By NICHOLAS BAKALAR Many people use copper bracelets and magnetic wrist straps to alleviate the pain of arthritis, but a new randomized, double-blinded, placebo-controlled study concludes they do not work. British researchers randomized 65 patients with rheumatoid arthritis to receive one of four treatments: wearing a powerful magnetic wrist strap, a weak magnetic strap, a non-magnetic strap and a copper bracelet. Each patient wore each device for five weeks and completed pain surveys. The study appears in the September issue of PLoS One. The patients reported pain levels using a visual scale, ranging from “no pain” to “worst pain ever,” and recorded how often their joints felt tender and swollen. Researchers used questionnaires to assess physical limitations, and tested for inflammation by measuring blood levels of C-reactive protein and plasma viscosity. There was no statistically significant difference in any of these measures regardless of which type of device patients were wearing. Stewart J. Richmond, a researcher at the University of York who led the study, acknowledged that the devices may have some benefits as a placebo. “People swear by these things,” he said. “Is it ethically correct to allow patients to live in blissful ignorance? Or is it better to provide them with the facts? We can’t deceive patients. We have to be honest with them.” Copyright 2013 The New York Times Company

Keyword: Pain & Touch
Link ID: 18695 - Posted: 09.24.2013

Virginia Hughes Enzymes called topoisomerases are crucial for the expression of extremely long genes in neurons, according to a study published 5 September in Nature1. More than one-quarter of these genes are known autism candidates, the study found. In the process of doing these analyses, the researchers stumbled on something surprising about autism genes in general: They're three to four times longer than the average gene expressed in neurons. "It's pretty remarkable that, at least to my knowledge, no one had noticed this before," notes Benjamin Philpot, associate professor of cell biology and physiology at the University of North Carolina, Chapel Hill, and one of the study's leaders. "But the genes are definitely much longer. It's very striking." The findings suggest that defects in topoisomerases — whether caused by genetic mutations or environmental influences — may contribute to some cases of autism and other developmental disorders, the researchers say. If it's true that long genes are preferentially affected in autism, "the implications are really quite fascinating," notes James Sutcliffe, associate professor of molecular physiology and biophysics at Vanderbilt University in Nashville, Tennessee, who was not involved in the research. In genetic sequencing studies, for example, mutations found in long genes tend to be discounted in statistical analyses. That’s because the longer a gene is, the more likely it is to harbor a mutation just by chance. But the new study suggests that mutations in long genes should be considered more carefully.

Keyword: Autism; Genes & Behavior
Link ID: 18694 - Posted: 09.24.2013

By Laura Geggel and SFARI.org Boredom, tiredness, hunger and stress can all set off a yawn. People can even 'catch' a bout of yawning when they see or hear another person in the throes of the involuntary gesture, a phenomenon known as social yawning. Researchers speculate that this shared behavior is a form of empathy that strengthens the bonds of a group: One drowsy person’s yawn that triggers others to do the same could lead to a unanimous call for bedtime, for example. Humans aren't the only species to yawn sympathetically: Dogs yawn in response to human yawns, and chimpanzees and baboons yawn in concert with one another. Children with autism apparently don’t respond to social yawning, however, prompting some researchers to blame their well-chronicled struggle with empathy. A new Japanese study suggests that, instead, children with the disorder miss facial cues, such as closed eyes, that make yawning contagious. The study was published 22 July in Autism Research and Treatment. The researchers say children with autism miss those cues because they avoid looking at people’s faces. But that may not entirely explain it. For example, a small 2009 study found that typically developing children yawn even when they’ve only heard another person do so, but children with autism do not. In the new study, the researchers set up two experiments to determine whether children with autism look at others’ faces enough to catch a social yawn. In the first test, 26 children with autism and 46 controls wore eye-tracking devices while watching video clips of people either yawning or remaining still. The researchers asked the children to count how many people in the clips were wearing glasses to make sure they looked at the people’s eyes. The video showed the person yawning only when the eye tracker verified that the children had fixed their gaze on the eyes. © 2013 Scientific American

Keyword: Autism; Emotions
Link ID: 18693 - Posted: 09.24.2013

By Fritz Andersen, It was hot that Sunday morning in February 2011 in Old San Juan. I had just retired after 40 years of cardiology practice in the suburbs of Washington, and my wife and I were spending the winter in Puerto Rico. A couple of friends had arrived by cruise ship, and I took them to see the 450-year-old Spanish fortress that sits above the entrance of the harbor. The fortress walls radiated heat, and after reentering the city we walked to our home for a breather and a refreshing ceiling fan. While sitting in the kitchen and sipping a beer, I suddenly passed out. I woke up a bit dizzy and confused; my friend, an internist from Arlington, told me I had had a grand mal seizure. My wife, Carmen Alicia, called a local friend, also a cardiologist, who sent us to a nearby hospital; there, an MRI exam revealed a small spot on my brain. The neurologist felt it needed to be biopsied to obtain a tissue diagnosis. I immediately returned to Virginia and went to several specialists, who suggested further testing before I decided to have an invasive brain biopsy. I also had a blood test for cysticercosis, an infection that results from eating undercooked pork contaminated with Tenia solium. This common parasite produces cysts all over the body, including the brain. It is the most common reason for seizures in many countries, particularly in India, where children with seizures are first treated for this disease even before other studies are done. My blood test was strongly positive. I started a course of oral medicine to treat it. The test reassured me. Unfortunately, my spot grew a bit over the course of three months, reaching the size of a grape. A biopsy and excision were now indicated. © 1996-2013 The Washington Post

Keyword: Genes & Behavior
Link ID: 18692 - Posted: 09.24.2013

By PETER ANDREY SMITH In a cavernous basement laboratory at the University of Minnesota, Thomas Stoffregen thrusts another unwitting study subject — well, me — into the “moving room.” The chamber has a concrete floor and three walls covered in faux marble. As I stand in the middle, on a pressure sensitive sensor about the size of a bathroom scale, the walls lurch inward by about a foot, a motion so disturbing that I throw up my arms and stumble backward. Indeed, the demonstration usually throws adults completely off balance. I’m getting off lightly. Dr. Stoffregen, a professor of kinesiology, uses the apparatus to study motion sickness, and often subjects must stand and endure subtle computer-driven oscillations in the walls until they are dizzy and swaying. Dr. Stoffregen’s research has also taken him on cruises — cruise ships are to motion sickness what hospitals are to pneumonia. “No one’s ever vomited in our lab,” he said. “But our cruises are a different story.” For decades now, Dr. Stoffregen, 56, director of the university’s Affordance Perception-Action Laboratory, has been amassing evidence in support of a surprising theory about the causes of motion sickness. The problem does not arise in the inner ear, he believes, but rather in a disturbance in the body’s system for maintaining posture. The idea, once largely ignored, is beginning to gain grudging recognition. “Most theories say when you get motion sick, you lose your equilibrium,” said Robert Kennedy, a psychology professor at the University of Central Florida. “Stoffregen says because you lose your equilibrium, you get motion sick.” Motion sickness is probably a problem as old as passive transportation. The word “nausea” derives from the Greek for “boat,” but the well-known symptoms arise from a variety of stimuli: lurching on the back of a camel, say, or riding the Tilt-a-Whirl at a fair. “Pandemonium,” the perpetually seasick Charles Darwin called it. Copyright 2013 The New York Times Company

Keyword: Hearing; Vision
Link ID: 18691 - Posted: 09.24.2013

At Pimlico Race Course in Baltimore every May, the winning horse in the Preakness Stakes is draped with a blanket covered with what appear to be the Maryland state flower, the black-eyed Susan. But the flower doesn't bloom until later in the season. Those crafting the victory blanket must resort to using yellow Viking daisies — and painting the centers black. That might fool race fans, but bees can see through the ruse. With eyes equipped to detect ultraviolet light, a bee can pick out an additional band in the black-eyed Susan's bull's-eye. The insect's livelihood depends on it. At the center of the target is the flower's nutritional payload, nectar and pollen, which also glows in UV light. As with other members of the sunflower family, black-eyed Susan flower heads are composed of two kinds of florets. The dark center is made up of numerous disc florets, each of which contains male and female reproductive components. When a bee or other pollinator fertilizes a disc floret, it develops a single seed that ripens and falls from the flower head in the autumn. Seeds can remain viable for more than 30 years. Circling the disc florets are bright yellow ray florets, which flag down pollinators and act as landing strips. The inner portion of each ray floret contains several compounds that absorb UV rays. The outer portion reflects UV rays, contributing a visually energetic outer ring to the pattern — provided you're a bee. Black-eyed Susan, Rudbeckia hirta. © 1996-2013 The Washington Post

Keyword: Vision; Evolution
Link ID: 18690 - Posted: 09.24.2013

By Laura Sanders A nap can ease the burden of a painful memory. While fast asleep, people learned that a previously scary situation was no longer threatening, scientists report September 22 in Nature Neuroscience. The results are the latest to show that sleep is a special state in which many sorts of learning can happen. And the particular sort of learning in the new study blunted a fear memory, a goal of treatments for disorders such as phobias and post-traumatic stress disorder. “It’s a remarkable finding,” says sleep neuroscientist Edward Pace-Schott of Harvard Medical School and Massachusetts General Hospital. Researchers led by Katherina Hauner of Northwestern University’s Feinberg School of Medicine first taught 15 (awake) volunteers to fear the combination of a face and odor. Participants saw a picture of a certain man’s face and at the same time smelled a distinctive scent, such as lemon. This face-odor combo was paired with a nasty shock, so that the volunteers quickly learned to expect something bad when they saw that particular face and smelled the associated odor. Then the volunteers tucked in for a nap in the laboratory. When the participants hit the deepest stage of sleep, called slow-wave sleep, Hauner and her colleagues redelivered the smell that had earlier come with a shock. During the nap, some participants had learned that the smell was safe. The volunteers sweated less (a measure of fear) when the face-odor combination appeared after the nap, the scientists found. When the odor wasn’t presented during sleep, volunteers’ responses to the associated face were unchanged. © Society for Science & the Public 2000 - 2013

Keyword: Sleep; Learning & Memory
Link ID: 18689 - Posted: 09.23.2013

By Arielle Duhaime-Ross The flatworms known as planarians are neuroscience darlings. Their centralized brain, complex sensory abilities and rapid regenerative capacities make these nonparasitic worms ideal for studying the mechanisms that regulate stem cell function, neuronal development and limb regrowth. To this repertoire, scientists have now added a new trick: these invertebrates can store memories outside their brain and retrieve them after losing their head and growing a new one. Researchers at Tufts University tested the worms' recall by leveraging a quirk of planarian behavior: worms that recognize a familiar locale will settle in to feed more quickly than planarians that find themselves in a new environment. Such newcomers typically need time to explore their surroundings to ensure their safety before they eat. So the researchers introduced planarians to a textured petri dish and allowed them to get acquainted with their environs. Next they decapitated the worms and waited two weeks for their heads to grow back. The scientists then jogged the worms' memory by briefly returning them to the dish and feeding them. The idea was to revive the dormant memory from the body through a short exposure to familiar turf. “For the worm, automatically imprinting the new brain tissue with an old memory that could end up being completely irrelevant would be a waste,” says study co-author Michael Levin, a Tufts developmental biologist. “So the brief exposure tells the brain that the memory is indeed relevant.” When the researchers returned the trained flatworms to the same dish, the planarians initiated feeding much more quickly than worms that had gone through the same routine but had not explored the dish prior to decapitation. © 2013 Scientific American

Keyword: Learning & Memory
Link ID: 18688 - Posted: 09.23.2013

By Neuroskeptic Neuroscientists are interested in how brains interact socially. One of the main topics of study is ‘mentalizing’ aka ‘theory of mind’, the ability to accurately attribute mental states – such as beliefs and emotions – to other people. It is widely believed that the brain has specific areas for this – i.e. social “modules” (although today most neuroscientists are shy about using that word, it’s basically what’s at issue.) But two new papers out this week suggest that people can still mentalize successfully after damage to “key parts of the theory of mind network”. Herbet et al, writing in Cortex, showed few effects of surgical removal of the right frontal lobe in 10 brain tumour patients. On two different mentalizing tasks, they showed that removal caused either no decline in performance, or only a transient one. Meanwhile Michel et al report that the left temporal pole is dispensable for mentalizing as well, in a single case report in the Journal of Cognitive Neuroscience. They describe a patient suffering from frontotemporal dementia (FTD), whose left temporal lobe was severely atrophied. He’d lost the use of language, but he did quite normally on theory of mind tests adapted to be non-linguistic. In both papers, these patients don’t have those parts of the brain that are most activated in fMRI studies of mentalizing. Where the blobs on the brain normally go, they have no brain.

Keyword: Attention
Link ID: 18687 - Posted: 09.23.2013

Joseph Brean U.S. President Barack Obama’s much-hyped BRAIN initiative to crack the mysteries of consciousness via a finely detailed map of the brain in action took its first big step this week, with the release of a strategy report that foresees “revolutionary advances” in the $100-million effort to “crack the brain’s code,” perhaps in as little as “a few years.” “We stand on the verge of a great journey into the unknown,” the report says, explicitly comparing BRAIN to the Apollo moon shot, and predicting it will “change human society forever.” As a grand challenge, Apollo was an unambiguous success, despite the vast expense and human costs, but there is a growing sense among scientists, if not legacy-minded politicians, that the road ahead for modern neuroscience will be pocked with disappointment, with more impenetrable mysteries than solvable problems. As the world approaches what some are calling “peak neuro,” after three decades of over-hyped “brain porn,” the optimistic hope is that Mr. Obama’s BRAIN project will lead to a detailed and dynamic map of the brain, and thus reveal both how it works and how it fails in such diseases as Alzheimer’s or autism. The pessimistic fear, however, is that the “speed of thought,” as Mr. Obama described it, is just too quick for our current brain imaging technologies, primarily functional magnetic resonance imaging (fMRI). As the anonymous blogger Neuroskeptic, a British brain scientist who tracks the misinterpretation of brain scan studies by both scientists and media, put it in an email, “there’s just as much hype and misrepresentation as ever.” The more we learn about the brain, the less we seem to know. With its potential overstated and its aspirations presented as foregone conclusions, the relatively new field of neuroscience is in a period of self-reflection, said Jackie Sullivan, a philosopher of neuroscience at Western University in London Ont. “The vast majority of neuroscientists are well aware that the goals going forward need to be more modest,” she said. © 2013 National Post

Keyword: Consciousness; Brain imaging
Link ID: 18686 - Posted: 09.23.2013

By JOHN SCHWARTZ Candace Pert, a neuroscientist who helped discover a fundamental element of brain chemistry as a graduate student and went on to become a major proponent of alternative medicine, died on Sept. 12 at her home in Potomac, Md. She was 67. The cause was cardiac arrest, said her sister, Deane Beebe. Dr. Pert was working at the Johns Hopkins University School of Medicine in the 1970s when a team she was on found one of the most sought-after objects in brain research: the receptor in the brain that opiates like morphine fit into, like a key in a lock, allowing the drug’s effects to work. The discovery of the opioid receptor would, in 1978, earn the coveted Albert Lasker Award, often a precursor to the Nobel Prize. The award went to Solomon H. Snyder, who headed the lab. Neither Dr. Pert nor any of the other lab assistants was cited. Such omissions are common in the world of science; the graduate student in the lab rarely gets credit beyond being the first name on the papers describing the research. But Dr. Pert did something unusual: she protested, sending a letter to the head of the foundation that awards the prize, saying she had “played a key role in initiating the research and following it up” and was “angry and upset to be excluded.” Her letter caused a sensation in the field. Some saw her exclusion as an example of the burdens and barriers women face in science careers. In a 1979 article about Dr. Pert in the The Washington Post, Dr. Snyder, who had lauded Dr. Pert’s contributions in his Lasker acceptance speech, argued that “that’s the way the game is played,” adding that today’s graduate students will be tomorrow’s lab chiefs, and that “when they have students, it will be the same.” © 2013 The New York Times Company

Keyword: Pain & Touch
Link ID: 18685 - Posted: 09.21.2013

By Julianne Chiaet It has taken a century so far for scientists to not figure out the cause of multiple sclerosis (MS). The inflammatory disease, which affects more than 2.1 million people worldwide, has been blamed on toxins, viruses and even food. Most recently, scientists have placed their bets on two major ideas: The first (and far more popular) hypothesis suggests MS begins in white matter, which influences how parts of the brain work together. White matter consists of bundles of axons covered in myelin, a white insulating fatty layer. In people with MS myelin degrades and nerve fibers are left exposed, causing problems in motor coordination and loss of senses. The second hypothesis suggests that MS begins in the gray matter, which affects thinking and learning. The white matter hypothesis overshadows its alternative in part because white matter’s impact is easier to observe. When using a microscope to look at brain tissue, scientists are struck by the degradation in the myelin in samples from patients with MS. And when analyzing MS in the clinic, the overt symptoms experienced by a person with the disease can be attributed to the myelin. Symptoms associated with dysfunctions in gray matter are less obvious, such as the loss of an IQ point. Now, new evidence lends support to the less-favored gray matter hypothesis. Scientists at Rutgers University in Newark tried a new approach to look into the gray matter of MS patients. They analyzed proteins in cerebrospinal fluid (CSF), which can be thought of as the central nervous system’s “blood.” By comparing the quantity of specific CSF proteins in patients who were newly diagnosed or had the relapsing remitting variety of MS with that of healthy patients, the researchers found an uneven distribution of 20 proteins among the three groups. © 2013 Scientific American

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 18684 - Posted: 09.21.2013

by Andy Coghlan Parts of the brain may still be alive after a person's brain activity is said to have flatlined. When someone is in a deep coma, their brain activity can go silent. An electroencephalogram measuring this activity may eventually show a flatline, usually taken as a sign of brain death. However, while monitoring a patient who had been placed in a deep coma to prevent seizures following a cardiac arrest, Bogdan Florea, a physician at the Regina Maria Medical Centre in Cluj-Napoca, Romania, noticed a strange thing – some tiny intermittent bursts of activity were interrupting an otherwise flatline signal, each lasting a few seconds. He asked Florin Amzica of the University of Montreal in Canada and his colleagues to investigate what might be happening. To imitate what happened in the patient, Amzica's team put cats into a deep coma using a high dose of anaesthesia. While EEG recordings taken from the surface of the brain – the cortex – showed a flatline, recordings from deep-brain electrodes revealed tiny bursts of activity originating in the hippocampus, responsible for memory and learning, which spread within minutes to the cortex. "These ripples build up a synchrony that rises in a crescendo to reach a threshold where they can spread beyond the hippocampus and trigger activity in the cortex," says Amzica. © Copyright Reed Business Information Ltd.

Keyword: Consciousness
Link ID: 18683 - Posted: 09.21.2013

By John Horgan Once again, antidepressants have been linked to an episode of horrific violence. The New York Times reports that Aaron Alexis, who allegedly shot 12 people to death at a Navy facility in Washington, D.C., earlier this week, received a prescription for the antidepressant trazodone in August. When I first researched antidepressants almost 20 years ago, I encountered claims that they sometimes triggered violent episodes—for example, a 1989 incident in which a Kentucky man taking fluoxetine (brand name Prozac) shot to death eight co-workers and then himself. I dismissed the claims, reasoning that, because people prescribed psychiatric drugs are disturbed to begin with, it is not surprising that a tiny fraction hurt themselves and/or others. By 2004, however, in part because of lawsuits that forced pharmaceutical companies to disclose data on adverse effects, the FDA ordered antidepressant manufacturers to include a warning that antidepressants “increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders.” Alexis, who was 34, was reportedly seeking treatment for insomnia when he received his prescription for trazodone. Originally marketed as an antidepressant after its approval by the FDA in 1981, trazodone is also prescribed for anxiety and insomnia. Trazodone was a precursor of the extremely popular selective serotonin reuptake inhibitors (SSRIs); like the SSRIs, trazodone boosts levels of the neurotransmitter serotonin. © 2013 Scientific American

Keyword: Aggression; Depression
Link ID: 18682 - Posted: 09.21.2013

By T. M. LUHRMANN STANFORD, Calif. — THE specter of violence caused by mental illness keeps raising its head. The Newtown, Conn., school killer may have suffered from the tormenting voices characteristic of schizophrenia; it’s possible that he killed his mother after she was spooked by his strange behavior and tried to institutionalize him. We now know that Aaron Alexis, who killed 12 people at the Washington Navy Yard on Monday, heard voices; many observers assume that he, too, struggled with schizophrenia. To be clear: a vast majority of people with schizophrenia — a disease we popularly associate with violence — never commit violent acts. They are far more likely to be the victims of violence than perpetrators of it. But research shows us that the risk of violence from people with schizophrenia is real — significantly greater than it is in the broader population — and that the risk increases sharply when people have disturbing hallucinations and use street drugs. We also know that many people with schizophrenia hear voices only they can hear. Those voices feel real, spoken by an external, commanding authority. They are often mean and violent. An unsettling question is whether the violent commands from these voices reflect our culture as much as they result from the disease process of the illness. In the past few years I have been working with some colleagues at the Schizophrenia Research Foundation in Chennai, India, to compare the voice-hearing experience of people with schizophrenia in the United States and India. The two groups of patients have much in common. Neither particularly likes hearing voices. Both report hearing mean and sometimes violent commands. But in our sample of 20 comparable cases from each country, the voices heard by patients in Chennai are considerably less violent than those heard by patients in San Mateo, Calif. © 2013 The New York Times Company

Keyword: Schizophrenia; Aggression
Link ID: 18681 - Posted: 09.21.2013

By William Saletan In much of this country, over the last three years, pro-lifers have banned abortions 20 weeks after fertilization. They’ve justified these bans by asserting—contrary to the most authoritative studies—that fetuses at this stage of development can feel pain. Their assertions, in turn, are based on research by several doctors. But the doctors don’t buy the pro-lifers’ conclusions. They say their research doesn’t support the bans. The 12 state bans (several of which have been blocked or limited by courts) begin with legislative “findings.” The findings parrot a 33-page report posted by the National Right to Life Committee and other pro-life organizations. The report cites the work of a number of researchers. Pam Belluck, an enterprising New York Times correspondent, contacted the researchers and asked them about the abortion bans. It turns out there’s a big gap between the science and the legislation. The pro-life report cites Dr. Nicholas Fisk, a former president of the International Fetal Medicine and Surgery Society, 27 times. According to the report, Fisk’s work shows fetal “stress responses” that imply sensitivity to pain. But Fisk tells Belluck that he doesn’t buy the inference from stress hormones and cerebral blood flow to pain. Neural studies, he says, have persuaded him that until 24 weeks gestation—the current abortion limit in many states—fetal pain “is not possible at all.” The report also cites Dr. Mark Rosen, a fetal anesthesia pioneer, 16 times. Rosen’s work, the report suggests, shows that painkillers and anesthesia are common during fetal surgery because unborn children can feel pain. But Rosen tells Belluck that the real purpose of such drugs during fetal surgery is to minimize dangerous movement and harmful stress hormones, thereby facilitating recovery. The drugs don’t signify medical belief in fetal pain. Dr. Scott Adzick, another fetal surgery expert cited in the pro-life report, makes the same point. © 2013 The Slate Group, LLC

Keyword: Pain & Touch; Development of the Brain
Link ID: 18680 - Posted: 09.21.2013

By William Skaggs At the level of personal experience, there is nothing that seems easier to understand than pain. When I jam my finger in a doorway, I have no difficulty at all recognizing the sensation that results. But this superficial simplicity covers up a world of complexity at the level of brain mechanisms, and the complexities are even greater when we try to identify pain in other people or other species of animals. Some of the complexities are purely scientific, but others are caused by moral or philosophical issues getting mixed up with scientific issues. My provocation for writing this post was a blog post called Do Octopuses Feel Pain?, by Katherine Harmon, who writes the blog Octopus Chronicles, It’s basically a nice article—there’s nothing objectionable about it—but it pressed one of my buttons. She made a number of important points, and altogether what she wrote is well worth reading, but nevertheless the result left me with a feeling of dissatisfaction, as do most scientific discussions about pain in animals. I’d like to try to explain where that discomfort comes from. In her blog post, Harmon listed three elements that are involved in feeling pain: (1) nociception, that is, having mechanisms in the body that are capable of detecting damage and transmuting it into neural signals; (2) the experience of pain; (3) the ability to communicate pain information from sensation to perception. I’m not sure I understand the third aspect, but I take it to mean the ability to transform nociception into experience. In any case, the essence of pain as most people understand it is aspect 2. Most people think of pain as a particular type of experience—as something that happens inside our minds and can only be observed by ourselves. © 2013 Scientific American

Keyword: Pain & Touch
Link ID: 18679 - Posted: 09.21.2013

JoNel Aleccia NBC News A neurosurgery patient treated at a New Hampshire hospital this spring did have a rare brain disorder known as Creutzfeldt-Jakob Disease, health officials confirmed Friday. That means that 15 other people in three states may have been exposed to the invariably deadly infection through potentially tainted surgical equipment. Autopsy results came back positive for CJD from the National Prion Disease Pathology Surveillance Center and were reported to the New Hampshire Department of Health and Human Services and Catholic Medical Center, where the surgery took place. Earlier this month, New Hampshire officials notified eight patients who may have been exposed to CJD through shared equipment. Five others in Massachusetts and two in Connecticut were also warned of the risk, health officials in those states said. "Though we are not surprised by the test results, we are saddened by the toll this disease takes on families and our sympathies go out to all those affected," said Dr. Jose Montero, New Hampshire's director of public health, in a statement. The initial patient turned out to have sporadic CJD, which occurs spontaneously. It's not the variant form of the disease that causes a human type of "mad cow disease" and is associated with eating beef contaminated with the cattle version of the infection, called bovine spongiform encephalotpathy, or BSE, experts said. The problem arose because standard hospital disinfection techniques cannot eradicate the prion that causes CJD. A prion is a protein and the type that causes BSE and CJD is misfolded and somehow manages to transform other proteins into disease-causing shape.

Keyword: Prions
Link ID: 18678 - Posted: 09.21.2013

Billions of dollars have been spent on clinical trials of Alzheimer’s drugs that target amyloid plaques—the hallmark protein tangles that clog brain cells in people with the memory-robbing disease. So far, all have failed, leading some frustrated researchers to say it’s time to move on to other drug targets. Others say the drugs have not yet been fairly tested because they were administered too late, after brain damage is irreversible. Yesterday, the National Institutes of Health (NIH) announced that it is giving $33 million to a study that researchers hope will either revive the amyloid hypothesis, or put it to bed. The new trial—estimated to cost at least $100 million overall, with most of the remaining funds provided by partners in the pharmaceutical industry—will be part of the Alzheimer's Prevention Initiative, a large consortium of researchers attempting to identify biomarkers and treatments that can slow or stop the disease. Lead researchers Eric Reiman and Pierre Tariot of the Banner Alzheimer’s Institute in Phoenix plan to give a yet-to-be identified anti-amyloid drug, or placebo, to 650 people who carry two copies of the APOE4 gene—a genetic double whammy that confers a 10-fold increased risk of developing Alzheimer’s late in life. All participants will be between the ages of 60 and 75 and healthy, including free of recognized Alzheimer’s symptoms. Roughly a third will likely not have much amyloid in their brains yet, allowing the researchers to track whether the drug affects its accumulation, Reiman says. © 2012 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 18677 - Posted: 09.21.2013

David Hilfiker knows what's coming. He was diagnosed with Alzheimer's so early that he's had time to tell his family what he wants to happen once forgetfulness turns incapacitating. "When it's time to put me in an institution, don't have me at home and destroy your own life," said the retired physician, who is still well enough that he blogs about the insidious progress of the disease. "Watching the Lights Go Out," it's titled. Nearly half of all seniors who need some form of long-term care -— from help at home to full-time care in a facility — have dementia, the World Alzheimer Report said Thursday. It's a staggering problem as the global population ages, placing enormous strain on families who provide the bulk of that care at least early on, and on national economies alike. Indeed, cognitive impairment is the strongest predictor of who will move into a care facility within the next two years, 7.5 times more likely than people with cancer, heart disease or other chronic ailments of older adults, the report found. "It's astonishing," said Marc Wortmann, executive director of Alzheimer's Disease International, which commissioned the report and focused on the problems of caregiving. "What many countries try to do is keep people away from care homes because they say that's cheaper. Yes it's cheaper for the government or the health system, but it's not always the best solution." And dropping birth rates mean there are fewer children in families to take care of aging parents, too, said Michael Hodin of the Global Coalition on Aging. © CBC 2013

Keyword: Alzheimers
Link ID: 18676 - Posted: 09.21.2013