By Bahar Gholipour When Ryan Darby was a neurology resident, he was familiar with something called alien limb syndrome, but that did not make his patients’ behavior any less puzzling. Individuals with this condition report that one of their extremities—often a hand—seems to act of its own volition. It might touch and grab things or even unbutton a shirt the other hand is buttoning up. Patients are unable to control the rebellious hand short of grabbing or even sitting on it. They seem to have lost agency—that unmistakable feeling of ownership of one’s actions and an important component of free will. “It was one of those symptoms that really questioned the mind and how it brings about some of those bigger concepts,” says Darby, now an assistant professor of neurology at Vanderbilt University. Alien limb syndrome can arise after a stroke causes a lesion in the brain. But even though patients who have it report the same eccentric symptoms, their lesions do not occur in the same place. “Could the reason be that the lesions were just in different parts of the same brain network?” Darby wondered. To find out, he and his colleagues compiled findings from brain-imaging studies of people with the syndrome. They also looked into akinetic mutism—a condition that leaves patients with no desire to move or speak, despite having no physical impediment. Using a new technique, the researchers compared lesion locations against a template of brain networks—that is, groups of regions that often activate in tandem. © 2018 Scientific American

Keyword: Consciousness
Link ID: 25724 - Posted: 11.27.2018

Scientists at the National Eye Institute (NEI) have found that neurons in the superior colliculus, an ancient midbrain structure found in all vertebrates, are key players in allowing us to detect visual objects and events. This structure doesn’t help us recognize what the specific object or event is; instead, it’s the part of the brain that decides something is there at all. By comparing brain activity recorded from the right and left superior colliculi at the same time, the researchers were able to predict whether an animal was seeing an event. The findings were published today in the journal Nature Neuroscience. NEI is part of the National Institutes of Health. Perceiving objects in our environment requires not just the eyes, but also the brain’s ability to filter information, classify it, and then understand or decide that an object is actually there. Each step is handled by different parts of the brain, from the eye’s light-sensing retina to the visual cortex and the superior colliculus. For events or objects that are difficult to see (a gray chair in a dark room, for example), small changes in the amount of visual information available and recorded in the brain can be the difference between tripping over the chair or successfully avoiding it. This new study shows that this process – deciding that an object is present or that an event has occurred in the visual field – is handled by the superior colliculus. “While we’ve known for a long time that the superior colliculus is involved in perception, we really wanted to know exactly how this part of the brain controls the perceptual choice, and find a way to describe that mechanism with a mathematical model,” said James Herman, Ph.D., lead author of the study.

Keyword: Vision
Link ID: 25723 - Posted: 11.27.2018

Jef Akst After publishing a 2014 study showing that noninvasive magnetic stimulation of the brain boosted people’s ability to remember an association between two items, Northwestern University neuroscientist Joel Voss began fielding a lot of questions from patients and their families. “We’re of course guarded in the publication talking about what we found—small but reliable increases in memory ability,” he says (Science, 345:1054–57). But some of the news coverage of that paper alluded to the procedure’s potential to treat Alzheimer’s disease and other memory-related disorders. “I got calls—at least two a day for quite a long period of time—and emails: ‘My loved one is suffering from X, Y, or Z; thank God now you can cure it. How do we get to your lab?’” Voss says. He would have to explain to them that this was a scientific study, not an approved treatment. “There are a million steps between here and there, and maybe it would never work—we don’t really know.” But Voss’s team continues to connect those dots, in hopes that one day the technique—the use of magnetic fields to influence activity in neurons close to the brain’s surface—could help patients with any number of brain disorders, and perhaps cognitively healthy people as well. In August, the researchers reported that transcranial magnetic stimulation (TMS) could moderately improve episodic memory—the ability to remember people, events, and other things you’ve encountered in your life (as opposed to, say, how to do something)—when targeted at the correct part of the brain. Voss and his colleagues were interested in activating the hippocampus, a structure near the brain’s center that serves as a hub of memory production and storage. Because the hippocampus itself is inaccessible by TMS—the magnetic field falls off precipitously with depth, explains Voss—the researchers instead targeted areas of the brain where activity correlated with activity in the hippocampus, to try to activate the networks that link more-superficial regions with the deep-brain structure. © 1986 - 2018 The Scientist

Keyword: Learning & Memory
Link ID: 25722 - Posted: 11.27.2018

By Abby Goodnough DAYTON, Ohio — Dr. Randy Marriott clicked open the daily report he gets on drug overdoses in the county. Only one in the last 24 hours — stunningly low compared to the long lists he used to scroll through last year in a grim morning routine. “They just began to abruptly drop off,” said Dr. Marriott, who oversees the handoff of patients from local rescue squads to Premier Health, the region’s biggest hospital system. Overdose deaths in Montgomery County, anchored by Dayton, have plunged this year, after a stretch so bad that the coroner’s office kept running out of space and having to rent refrigerated trailers. The county had 548 overdose deaths by Nov. 30 last year; so far this year there have been 250, a 54 percent decline. Dayton, a hollowed-out manufacturing center at the juncture of two major interstates, had one of the highest opioid overdose death rates in the nation in 2017 and the worst in Ohio. Now, it may be at the leading edge of a waning phase of an epidemic that has killed hundreds of thousands of people in the United States over the last decade, including nearly 50,000 last year. For the first time in years, the number of opioid deaths nationwide has begun to dip, according to preliminary data from the Centers for Disease Control and Prevention — with totals for the preceding 12 months falling slightly but steadily between December 2017 and April 2018. The flattening curve — along with declining opioid prescription rates and survey data suggesting far fewer Americans tried heroin last year and more got addiction treatment — is the first encouraging news in a while. While it’s too soon to know if the improvement is part of a long-term trend, it is clear there are some lessons to be learned from Dayton. The New York Times spent several days here interviewing police and public health officials; doctors, nurses and other treatment providers; people recovering from opioid addiction and people who are still using heroin and other drugs. © 2018 The New York Times Company

Keyword: Drug Abuse
Link ID: 25721 - Posted: 11.26.2018

Robin McKie Science Editor Lawyers are bringing a case against a London hospital trust that could trigger major changes to the rules governing patient confidentiality. The case involves a woman who is suing doctors because they failed to tell her about her father’s fatal hereditary disease before she had her own child. The woman discovered – after giving birth – that her father carried the gene for Huntington’s disease, a degenerative, incurable brain condition. Later she found out she had inherited the gene and that her own daughter, now eight, has a 50% chance of having it. The woman – who cannot be named for legal reasons – says she would have had an abortion had she known about her father’s condition, and is suing the doctors who failed to tell her about the risks she and her child faced. It is the first case in English law to deal with a relative’s claim over issues of genetic responsibility. “This could really change the way we do medicine, because it is about the duty that doctors have to share genetic test results with relatives and whether the duty exists in law,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. Experts say that as more is discovered about the genetic components of medical conditions, including cancer and dementia, doctors will come under increasing pressure to consider not only their patients’ needs but also those of relatives who may share affected genes. The case also raises questions over how much effort clinicians need to put into tracing relatives, and whether they will be sued if their attempts do not go far enough. © 2018 Guardian News and Media Limited

Keyword: Huntingtons
Link ID: 25720 - Posted: 11.26.2018

By Lisa Sanders, M.D. “Something’s wrong,” the 27-year-old woman said to her new husband. “I think you need to take me to the hospital.” It was the day after their wedding. The woman’s husband and her best friend were car fanatics, and so the newlyweds had wanted to commemorate their union with pictures at a drift track in rural Toutle, Wash. The best friend would “drift cookies,” circling the couple in a tight, controlled skid. As another friend took pictures, the two embraced, wreathed by smoke and dust and barely contained chaos as the red Mustang fishtailed around them. In the photos, the couple look happy. But as they loaded up the car to go home, the young woman started to feel strange. She’d been a little jittery all day. She noticed she couldn’t stop talking. She figured it was just the excitement of the wedding’s aftermath. But suddenly her excitement felt out of control. Her heart, which was racing since she got up that morning, went into overdrive. It pounded so hard that it hurt her throat and chest. She couldn’t think. Her hands took on a life of their own — they opened and closed incessantly. Her new husband was confused and worried. They drove to a hospital a couple of towns over. It was a panic attack, they were told. Since the birth of the couple’s daughter a year before, the young woman had struggled with postpartum depression and anxiety. She’d just married and had these crazy pictures taken; it was no wonder she was panicking. The young woman accepted the diagnosis, but she couldn’t help feeling that this was different from the anxiety she sometimes experienced. She was given a medication to take if she had more symptoms and sent home. The pills didn’t seem to help. The next day she felt her heart pounding in her throat and the same spacy-headed jitters from the day before. She tried the medicine again but after that, her memory is just fragments. © 2018 The New York Times Company

Keyword: Schizophrenia; Neuroimmunology
Link ID: 25719 - Posted: 11.26.2018

At 35, Sharon Jakab knew something was wrong when she started hallucinating. "I saw my grandmother on the wall in the room. She was talking to me. I wasn't sleeping, and I was a mess," she says from her home in Burlington, Ont. Jakab had been suffering from postpartum depression following the birth of her daughter. About a year and a half later, Jakab had another episode of postpartum depression following an ectopic pregnancy. It became so bad, she was suicidal. "There was a gun in the house and there were cartridges. I was all set to kill myself." She had to suicide-proof her home by taking away all dangerous objects, even skates, which have sharp blades. Now 61, Jakab has been in and out of hospitals, dealing with what she calls "waves of depression" that have lasted most of her adult life. She's tried about a dozen medications, including the antipsychotic drug clozapine. "Clozapine really helped me a lot, but I still suffered from depression, psychosis and mania." Because standard treatment like medication and therapy weren't effective, Jakab was diagnosed with treatment-resistant depression, a severe form of depression that close to a million Canadians experience. Electroconvulsive therapy or ECT, better known as shock treatment, is still considered the go-to treatment but comes with the common side effect of memory loss. So doctors are now exploring less invasive experimental approaches like brain stimulation that rewires the brain's circuits. ©2018 CBC/Radio-Canada

Keyword: Depression
Link ID: 25718 - Posted: 11.26.2018

By Mitch Leslie Unlike most cells in our bodies, the neurons in our brain can scramble their genes, scientists have discovered. This genome tampering may expand the brain’s protein repertoire, but it may also promote Alzheimer’s disease, their study suggests. “It’s potentially one of the biggest discoveries in molecular biology in years,” says Geoffrey Faulkner, a molecular biologist at the University of Queensland in Brisbane, Australia, who wasn’t connected to the research. “It is a landmark study,” agrees clinical neurologist Christos Proukakis of University College London. Scientists first discovered that certain cells could shuffle and edit DNA in the 1970s. Some immune cells snip out sections of genes that code for proteins that detect or fight pathogens and splice the remaining pieces together to create new varieties. Our B cells, for example, can potentially spawn about 1 quadrillion types of antibodies, enough to fend off an enormous range of bacteria, viruses, and other attackers. Scientists have seen hints that such genomic reshuffling—known as somatic recombination—happens in our brain. Neurons there often differ dramatically from one another. They often have more DNA or different genetic sequences than the cells around them. To look for definitive evidence of somatic recombination in the brain, neuroscientist Jerold Chun of the Sanford Burnham Prebys Medical Discovery Institute in San Diego, California, and colleagues analyzed neurons from the donated brains of six healthy elderly people and seven patients who had the noninherited form of Alzheimer’s disease, which accounts for most cases. The researchers tested whether the cells harbored different versions of the gene for the amyloid precursor protein (APP), the source of the plaques in the brains of people with Alzheimer’s disease. APP’s gene was a good candidate to examine, the researchers thought, because one of their previous studies suggested neurons from patients with Alzheimer’s disease can harbor extra copies of the gene, an increase that could arise from somatic recombination. © 2018 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 25716 - Posted: 11.24.2018

Sara Reardon Drug companies have spent billions of dollars searching for therapies to reverse or significantly slow Alzheimer’s disease, to no avail. Some researchers argue that the best way to make progress is to create better animal models for research, and several teams are now developing mice that more closely simulate how the disease devastates people’s brains. The US National Institutes of Health (NIH), the UK Dementia Research Institute and Jackson Laboratory (JAX) — one of the world’s biggest suppliers of lab mice — are among the groups trying to genetically engineer more sophisticated rodents. Scientists are also probing the complex web of mutations that influences neurological decline in mice and people. “We appreciate that the models we had were insufficient,” says Bruce Lamb, a neuroscientist at Indiana University in Indianapolis who directs the NIH-funded programme. “I think it’s sort of at a critical juncture right now.” Alzheimer’s is marked by cognitive impairment and the build-up of amyloid-protein plaques in the brains of people, but the disease does not occur naturally in mice. Scientists get around this by studying mice that have been genetically modified to produce high levels of human amyloid protein. These mice develop plaques in their brains, but they still do not display the memory problems seen in people. Many experimental drugs that have successfully removed plaques from mouse brains have not lessened the symptoms of Alzheimer’s disease in people. One high-profile stumble came last month, when three companies reported that their Alzheimer’s drugs — from a class called BACE inhibitors — had failed in large, late-stage clinical trials. Although the drugs successfully blocked the accumulation of amyloid protein in mice, they seemed to worsen cognitive decline and brain shrinkage in people. © 2018 Springer Nature Limited.

Keyword: Alzheimers
Link ID: 25715 - Posted: 11.24.2018

Shawna Williams In 1987, political scientist James Flynn of the University of Otago in New Zealand documented a curious phenomenon: broad intelligence gains in multiple human populations over time. Across 14 countries where decades’ worth of average IQ scores of large swaths of the population were available, all had upward swings—some of them dramatic. Children in Japan, for example, gained an average of 20 points on a test known as the Wechsler Intelligence Scale for Children between 1951 and 1975. In France, the average 18-year-old man performed 25 points better on a reasoning test in 1974 than did his 1949 counterpart.1 Flynn initially suspected the trend reflected faulty tests. Yet in the ensuing years, more data and analyses supported the idea that human intelligence was increasing over time. Proposed explanations for the phenomenon, now known as the Flynn effect, include increasing education, better nutrition, greater use of technology, and reduced lead exposure, to name but four. Beginning with people born in the 1970s, the trend has reversed in some Western European countries, deepening the mystery of what’s behind the generational fluctuations. But no consensus has emerged on the underlying cause of these trends. A fundamental challenge in understanding the Flynn effect is defining intelligence. At the dawn of the 20th century, English psychologist Charles Spearman first observed that people’s average performance on a variety of seemingly unrelated mental tasks—judging whether one weight is heavier than another, for example, or pushing a button quickly after a light comes on—predicts our average performance on a completely different set of tasks. Spearman proposed that a single measure of general intelligence, g, was responsible for that commonality. © 1986 - 2018 The Scientist

Keyword: Intelligence; Learning & Memory
Link ID: 25714 - Posted: 11.24.2018

Ashley Yeager For an hour a day, five days a week, mice in Hiroshi Maejima’s physiology lab at Hokkaido University in Sapporo, Japan, hit the treadmill. The researcher’s goal in having the animals follow the exercise routine isn’t to measure their muscle mass or endurance. He wants to know how exercise affects their brains. Researchers have long recognized that exercise sharpens certain cognitive skills. Indeed, Maejima and his colleagues have found that regular physical activity improves mice’s ability to distinguish new objects from ones they’ve seen before. Over the past 20 years, researchers have begun to get at the root of these benefits, with studies pointing to increases in the volume of the hippocampus, development of new neurons, and infiltration of blood vessels into the brain. Now, Maejima and others are starting to home in on the epigenetic mechanisms that drive the neurological changes brought on by physical activity. In October, Maejima’s team reported that the brains of rodents that ran had greater than normal histone acetylation in the hippocampus, the brain region considered the seat of learning and memory.1 The epigenetic marks resulted in higher expression of Bdnf, the gene for brain-derived neurotrophic factor (BDNF). By supporting the growth and maturation of new nerve cells, BDNF is thought to promote brain health, and higher levels of it correlate with improved cognitive performance in mice and humans. With a wealth of data on the benefits of working out emerging from animal and human studies, clinicians have begun prescribing exercise to patients with neurodegenerative diseases such as Parkinson’s and Alzheimer’s, as well as to people with other brain disorders, from epilepsy to anxiety. Many clinical trials of exercise interventions for neurodegenerative diseases, depression, and even aging are underway. Promising results could bolster the use of exercise as a neurotherapy. © 1986 - 2018 The Scientist

Keyword: Learning & Memory; Muscles
Link ID: 25713 - Posted: 11.24.2018

Marshall Allen Last March, Tony Schmidt discovered something unsettling about the machine that helps him breathe at night. Without his knowledge, it was spying on him. From his bedside, the device was tracking when he was using it and sending the information not just to his doctor, but to the maker of the machine, to the medical supply company that provided it and to his health insurer. Schmidt, an information technology specialist from Carrollton, Texas, was shocked. "I had no idea they were sending my information across the wire." Schmidt, 59, has sleep apnea, a disorder that causes worrisome breaks in his breathing at night. Like millions of people, he relies on a continuous positive airway pressure, or CPAP, machine that streams warm air into his nose while he sleeps, keeping his airway open. Without it, Schmidt would wake up hundreds of times a night; then, during the day, he'd nod off at work, sometimes while driving and even as he sat on the toilet. "I couldn't keep a job," he recalls. "I couldn't stay awake." The CPAP, he says, saved his career, maybe even his life. As many CPAP users discover, the life-altering device comes with caveats: Health insurance companies are often tracking whether patients use them. If they aren't, the insurers might not cover the machines or the supplies that go with them. And, faced with the popularity of CPAPs — which can cost $400 to $800 — and their need for replacement filters, face masks and hoses, health insurers have deployed a host of tactics that can make the therapy more expensive or even price it out of reach. Patients have been required to rent CPAPs at rates that total much more than the retail price of the devices, or they've discovered that the supplies would be substantially cheaper if they didn't have insurance at all. © 2018 npr

Keyword: Sleep
Link ID: 25712 - Posted: 11.24.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25711 - Posted: 11.24.2018

Selene Meza-Perez, Troy D. Randall Fat is a loaded tissue. Not only is it considered unsightly, the excess flab that plagues more than two-thirds of adults in America is associated with many well-documented health problems. In fact, obesity (defined as having a body mass index of 30 or more) is a comorbidity for almost every other type of disease. But, demonized as all body fat is, deep belly fat known as visceral adipose tissue (VAT) also has a good side: it’s a critical component of the body’s immune system. VAT is home to many cells of both the innate and adaptive immune systems. These cells influence adipocyte biology and metabolism, and in turn, adipocytes regulate the functions of the immune cells and provide energy for their activities. Moreover, the adipocytes themselves produce antimicrobial peptides, proinflammatory cytokines, and adipokines that together act to combat infection, modify the function of immune cells, and maintain metabolic homeostasis. Unfortunately, obesity disrupts both the endocrine and immune functions of VAT, thereby promoting inflammation and tissue damage that can lead to diabetes or inflammatory bowel disease. As researchers continue to piece together the complex connections between immunity, gut microbes, and adipose tissues, including the large deposit of fat in the abdomen known as the omentum, they hope not only to gain an understanding of how fat and immunity are linked, but to also develop fat-targeted therapeutics that can moderate the consequences of infectious and inflammatory diseases. © 1986 - 2018 The Scientist.

Keyword: Obesity; Neuroimmunology
Link ID: 25710 - Posted: 11.24.2018

Abby Olena Anticipating something tasty can lead to a watering mouth and grumbling stomach, but these familiar responses aren’t the only ways the body prepares for nourishment. According to a study published today (November 15) in Cell, sensing food primes mice to process incoming nutrients by directions from the central nervous system to the liver. “It’s a great tour de force combining [several strategies] in one paper to then identify pathways by which food anticipation could alter hepatic metabolism,” says Christoph Buettner, a physician and researcher at Icahn School of Medicine at Mount Sinai in New York who was not involved in the study. “It’s interesting that even before your food hits your tongue or ends up in your stomach, there are changes that prepare an organism for nutrient storage.” Two types of cells in the brain’s hypothalamus have been shown in previous studies to play opposing roles in regulating how much an organism eats. AgRP neurons are turned on when energy stores are low, making an animal seek out food, while POMC neurons, activated when an animal is sated, inhibit eating. Up until a few years ago, the prevailing wisdom was that ingested food resulted in hormonal changes and subsequent neuronal activation after some lag time, says Jens Brüning, an endocrinologist and geneticist at the Max Planck Institute for Metabolism Research in Germany. But in 2015, researchers from the University of California, San Francisco, showed in mice that these neurons change their state of activation nearly instantaneously in response to the sight or smell of food. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25709 - Posted: 11.24.2018

By Sharon Begley, The brain surgeon began as he always does, making an incision in the scalp and gently spreading it apart to expose the skull. He then drilled a 3-inch circular opening through the bone, down to the thick, tough covering called the dura. He sliced through that, and there in the little porthole he’d made was the glistening, blood-flecked, pewter-colored brain, ready for him to approach the way spies do a foreign embassy: He bugged it. Dr. Ashesh Mehta, a neurosurgeon at the Feinstein Institute for Medical Research on Long Island, was operating on his epilepsy patient to determine the source of seizures. But the patient agreed to something more: to be part of an audacious experiment whose ultimate goal is to translate thoughts into speech. While he was in there, Mehta carefully placed a flat array of microelectrodes on the left side of the brain’s surface, over areas involved in both listening to and formulating speech. By eavesdropping on the electrical impulses that crackle through the gray matter when a person hears in the “mind’s ear” what words he intends to articulate (often so quickly it’s barely conscious), then transmitting those signals wirelessly to a computer that decodes them, the electrodes and the rest of the system hold the promise of being the first “brain-computer interface” to go beyond movement and sensation. If all goes well, it will conquer the field’s Everest: developing a brain-computer interface that could enable people with a spinal cord injury, locked-in syndrome, ALS, or other paralyzing condition to talk again. © 2018 Scientific America

Keyword: Brain imaging; Robotics
Link ID: 25708 - Posted: 11.21.2018

By Gina Kolata Whenever I see a photo from the 1960s or 1970s, I am startled. It’s not the clothes. It’s not the hair. It’s the bodies. So many people were skinny. In 1976, 15 percent of American adults were obese. Now the it’s nearly 40 percent. No one really knows why bodies have changed so much. Scientists do a lot of hand-waving about our “obesogenic environment” and point to favorite culprits: the abundance of cheap fast foods and snacks; food companies making products so tasty they are addictive; larger serving sizes; the tendency to graze all day. Whatever the combination of factors at work, something about the environment is making many people as fat as their genetic makeup permits. Obesity has always been with us, but never has it been so common. Everyone — from doctors to drug companies, from public health officials to overweight people themselves — would love to see a cure, a treatment that brings weight to normal and keeps it there. Why hasn’t anyone discovered one? It’s not for lack of trying. Yes, some individuals have managed to go from fat to thin with diets and exercise, and have kept off the weight. But they are the rare exceptions. Most spend years dieting and regaining, dieting and regaining, in a fruitless, frustrating cycle. There is just one almost uniformly effective treatment, and it is woefully underused: only about 1 percent of the 24 million American adults who are eligible get the procedure. That treatment is bariatric surgery, a drastic operation that turns the stomach into a tiny pouch and, in one version, also reroutes the intestines. Most who have it lose significant amounts of weight — but many of them remain overweight, or even obese. Their health usually improves anyway. Many with diabetes no longer need insulin. Cholesterol and blood pressure levels tend to fall. Sleep apnea disappears. Backs, hips and knees stop aching. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25707 - Posted: 11.21.2018

National Institutes of Health scientists and their colleagues have found evidence of the infectious agent of sporadic Creutzfeldt-Jakob disease (CJD) in the eyes of deceased CJD patients. The finding suggests that the eye may be a source for early CJD diagnosis and raises questions about the safety of routine eye exams and corneal transplants. Sporadic CJD, a fatal neurodegenerative prion disease of humans, is untreatable and difficult to diagnose. Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the body and brain. Scientists hope that early diagnosis of prion and related diseases—such as Alzheimer’s, Parkinson’s and dementia with Lewy bodies—could lead to effective treatments that slow or prevent these diseases. Scientists from NIH’s National Institute of Allergy and Infectious Diseases (NIAID) collaborated on the research with colleagues from the University of California at San Diego and UC-San Francisco. About 40 percent of sporadic CJD patients develop eye problems that could lead to an eye exam, meaning the potential exists for the contamination of eye exam equipment designed for repeat use. Further, cadaveric corneal transplants from undiagnosed CJD patients have led to two probable and three possible cases of disease transmission, the researchers say. Previous studies have shown that the eyes of CJD patients contain infectious prions, though the distribution of prions among the various components of the eye was not known. To address this question, the scientists recruited 11 CJD patients who agreed to donate their eyes upon death. The researchers found evidence of prion infection throughout the eyes of all 11 deceased patients using real time quaking-induced conversion (RT-QuIC), a highly sensitive test NIAID scientists developed that detects prion seeding activity in a sample as evidence of infection.

Keyword: Prions; Vision
Link ID: 25706 - Posted: 11.21.2018

By Virginia Morell Like any fad, the songs of humpback whales don’t stick around for long. Every few years, males swap their chorus of squeaks and groans for a brand new one. Now, scientists have figured out how these “cultural revolutions” take place. All male humpbacks in a population sing the same song, and they appear to learn new ones somewhat like people do. Males in the eastern Australian population of humpbacks, for example, pick up a new song every few years from the western Australian population at shared feeding grounds or while migrating. Over the next few years, the songs spread to all South Pacific populations. To understand how the whales learn the novel ballads, scientists analyzed eastern Australian whale songs over 13 consecutive years. Using spectrograms of 412 song cycles from 95 singers, the scientists scored each tune’s complexity for the number of sounds and themes, and studied the subtle variations individual males can add to stand out. Complexity increased as the songs evolved (as heard in the video below), the team reports today in the Proceedings of the Royal Society B. But after a song revolution, the ballads became shorter with fewer sounds and themes. The revolutionary songs may be less complex than the old ones because the whales can only learn a certain amount of new material at a time, the scientists conclude. That could mean that although humpback whales are still the crooners of the sea, their learning skills are a bit limited. © 2018 American Association for the Advancement of Scienc

Keyword: Animal Communication; Language
Link ID: 25705 - Posted: 11.21.2018

By Pam Belluck It’s a rare person in America who doesn’t know of someone with Alzheimer’s disease. The most common type of dementia, it afflicts about 44 million people worldwide, including 5.5 million in the United States. Experts predict those numbers could triple by 2050 as the older population increases. So why is there still no effective treatment for it, and no proven way to prevent or delay its effects? Why is there still no comprehensive understanding of what causes the disease or who is destined to develop it? The answer, you could say, is: “It’s complicated.” And that is certainly part of it. For nearly two decades, researchers, funding agencies and clinical trials have largely focused on one strategy: trying to clear the brain of the clumps of beta amyloid protein that form the plaques integrally linked to the disease. But while some drugs have reduced the accumulation of amyloid, none have yet succeeded in stopping or reversing dementia. And amyloid doesn’t explain everything about Alzheimer’s — not everyone with amyloid plaques has the disease. “It’s not that amyloid is not an important factor,” said Dr. John Morris, director of the Knight Alzheimer’s Disease Research Center at the Washington University School of Medicine in St. Louis. “On the other hand, we’ve had some 200-plus trials since 2001 that have been negative.” Not all trials have targeted amyloid. Some have focused on tau, a protein that, in Alzheimer’s, forms threads that stick together in tangles inside neurons, sandbagging their communications with one another. Tau tangles seem to spread after amyloid accumulates into plaques between neurons. But so far, anti-tau drugs haven’t successfully attacked Alzheimer’s itself. Only five drugs have been approved to treat this dementia, but they address early symptoms and none have been shown to work very well for very long. It’s been 15 years since the last one was approved. © 2018 The New York Times Company

Keyword: Alzheimers
Link ID: 25704 - Posted: 11.20.2018