By GRETCHEN REYNOLDS Exercise may help the brain to build durable memories, through good times and bad. Stress and adversity weaken the brain’s ability to learn and retain information, earlier research has found. But according to a remarkable new neurological study in mice, regular exercise can counteract those effects by bolstering communication between brain cells. Memory has long been considered a biological enigma, a medley of mental ephemera that has some basis in material existence. Memories are coded into brain cells in the hippocampus, the brain’s memory center. If our memories were not written into those cells, they would not be available for later, long-term recall, and every brain would be like that of Dory, the memory-challenged fish in “Finding Nemo.” But representations of experience are extremely complex, and aspects of most memories must be spread across multiple brain cells, neuroscientists have determined. These cells must be able to connect with one another, so that the memory, as a whole, stays intact. The connections between neurons, known as synapses, are composed of electrical and chemical signals that move from cell to cell, like notes passed in class. The signals can be relatively weak and sporadic or flow with vigor and frequency. In general, the stronger the messages between neurons, the sturdier and more permanent the memories they hold. Neuroscientists have known for some time that the potency of our synapses depends to some degree on how we live our lives. Lack of sleep, alcohol, diet and other aspects of our lifestyles, especially stress, may dampen the flow of messages between brain cells, while practice fortifies it. Repeat an action and the signals between the cells maintaining the memory of that action can strengthen. That is learning. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24683 - Posted: 02.21.2018

Heavy drinkers are putting themselves at risk of dementia, according to the largest study of its kind ever conducted. Research published in the Lancet Public Health journal provides powerful evidence that people who drink enough to end up in hospital are putting themselves at serious risk of vascular dementia and Alzheimer’s disease. It will also raise questions for moderate drinkers about the possible long-term consequences of their social habit. The study, which used the French National Hospital Discharge database, looked at more than a million people diagnosed with dementia between 2008 and 2013. More than a third – 38% of the 57,000 cases of early-onset dementia – were directly alcohol-related and 18% had an additional diagnosis of alcohol use disorders. Overall, alcohol use disorders were associated with a three times greater risk of all types of dementia. Dr Sara Imarisio, head of research at Alzheimer’s Research UK, said: “As this study only looked at the people who had been admitted to hospital due to chronic heavy drinking, it doesn’t reveal the full extent of the link between alcohol use and dementia risk. Previous research has indicated that even moderate drinking may have a negative impact on brain health and people shouldn’t be under the impression that only drinking to the point of hospitalisation carries a risk.” Experts said the new research should change attitudes. “What is most surprising about this paper is that it has taken us so long to recognise that alcohol misuse and dependence are such potent risk factors for the development of dementia,” said Robert Howard, professor of old age psychiatry at University College London.

Keyword: Drug Abuse; Alzheimers
Link ID: 24682 - Posted: 02.21.2018

By CHRISTOPHER MELE A persistent noise of unknown origin, sometimes compared to a truck idling or distant thunder, has bedeviled a Canadian city for years, damaging people’s health and quality of life, numerous residents say. Those who hear it have compared it to a fleet of diesel engines idling next to your home or the pulsation of a subwoofer at a concert. Others report it rattling their windows and spooking their pets. Known as the Windsor Hum, this sound in Windsor, Ontario, near Detroit, is unpredictable in its duration, timing and intensity, making it all the more maddening for those affected. “You know how you hear of people who have gone out to secluded places to get away from certain sounds or noises and the like?” Sabrina Wiese posted in a private Facebook group dedicated to finding the source of the noise. “I’ve wanted to do that many times in the past year or so because it has gotten so bad,” she wrote. “Imagine having to flee all you know and love just to have a chance to hear nothing humming in your head for hours on end.” Since reports of it surfaced in 2011, the hum has been studied by the Canadian government, the University of Western Ontario and the University of Windsor. Activists have done their own sleuthing. Over six years, Mike Provost of Windsor, who helps run the Facebook page, has amassed more than 4,000 pages of daily observations about the duration, intensity and characteristics of the sound and the weather conditions at the time. © 2018 The New York Times Company

Keyword: Hearing; Brain Injury/Concussion
Link ID: 24681 - Posted: 02.19.2018

Jon Hamilton Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one. Neuroscientists Robert Moir and Rudolph Tanzi were sipping Coronas in separate offices during "attitude adjustment hour" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system. Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. "I cruise wherever my fancy takes me," he says. And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain. One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized. These peptides are "extremely important," Moir says. "They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours." As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia. © 2018 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 24680 - Posted: 02.19.2018

Nicola Davis Adults who have experienced a stroke may one day be able to take a drug to help their brain “rewire” itself, so that tasks once carried out by now-damaged areas can be taken over by other regions, researchers have claimed. The ability for the brain to rewire, so-called “brain plasticity”, is thought to occur throughout life; however, while children have a high degree of brain plasticity, adult brains are generally thought to be less plastic. Research looking at children and young adults who had a stroke as a baby – a situation thought to affect at least one in 4,000 around the time of their birth – has highlighted the incredible ability of the young brain to rewire. Elissa Newport, a professor of neurology at Georgetown University school of medicine in Washington DC, detailed a new study involving 12 such individuals, aged between 12 and 25. “What you see is the right hemisphere, which is never in control of language in anyone who is healthy, is apparently capable of taking over language if you lose left hemisphere,” said Newport, who presented the findings at a meeting of the American Association for the Advancement of Science in Austin, Texas. “This does not happen in adults,” she added. © 2018 Guardian News and Media Limited

Keyword: Stroke
Link ID: 24679 - Posted: 02.19.2018

Laurel Hamers AUSTIN, Texas — Babies’ stroke-damaged brains can pull a mirror trick to recover. A stroke on the left side of the brain often damages important language-processing areas. But people who have this stroke just before or after birth recover their language abilities in the mirror image spot on the right side, a study of teens and young adults shows. Those patients all had normal language skills, even though as much as half of their brain had withered away, researchers reported February 17 at the annual meeting of the American Association for the Advancement of Science. Researchers so far have recruited 12 people ages 12 to 25 who had each experienced a stroke to the same region of their brain’s left hemisphere just before or after birth. People who have this type of stroke as adults often lose their ability to use and understand language, said study coauthor Elissa Newport, a neurology researcher at Georgetown University Medical Center in Washington, D.C. MRI scans of healthy siblings of the stroke patients showed activity in language centers in the left hemisphere of the brain when the participants heard speech. The stroke patients showed activity in the exact same areas — just on the opposite side of the brain. It’s well established that if an area of the brain gets damaged, other brain areas will sometimes compensate. But the new finding suggests that while young brains have an extraordinary capacity to recover, there might be limits on which areas can pinch-hit. |© Society for Science & the Public 2000 - 2018.

Keyword: Laterality; Stroke
Link ID: 24678 - Posted: 02.19.2018

by Sandra G. Boodman “What are you doing ?” Laura Hsiung’s friends asked as she slowly loped across a Maryland handball court, her ankle off-kilter so that she was walking on the outside of her left foot. Hsiung recalls wondering the same thing. One minute she was walking normally, and then all of a sudden, she wasn’t. “I couldn’t figure it out,” Hsiung said. “I hadn’t rolled my ankle. But my left foot just would not function normally.” For the next two years, Hsiung consulted specialist after specialist — orthopedists, a podiatrist and a neurologist — each of whom was unable to explain what was causing her weird walk. She underwent surgery which didn’t help and felt increasingly desperate about the problem, which did not affect her right foot. “Doctors would literally say, ‘I don’t know what’s wrong with you,’ ” said Hsiung, who lives in Montgomery County. Nor, she said, did most of them seem interested in unearthing a probable cause. After nearly two years of frustration and anxiety, a consultation with a physical therapist ultimately led to a diagnosis, followed by treatment that has helped alleviate Hsiung’s unusual disorder. Although they met only twice, the impact of her encounters with that physical therapist had a galvanizing effect on another aspect of Hsiung’s life, pushing her to make a midlife career change she had been contemplating. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 24677 - Posted: 02.19.2018

By Linda Qiu and Justin Bank A heavily armed young man is accused of killing 17 people after opening fire on terrified students and teachers at Marjory Stoneman Douglas High School in Parkland, Fla., on Wednesday. It was the third mass shooting in the past four months in the United States. Nikolas Cruz, who has been linked to a history of mental illness, is believed to have used a legally obtained AR-15 in the shooting. The attack has led to widespread conversations about links between gun violence and mental illness, and how lawmakers and interest groups are debating potential policy responses. Below is a look at some facts and falsehoods uttered by Speaker Paul D. Ryan, Republican of Wisconsin; Senator Bernie Sanders, independent of Vermont; and others in the wake of Wednesday’s shooting. “Mental health is often a big problem underlying these tragedies.” — House Speaker Paul Ryan There’s a link, but it’s more limited than widely thought. Mr. Ryan’s claim reflects a common misconception. According to various polls, roughly half of Americans either believe that failing to identify people with mental health problems is the primary cause of gun violence or that addressing mental health issues would be a major deterrent. That conclusion is not shared by experts or widely accepted research. In an analysis of 235 mass killings, many of which were carried out with firearms, 22 percent of the perpetrators could be considered mentally ill. Overall, mass shootings by people with serious mental illness represent 1 percent of all gun homicides each year, according to the book “Gun Violence and Mental Illness” published by the American Psychiatric Association in 2016. To be sure, gun violence experts contacted by New York Times reporters have said that barring sales to people who are deemed dangerous by mental health providers could help prevent mass shootings. But the experts said several more measures — including banning assault weapons and barring sales to convicted violent criminals — more effective. © 2018 The New York Times Company

Keyword: Aggression
Link ID: 24676 - Posted: 02.17.2018

Dan Garisto If you’ve ever felt the urge to tap along to music, this research may strike a chord. Recognizing rhythms doesn’t involve just parts of the brain that process sound — it also relies on a brain region involved with movement, researchers report online January 18 in the Journal of Cognitive Neuroscience. When an area of the brain that plans movement was disabled temporarily, people struggled to detect changes in rhythms. The study is the first to connect humans’ ability to detect rhythms to the posterior parietal cortex, a brain region associated with planning body movements as well as higher-level functions such as paying attention and perceiving three dimensions. “When you’re listening to a rhythm, you’re making predictions about how long the time interval is between the beats and where those sounds will fall,” says coauthor Jessica Ross, a neuroscience graduate student at the University of California, Merced. These predictions are part of a system scientists call relative timing, which helps the brain process repetitive sounds, like a musical rhythm. “Music is basically sounds that have a structure in time,” says Sundeep Teki, a neuroscientist at the University of Oxford who was not involved with the study. Studies like this, which investigate where relative timing takes place in the brain, could be crucial to understanding how the brain deciphers music, he says. |© Society for Science & the Public 2000 - 2018.

Keyword: Hearing
Link ID: 24675 - Posted: 02.17.2018

By John Carroll, For years now the gold standard for R&D in Alzheimer’s disease has focused on generating convincing evidence that any new therapy being studied could slow the cognitive decline of patients and help preserve their ability to perform the kind of daily functions that can keep a patient independent for a longer period of time. That’s a hurdle no one has managed to clear for well over a decade. So now, with late-stage clinical failures piling up, the U.S. Food and Drug Administration (FDA) has set off down a path to adapt those standards as researchers are pushed inexorably into earlier and earlier forms of the disease, ahead of the brain damage inflicted by Alzheimer’s. In a set of draft guidances, the agency essentially proposed to offer an approval pathway for new drugs that could prevent the onset of the devastating symptoms of Alzheimer’s if drug developers could hit acceptable biomarkers that indicate the drug is working. And they’re likely going to continue with a new gold standard that will focus on long-term cognition alone, lowering the bar for drugs for an enormous and growing market. David Miller, the clinical vice president of Bracket, a Washington, D.C.-based tech provider which specializes in Alzheimer’s studies, tells me the draft guidance hit just after a meeting of the Washington, D.C.-based Alzheimer’s Association research group, which was discussing how you might be able to use a mix of markers for amyloid β and tau—two toxic proteins frequently cited as likely triggers—alongside neurodegenerative markers to identify patients who could be enrolled at a very early point in the disease. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 24674 - Posted: 02.17.2018

Nicola Davis Pilot studies have shown that changes in vesicles in men’s semen mirror that in their sperm, suggesting that, as in mice, the two interact. Pilot studies have shown that changes in vesicles in men’s semen mirror that in their sperm, suggesting that, as in mice, the two interact. Photograph: Alamy Stressed fathers may end up with changes to their sperm that could affect behaviour in their offspring, research in mice has shown. Previous work by the team found that male mice who were exposed to a mildly stressful event, such as being restrained, produced sperm that was richer in certain types of molecules called microRNAs. Crucially, the higher levels of these microRNAs in the sperm seemed to result in offspring with a dampened response to stress. That, scientists have noted, could affect the mental health of offspring, since an inability to respond appropriately to stress has been linked to neuropsychiatric disorders such as PTSD and depression. “The hypothalamus, the part of the brain that determines your stress response, has been wired differently,” said Tracy Bale, professor of neuroscience at the University of Maryland School of Medicine, who is presenting the new research at the meeting of the American Association for the Advancement of Science in Austin, Texas. Now the researchers say they have unpicked what is going on through work in both mice and cultured cells – experiments known as “stress in the dish”.

Keyword: Stress; Epigenetics
Link ID: 24673 - Posted: 02.17.2018

By Roni Dengler AUSTIN—Babies are as primed to learn a visual language as they are a spoken one. That’s the conclusion of research presented here today at the annual meeting of AAAS, which publishes Science. Parents and scientists know babies are learning sponges that can pick up any language they’re born into. But not as much is known about whether that includes visual language. To find out if infants are sensitive to visual language, Rain Bosworth, a psychologist at the University of California, San Diego, tracked 6-month-olds’ and 1-year-olds’ eye movements as they watched a video of a woman performing self-grooming gestures, such as tucking her hair behind her ear, and signing. The infants watched the signs 20% more than the 1-year-old children did. That means babies can distinguish between what’s language and what’s not, even when it’s not spoken, but 1-year-olds can’t. That’s consistent with what researchers know about how babies learn spoken language. Six-month-olds home in on their native language and lose sensitivity to languages they’re not exposed to, but by 12 months old that’s more or less gone, Bosworth says. The researchers also watched babies’ gazes as they observed a signer “fingerspelling,” spelling out words with individually signed letters. The signer executed the fingerspelling cleanly or sloppily. Again, researchers found the 6-month-old babies, who had never seen sign language before, favored the well-formed letters, whereas the 12-month-olds did not show a preference. Together that means there’s a critical developmental window for picking up even nonverbal languages. As 95% of deaf children are born to hearing parents, they are at risk for developmental delays because they need that language exposure early on, the scientists say. © 2018 American Association for the Advancement of Science

Keyword: Language; Development of the Brain
Link ID: 24672 - Posted: 02.17.2018

By GINA KOLATA A group of American diplomats stationed in Havana appear to have symptoms of concussion without ever having received blows to their heads, medical experts have found. The diplomats originally were said to have been victims of a “sonic attack,” a possibility that the Federal Bureau of Investigation reportedly ruled out in January. The experts’ report, published late Wednesday in the journal JAMA, does not solve the mystery, instead raising even more questions about what could have caused the brain injuries. The incidents occurred in 2016, when 18 of the 21 affected diplomats reported they heard strange sounds in their homes or hotel rooms. The noises were loud and sounded like buzzing or grinding metal, or piercing squeals or humming, the diplomats recalled. Many said they felt increased air pressure, as if they were riding in a car with the windows rolled partway down. Three diplomats said they felt a vibration. All but one reported immediate symptoms: headache, pain in one ear, loss of hearing. Days or weeks later, other symptoms emerged, including memory problems, an inability to concentrate, mood problems, headaches and fatigue. The State Department asked researchers at the University of Pennsylvania to investigate. Their report confirmed neurological problems in the diplomats, including signs of what appear to be concussions. “The study was conducted by the top concussion research team in the world utilizing state-of-the-art methods,” said C. Edward Dixon, a professor of neurological surgery at the University of Pittsburgh, who was not involved in the research. The findings suggest “a significant brain insult,” he said. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 24671 - Posted: 02.16.2018

By Richard Stone U.S. diplomats who fell ill in Cuba are victims of a new neurological syndrome, according to brain researchers at the University of Pennsylvania. But the team was unable to shed light on the malady’s mysterious cause, which the U.S. State Department has characterized as a “health attack.” From late 2016 through August 2017, as many as 24 U.S. citizens affiliated with the U.S. Embassy in Havana reported symptoms ranging from vertigo and sleeplessness to cognitive impairment. Many described hearing loud or disconcerting sounds before the onset of symptoms, or pressure sensations in their ears akin to the baffling that occurs in a moving car with the windows cracked open. “They felt something weird going on,” and when they moved away from the perceived exposure, some of “the symptoms abated,” says Douglas Smith, director of Penn’s Center for Brain Injury and Repair. The State Department called in the Penn group after initial examinations of diplomats at the University of Miami in Florida revealed persistent and inexplicable symptoms. The Penn team’s report on the diplomats’ health appears in today’s issue of The Journal of the American Medical Association (JAMA). The coincidence of the diplomats’ impairment and the auditory phenomena fueled speculation they were victims of a “sonic attack.” Last summer, citing what it saw as Cuba’s inability to protect U.S. diplomats, the State Department pulled most of its personnel out of Cuba and expelled from the U.S. a corresponding number of Cuban diplomats. The Cuban government has denied knowledge of an attack and has cooperated with the U.S. investigation, which is being spearheaded by the FBI. © 2018 American Association for the Advancement of Science

Keyword: Brain Injury/Concussion
Link ID: 24670 - Posted: 02.16.2018

A small group of cells in the brain can have a big effect on seizures and memory in a mouse model of epilepsy. According to a new study in Science, loss of mossy cells may contribute to convulsive seizures in temporal lobe epilepsy (TLE) as well as memory problems often experienced by people with the disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The role of mossy cells in epilepsy has been debated for decades. This study reveals how critical these cells are in the disease, and the findings suggest that preventing loss of mossy cells or finding ways to activate them may be potential therapeutic targets,” said Vicky Whittemore, Ph.D., program director at NINDS. Mossy cells, named for the dense moss-like protrusions that cover their surface, are located in the hippocampus, a brain area that is known to play key roles in memory. Loss of mossy cells is associated with TLE, but it is unknown what role that plays in the disease. Using state-of-the-art tools, Ivan Soltesz, Ph.D., professor of neurosurgery and neurosciences at Stanford University, Palo Alto, California, and his team were able to turn mossy cells on and off to track their effects in a mouse model of epilepsy. “This study would not have been possible without the rapid advancement of technology, thanks in part to the BRAIN Initiative, which has encouraged scientists to develop innovative instruments and new ways to look at the brain,” said Dr. Soltesz. “It’s remarkable that we can manipulate specific brain cells in the hippocampus of a mouse. Using 21st century tools brings us closer than ever to unlocking the mysteries behind this debilitating disease.”

Keyword: Epilepsy; Learning & Memory
Link ID: 24669 - Posted: 02.16.2018

Blood-thinning drugs may increase rather than cut the risk of stroke in some people over 65 who have an irregular heartbeat and also chronic kidney disease, according to a new study. The researchers are calling on doctors to be more cautious in prescribing the drugs, called anticoagulants, until there has been more research. Research led by scientists at University College London highlights the problems with polypharmacy – the use of multiple drugs for people with more than one health issue. Older people are especially likely to be on medication for more than one complaint. The researchers enrolled nearly 7,000 patients who had chronic kidney disease and were then diagnosed with atrial fibrillation – the most common form of irregular heartbeat. It affects at least 33.5 million people over the age of 55 worldwide and accounts for 1% of the NHS health budget in the UK. Chronic kidney disease is also common, says the paper in the British Medical Journal, affecting 10-15% of adults. A third also have atrial fibrillation. About half a million people in the UK have both conditions and could be prescribed blood-thinning drugs. The researchers monitored the participants, half of whom were on blood-thinning drugs and half not, for 506 days. They found those on the medication were 2.6 times as likely as those not on anticoagulants to have a stroke, and 2.4 times as likely to have a haemorrhage. There was not, however, an increased risk of death.

Keyword: Stroke
Link ID: 24668 - Posted: 02.16.2018

By Ashley Yeager Wandering through a maze with striped gray walls, a mouse searches for turns that will take it to a thirst-quenching reward. Although the maze seems real to the mouse, it is, in fact, a virtual world. Virtual reality (VR) has become a valuable tool to study brains and behaviors because researchers can precisely control sensory cues, correlating nerve-cell activity with specific actions. “It allows experiments that are not possible using real-world approaches,” neurobiologist Christopher Harvey of Harvard Medical School and colleagues wrote in 2016 in a commentary in Nature (533:324–25). Studies of navigation are perfect examples. Extraneous sounds, smells, tastes, and textures, along with internal information about balance and spatial orientation, combine with visual cues to help a mouse move through a maze. In a virtual environment, researchers can add or remove any of these sensory inputs to see how each affects nerve-cell firing and the neural patterns that underlie exploration and other behaviors. But there’s a catch. Many VR setups severely restrict how animals move, which can change nerve cells’ responses to sensory cues. As a result, some researchers have begun to build experimental setups that allow animals to move more freely in their virtual environments, while others have starting using robots to aid animals in navigation or to simulate interactions with others of their kind. Here, The Scientist explores recent efforts in both arenas, which aim to develop a more realistic sense of how the brain interprets reality. © 1986-2018 The Scientist

Keyword: Learning & Memory
Link ID: 24667 - Posted: 02.16.2018

Aimee Cunningham Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine. The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques. Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear. One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients. |© Society for Science & the Public 2000 - 2018.

Keyword: Alzheimers
Link ID: 24666 - Posted: 02.15.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Prions
Link ID: 24665 - Posted: 02.15.2018

By Matt Warren The anesthesia medication ketamine has shown promise in treating depression, but its exact effects on the brain are unclear. Now, researchers have discovered that the drug changes the firing patterns of cells in a pea-size structure hidden away in the center of the brain. This could explain why ketamine is able to relieve symptoms of depression so quickly—and may provide a fresh target for scientists developing new antidepressants. “It’s a spectacular study,” says Roberto Malinow, a neuroscientist at the University of California, San Diego, who was not involved in the work. “It will make a lot of people think.” In clinical trials, ketamine appears to act much faster than existing antidepressants, improving symptoms within hours rather than weeks. “People have tried really hard to figure out why it’s working so fast, because understanding this could perhaps lead us to the core mechanism of depression,” says Hailan Hu, a neuroscientist at Zhejiang University School of Medicine in Hangzhou, China, and a senior author on the new study. Hu suspected the drug might target a tiny region in the middle of the brain called the lateral habenula, the so-called “anti–reward center.” This region inhibits nearby reward areas, which can be useful in learning; for example, if a monkey pulls a lever expecting a treat but never receives it, the lateral habenula will reduce the activity of reward areas, and the monkey will be less likely to pull the lever in the future. But research over the past decade has suggested that the area may be overactive in depression, dampening down those reward centers too much. © 2018 American Association for the Advancement of Science.

Keyword: Depression; Drug Abuse
Link ID: 24664 - Posted: 02.15.2018