main ingredient in the brain’s reward system. Pleasurable activities such as eating, sex, and some drugs all trigger bursts of dopamine, essentially telling the brain, “Hey, that was great—let’s do it again soon.” Scientists know that drug abuse can wreak havoc on the dopamine system. Cocaine and alcohol abusers, for example, are known to produce far less dopamine in their brains than people who aren’t addicted to those drugs. But past studies had hinted that the same might not be true for those who abuse marijuana. © 2014 American Association for the Advancement of Science
Keyword: Drug Abuse
Link ID: 19832 - Posted: 07.15.2014
By ALEX STONE Last summer, in a failed attempt at humor, Clorox ran an online ad that declared, “Like dogs or other house pets, new dads are filled with good intentions but lacking the judgment and fine motor skills to execute well.” Although the company pulled the ad amid a flurry of scorn from the online commentariat, it nevertheless played to a remarkably widespread stereotype — that fathers are somehow unfit to raise children. In “Do Fathers Matter?” — spoiler alert: they do — the veteran science writer Paul Raeburn jumps to Dad’s defense, drawing on several decades of research and his own experience as a five-time father. What emerges is a thought-provoking field piece on the science of fatherhood, studded with insights on how to apply it in the real world. Historically, developmental psychologists have largely dismissed fathers as irrelevant. Nearly half the articles on child and adolescent psychology published in leading journals from 1997 to 2005, for example, make no mention of fathers; before 1970, when fathers weren’t even allowed in delivery rooms, less than a fifth of the research on parental bonding took them into account. This bias reflects a deeply ingrained assumption that fathers play a marginal role in how their children turn out, a belief enshrined in the theory of infant attachment, which grew out of the work of the British psychiatrist John Bowlby in the second half of the 20th century. “It focused exclusively on mothers,” Mr. Raeburn writes. “The role of the father, Bowlby believed, was to provide support for the mother. In the drama of childhood, he was merely a supporting actor.” This was more or less the established view until a few decades ago, when psychologists, motivated in part by the growing number of women entering the work force, finally started paying attention to fathers. © 2014 The New York Times Company
by Azeen Ghorayshi Food could be a new weapon in shaking off the effects of jet lag after research in mice showed that the insulin released as a result of eating can be a key factor in restoring a disrupted body clock. Miho Sato and her colleagues at The Research Institute for Time Studies at Yamaguchi University in Japan did experiments in mice and tissue cultures to show, for the first time, that increases in insulin affect circadian rhythms. These daily rhythms affect alertness, sleep patterns, and mediate many other physiological processes. Your biological clock is regulated by two broad factors: first, the central rhythm is reset daily by light, as sensory input from the eyes is processed by a small part of the brain called the suprachiasmatic nucleus. The rise and fall of hormones linked to sleep, for example, match this rhythm. But circadian rhythms are also present in peripheral "clocks" in a wide range of cell types in the body. Some of these can be influenced by food. Sato demonstrated the role of insulin by shifting the peripheral body clock in the livers of mice by feeding them only at night. They then split the mice into two groups, supressed insulin levels in one group, and returned all the mice to daytime feeding. Four days later, the livers of the non-supressed mice had readjusted to a normal daily rhythm, as revealed by the daily rise and fall of liver-gene expression. The livers of the insulin-suppressed mice had still not returned to normal. © Copyright Reed Business Information Ltd.
Keyword: Biological Rhythms
Link ID: 19830 - Posted: 07.15.2014
By Neuroskeptic An entertaining paper just out in Frontiers in Systems Neuroscience offers a panoramic view of the whole of neuroscience: Enlarging the scope: grasping brain complexity The paper is remarkable not just for its content but also for its style. Some examples: How does the brain work? This nagging question is an habitué from the top ten lists of enduring problems in Science’s grand challenges. Grasp this paradox: how is one human brain – a chef d’oeuvre of complexity honed by Nature – ever to reach such a feast as to understand itself? Where one brain may fail at this notorious philosophical riddle, may be a strong and diversely-skilled army of brains may come closer. Or It remains an uneasy feeling that so much of Brain Science is built upon the foundation of a pair of neurons, outside the context of their networks, and with two open-ended areas of darkness at either of their extremities that must be thought of as the entire remainder of the organism’s brain (and body). And my favorite: As humans tend to agree, increased size makes up for smarter brains (disclosure: both authors are human) I love it. I’m not sure I understand it, though. The authors, Tognoli and Kelso, begin by framing a fundamental tension between directed information transfer and neural synchrony, pointing out that neurons firing perfectly in synch with each other could not transfer information between themselves.
Link ID: 19829 - Posted: 07.15.2014
|By Maria Burke and ChemistryWorld The world needs to tackle head-on the market failures undermining dementia research and drug development, UK Prime Minister David Cameron told a summit of world health and finance leaders in London in June. He announced an investigation into how to get medicines to patients earlier, extend patents and facilitate research collaborations, to report this autumn. But just how much difference will these sorts of measures make when scientists are still grappling with exactly what causes different types of dementia? Added to these problems is that dementia has become a graveyard for a large number of promising drugs. A recent study looked at how 244 compounds in 413 clinical trials fared for Alzheimer's disease between 2002 and 2012. The researchers findings paint a gloomy picture. Of those 244 compounds, only one was approved. The researchers report that this gives Alzheimer's disease drug candidates one of the highest failures rates of any disease area – 99.6%, compared with 81% for cancer. ‘Dementia is a ticking bomb costing the global economy £350 billion and yet progress with research is achingly slow,’ warned the World Dementia Envoy, Dennis Gillings. Businesses need incentives to invest in research and bring in faster, cheaper clinical trials, or the world won’t meet the ambition to find a cure or disease-modifying therapy by 2025, he added. ‘We need to free up regulation so that we can test ground-breaking new drugs, and examine whether the period for market exclusivity could be extended.’ © 2014 Scientific American
Link ID: 19828 - Posted: 07.15.2014
By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014
|By William Skaggs Jet lag is a pain. Besides the inconvenience and frustration of traveling more than a few time zones, jet lag likely causes billions of dollars in economic losses. The most effective treatment, according to much research, is structured exposure to light, although the drug melatonin may also sometimes be helpful at bedtime. Both approaches have been used for more than 20 years, and during that time no viable new interventions have appeared. Recently, however, research into the molecular biology of circadian rhythms has raised the prospect of developing new drugs that might produce better results. Jet lag occurs when the “biological clock” in the brain becomes misaligned with the local rhythm of daily activity. The ultimate goal of circadian medicine is a treatment that instantly resets the brain's clock. Failing that, it would be helpful to have treatments that speed the rate of adjustment. Four recent discoveries suggest new possibilities. The first involves vasopressin, which is the main chemical signal used to synchronize cellular rhythms of activity in the brain area that is responsible for our biological clock. Blocking vasopressin makes it much easier to reset this clock. Potentially, a drug that interferes with vasopressin could work as a fast-acting treatment for jet lag. The second and third possibilities involve a pair of brain chemicals called salt-inducible kinase 1 (SIK1) and casein kinase 1ε (CK1ε), both of which limit the ability of light to reset the brain's clock. Drugs already exist that interfere with their action and greatly increase the effectiveness of light exposure. The existing drugs are not viable jet-lag treatments, because they are hard to administer and have unpleasant side effects, but researchers hope better drugs can be developed that work in a similar way. © 2014 Scientific American,
By Fredrick Kunkle Sleep disturbances such as apnea may increase the risk of Alzheimer’s disease, while moderate exercise in middle age and mentally stimulating games, such as crossword puzzles, may prevent the onset of the dementia-causing disease, according to new research to be presented Monday. The findings — which are to be introduced during the six-day Alzheimer’s Association International Conference in Copenhagen — bolster previous studies that suggest sleep plays a critical role in the aging brain’s health, perhaps by allowing the body to cleanse itself of Alzheimer's-related compounds during down time. The studies also add to a growing body of literature that suggests keeping the brain busy keeps it healthy. The battle against Alzheimer’s disease has become more urgent for the United States and other developing nations as their populations turn increasingly gray. The disease is the leading cause of dementia in older people and afflicts more than 5 million Americans. At its current pace, the number is expected to soar to 16 million people by 2050. In 2012, the United States adopted a national plan to combat the disease and the G-8 nations last year adopted a goal of providing better treatment and prevention by 2025. Erin Heintz, a spokeswoman for the Alzheimer’s Association, said U.S. government funding to combat the disease now stands at about $500 million a year. To reach its 2025 goal, the United States should be spending $2 billion a year, she said.