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

Keyword: Alzheimers
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

Keyword: Depression
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

Keyword: Learning & Memory; Aggression
Link ID: 19834 - Posted: 07.15.2014

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.

Keyword: Genes & Behavior; Aggression
Link ID: 19833 - Posted: 07.15.2014

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

Keyword: Development of the Brain; Aggression
Link ID: 19831 - Posted: 07.15.2014

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.

Keyword: Consciousness
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

Keyword: Alzheimers
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

Keyword: Depression; Aggression
Link ID: 19827 - Posted: 07.14.2014

|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,

Keyword: Biological Rhythms; Aggression
Link ID: 19826 - Posted: 07.14.2014

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.

Keyword: Alzheimers; Aggression
Link ID: 19825 - Posted: 07.14.2014

One in three cases of Alzheimer's disease worldwide is preventable, according to research from the University of Cambridge. The main risk factors for the disease are a lack of exercise, smoking, depression and poor education, it says. Previous research from 2011 put the estimate at one in two cases, but this new study takes into account overlapping risk factors. Alzheimer's Research UK said age was still the biggest risk factor. Writing in The Lancet Neurology, the Cambridge team analysed population-based data to work out the main seven risk factors for Alzheimer's disease. These are: Diabetes Mid-life hypertension Mid-life obesity Physical inactivity Depression Smoking Low educational attainment They worked out that a third of Alzheimer's cases could be linked to lifestyle factors that could be modified, such as lack of exercise and smoking. The researchers then looked at how reducing these factors could affect the number of future Alzheimer's cases. They found that by reducing each risk factor by 10%, nearly nine million cases of the disease could be prevented by 2050. In the UK, a 10% reduction in risk factors would reduce cases by 8.8%, or 200,000, by 2050, they calculated. BBC © 2014

Keyword: Alzheimers
Link ID: 19824 - Posted: 07.14.2014

By Fredrick Kunkle A simple test of a person’s ability to identify odors and noninvasive eye exams might someday help doctors learn whether their patients are at risk of Alzheimer’s disease, according to research to be presented Sunday. With Alzheimer’s disease growing fast among the world’s aging population, researchers are increasingly focused on the search for new ways to detect and treat the brain-killing disease in its earliest stages. In two separate studies on the connection between dementia and sense of smell, teams of researchers found that a decreased ability to detect odors in older people, as determined by a common scratch-and-sniff test, could point to brain cell loss and the onset of dementia. In two other studies, researchers showed that noninvasive eye exams also might offer a way to identify Alzheimer’s in its early stages. The findings — which are to be presented at the Alzheimer’s Association International Conference in Copenhagen on Sunday — raise hopes that doctors could develop simple, inexpensive diagnostic tools that would hunt down reliable biomarkers of a disease that affects more than 5 million people in the United States. Alzheimer’s is a progressive and incurable disease that begins in areas of the brain associated with memory. It is the leading cause of dementia in older people, usually striking after the age of 65. It robs people of their cognitive abilities, speech and, ultimately, their identities. Eventually, it shuts down the most basic body functions, resulting in death.

Keyword: Alzheimers
Link ID: 19823 - Posted: 07.14.2014

|By Roni Jacobson Prozac, Paxil, Celexa, Zoloft, Lexapro. These so-called selective serotonin reuptake inhibitors (SSRIs) are among the most widely prescribed drugs in the U.S. Although they are typically used to treat depression and anxiety disorders, they are also prescribed off-label for conditions such as chronic pain, premature ejaculation, bulimia, irritable bowel syndrome, premenstrual syndrome and hot flashes. Even if you have never taken an SSRI, chances are you know someone who has. About one in every 10 American adults is being prescribed one now. For women aged 40 to 59 years old, the proportion increases to one in four. SSRIs block the body from reabsorbing serotonin, a neurotransmitter mostly found in the brain, spinal cord and digestive tract whose roles include regulation of mood, appetite, sexual function and sleep. Specifically, SSRIs bind to the protein that carries serotonin between nerve cells—called SERT, for serotonin transporter—intercepting it before it can escort the released neurotransmitter back into the cell. This action leaves more active serotonin in the body, a chemical effect that is supposed to spur feelings of happiness and well-being. But there are hints that SSRIs are doing something other than simply boosting serotonin levels. First, people vary in their response to SSRIs: Studies have shown that the drugs are not very effective for mild to moderate depression, but work well when the disorder is severe. If low serotonin were the only culprit in depression, SSRIs would be more uniformly helpful in alleviating symptoms. Second, it takes weeks after starting an SSRI for depression and anxiety to lift even though changes in serotonin ought to happen pretty much right away. © 2014 Scientific American

Keyword: Depression; Aggression
Link ID: 19822 - Posted: 07.14.2014

Posted by alison abbott Cautious efforts to restore unity to the billion-euro Human Brain Project have begun. Both the European Commission and the project’s leaders have now responded to a scorching open letter in which angry neuroscientists condemn the flagship project, and pledge to boycott it. Signed by 156 top neuroscientists, including many research institute directors in Europe, the letter was sent on 7 July to the European Commission, which is funding the project’s first phase. It expresses concern about both the scientific approach in the neuroscience arm of the project, which aims to simulate brain function in supercomputers, and the general project management. The letter makes a series of demands for changes that it claims are needed to make the management and governance of the Human Brain Project more transparent and representative of the scientific views of the whole community. Since it was sent, a further 408 neuroscientists have added their signatures. On 10 July, the European Commission sent a bland statement to Nature, stating that “it is too early to draw conclusions on the success or failure of the project”, given that it has only been running for nine months. The Commission’s response also says that a “divergence of views” is not unusual in large-scale projects, particularly at their beginnings and that the Commission will “continue to engage with all partners in this ambitious project”. © 2014 Macmillan Publishers Limited

Keyword: Brain imaging
Link ID: 19821 - Posted: 07.14.2014

Sara Reardon For chimps, nature and nurture appear to contribute equally to intelligence. Smart chimpanzees often have smart offspring, researchers suggest in one of the first analyses of the genetic contribution to intelligence in apes. The findings, published online today in Current Biology1, could shed light on how human intelligence evolved, and might even lead to discoveries of genes associated with mental capacity. A team led by William Hopkins, a psychologist at Georgia State University in Atlanta, tested the intelligence of 99 chimpanzees aged 9 to 54 years old, most of them descended from the same group of animals housed at the Yerkes National Primate Research Center in Atlanta. The chimps faced cognitive challenges such as remembering where food was hidden in a rotating object, following a human’s gaze and using tools to solve problems. A subsequent statistical analysis revealed a correlation between the animals' performance on these tests and their relatedness to other chimpanzees participating in the study. About half of the difference in performance between individual apes was genetic, the researchers found. In humans, about 30% of intelligence in children can be explained by genetics; for adults, who are less vulnerable to environmental influences, that figure rises to 70%. Those numbers are comparable to the new estimate of the heritability of intelligence across a wide age range of chimps, says Danielle Posthuma, a behavioural geneticist at VU University in Amsterdam, who was not involved in the research. “This study is much overdue,” says Rasmus Nielsen, a computational biologist at the University of California, Berkeley. “There has been enormous focus on understanding heritability of intelligence in humans, but very little on our closest relatives.” © 2014 Nature Publishing Group

Keyword: Intelligence; Aggression
Link ID: 19820 - Posted: 07.12.2014

By Jules Wellinghoff A simple change in electric charge may make the difference between someone getting the medicine they need and a trip to the emergency room—at least if a new study bears out. Researchers investigating the toxicity of particles designed to ferry drugs inside the body have found that carriers with a positive charge on their surface appear to cause damage if they reach the brain. These particles, called micelles, are one type of a class of materials known as nanoparticles. By varying properties such as charge, composition, and attached surface molecules, researchers can design nanoparticles to deliver medicine to specific body regions and cell types—and even to carry medicine into cells. This ability allows drugs to directly target locations they would otherwise be unable to, such as the heart of tumors. Researchers are also looking at nanoparticles as a way to transport drugs across the blood-brain barrier, a wall of tightly connected cells that keeps most medication out of the brain. Just how safe nanoparticles in the brain are, however, remains unclear. So Kristina Bram Knudsen, a toxicologist at the National Research Centre for the Working Environment in Copenhagen, and colleagues tested two types of micelles, which were made from different polymers that gave the micelles either a positive or negative surface charge. They injected both versions, empty of drugs, into the brains of rats, and 1 week later they checked for damage. Three out of the five rats injected with the positively charged micelles developed brain lesions. The rats injected with the negatively charged micelles or a saline control solution did not suffer any observable harm from the injections, the team will report in an upcoming issue of Nanotoxicology. © 2014 American Association for the Advancement of Science

Keyword: Neurotoxins
Link ID: 19819 - Posted: 07.12.2014

By GARY MARCUS ARE we ever going to figure out how the brain works? After decades of research, diseases like schizophrenia and Alzheimer’s still resist treatment. Despite countless investigations into serotonin and other neurotransmitters, there is still no method to cure clinical depression. And for all the excitement about brain-imaging techniques, the limitations of fMRI studies are, as evidenced by popular books like “Brainwashed” and “Neuromania,” by now well known. In spite of the many remarkable advances in neuroscience, you might get the sinking feeling that we are not always going about brain science in the best possible way. This feeling was given prominent public expression on Monday, when hundreds of neuroscientists from all over the world issued an indignant open letter to the European Commission, which is funding the Human Brain Project, an approximately $1.6 billion effort that aims to build a complete computer simulation of the human brain. The letter charges that the project is “overly narrow” in approach and not “well conceived.” While no neuroscientist doubts that a faithful-to-life brain simulation would ultimately be tremendously useful, some have called the project “radically premature.” The controversy serves as a reminder that we scientists are not only far from a comprehensive explanation of how the brain works; we’re also not even in agreement about the best way to study it, or what questions we should be asking. The European Commission, like the Obama administration, which is promoting a large-scale research enterprise called the Brain Initiative, is investing heavily in neuroscience, and rightly so. (A set of new tools such as optogenetics, which allows neuroscientists to control the activity of individual neurons, gives considerable reason for optimism.) But neither project has grappled sufficiently with a critical question that is too often ignored in the field: What would a good theory of the brain actually look like? Different kinds of sciences call for different kinds of theories. Physicists, for example, are searching for a “grand unified theory” that integrates gravity, electromagnetism and the strong and weak nuclear forces into a neat package of equations. Whether or not they will get there, they have made considerable progress, in part because they know what they are looking for. © 2014 The New York Times Company

Keyword: Brain imaging
Link ID: 19818 - Posted: 07.12.2014