Chapter 13. Memory, Learning, and Development
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By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist
by Linda Rodriguez McRobbie If you ask Jill Price to remember any day of her life, she can come up with an answer in a heartbeat. What was she doing on 29 August 1980? “It was a Friday, I went to Palm Springs with my friends, twins, Nina and Michelle, and their family for Labour Day weekend,” she says. “And before we went to Palm Springs, we went to get them bikini waxes. They were screaming through the whole thing.” Price was 14 years and eight months old. What about the third time she drove a car? “The third time I drove a car was January 10 1981. Saturday. Teen Auto. That’s where we used to get our driving lessons from.” She was 15 years and two weeks old. The first time she heard the Rick Springfield song Jessie’s Girl? “March 7 1981.” She was driving in a car with her mother, who was yelling at her. She was 16 years and two months old. Price was born on 30 December 1965 in New York City. Her first clear memories start from around the age of 18 months. Back then, she lived with her parents in an apartment across the street from Roosevelt Hospital in Midtown Manhattan. She remembers the screaming ambulances and traffic, how she used to love climbing on the living room couch and staring out of the window down 9th Avenue. When she was five years and three months old, her family – her father, a talent agent with William Morris who counted Ray Charles among his clients; her mother, a former variety show dancer, and her baby brother – moved to South Orange, New Jersey. They lived in a three-storey, red brick colonial house with a big backyard and huge trees, the kind of place people left the city for. Jill loved it.
Keyword: Learning & Memory
Link ID: 23201 - Posted: 02.08.2017
By Julia Shaw We all have times of day when we are not at our best. For me, before 10am, and between 2-4pm, it’s as though my brain just doesn’t work the way it should. I labor to come up with names, struggle to keep my train of thought, and my eloquence drops to the level expected of an eight-year-old. In an effort to blame my brain for this, rather than my motivation, I reached out to a researcher in the area of sleep and circadian neuroscience. Andrea Smit, a PhD student working with Professors John McDonald and Ralph Mistlberger at Simon Fraser University in Canada, was happy to help me find excuses for why my memory is so terribly unreliable at certain times of day. Humans have daily biological rhythms, called circadian rhythms, which affect almost everything that we do. They inform our bodies when it is time to eat and sleep, and they dictate our ability to remember things. According to Smit, “Chronotype, the degree to which someone is a “morning lark” or a “night owl,” is a manifestation of circadian rhythms. In a recent study, Smit used EEG, a type of brain scan, to study the interaction between chronotypes and memory. “Testing extreme chronotypes at multiple times of day allowed us to compare attentional abilities and visual short term memory between morning larks and night owls. Night owls were worse at suppressing distracting visual information and had a worse visual short term memory in the morning as compared with the afternoon,” she says. “Our research shows that circadian rhythms interact with memories even at very early stages of processing within the brain.” © 2017 Scientific American
By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company
Diana Steele Generations of gurus have exhorted, “Live in the moment!” For Lonni Sue Johnson, that’s all she can do. In 2007, viral encephalitis destroyed Johnson’s hippocampus. Without that crucial brain structure, Johnson lost most of her memories of the past and can’t form new ones. She literally lives in the present. In The Perpetual Now, science journalist Michael Lemonick describes Johnson’s world and tells the story of her life before her illness, in which she was an illustrator (she produced many New Yorker covers), private pilot and accomplished amateur violist. Johnson can’t remember biographical details of her own life, recall anything about history or remember anything new. But remarkably, she can converse expertly about making art and she creates elaborately illustrated word-search puzzles. She still plays viola with expertise and expression and, though she will never remember that she has seen it before, she can even learn new music. Neuroscientists are curious about Johnson’s brain in part because her education and expertise before her illness contrast sharply with that of the most famous amnesiac known to science, Henry Molaison. Lemonick interweaves the story of “Patient H.M.,” as he was known, with Johnson’s biography. Molaison had experienced seizures since childhood and held menial jobs until surgery in his 20s destroyed his hippo-campus. At the time, in the 1950s, Molaison’s subsequent amnesia came as a surprise, prompting a 50-year study of his brain that provided a fundamental understanding of the central role of the hippocampus in forming conscious memories. © Society for Science & the Public 2000 - 2016.
Keyword: Learning & Memory
Link ID: 23189 - Posted: 02.06.2017
Hannah Devlin Science correspondent It sounds like torment for the smoker attempting to quit: handling packets of cigarettes and watching footage of people smoking, without being allowed to light up. However, scientists believe that lengthy exposure to environmental triggers for cravings could be precisely what smokers need to help them quit. The technique, known as extinction therapy, targets the harmful Pavlovian associations that drive addiction with the aim of rapidly “unlearning” them. The latest study, by scientists at the Medical University of South Carolina, found that after two one-hour sessions people smoked significantly fewer cigarettes one month after treatment compared to a control group. The study was not an unqualified success – many participants still relapsed after treatment – but the authors believe the work could pave the way for new approaches to treating addiction. Michael Saladin, the psychologist who led the work, said: “When I initially saw the results from this study it was pretty eye-opening.” In smokers, environmental triggers have typically been reinforced thousands of times so that the sight of a lighter, for instance, becomes inextricably linked to the rush of nicotine that the brain has learned will shortly follow. After quitting an addictive substance, these associations fade slowly over time, but people often flounder in the first days and weeks when cravings are most powerful. Saladin and others believe it is possible to fast-track this process in carefully designed training sessions, to help people over the initial hurdle. © 2017 Guardian News and Media Limited
Ah, to sleep, perchance … to shrink your neural connections? That's the conclusion of new research that examined subtle changes in the brain during sleep. The researchers found that sleep provides a time when thebrain's synapses — the connections among neurons—shrink back by nearly 20 percent. During this time, the synapses rest and prepare for the next day, when they will grow stronger while receiving new input—that is, learning new things, the researchers said. Without this reset, known as "synaptic homeostasis," synapses could become overloaded and burned out, like an electrical outlet with too many appliances plugged in to it, the scientists said. "Sleep is the perfect time to allow the synaptic renormalization to occur … because when we are awake, we are 'slaves' of the here and now, always attending some stimuli and learning something," said study co-author Dr. Chiara Cirelli of the University of Wisconsin-Madison Center for Sleep and Consciousness. "During sleep, we are much less preoccupied by the external world … and the brain can sample [or assess] all our synapses, and renormalize them in a smart way," Cirelli told Live Science. Cirelli and her colleague, Dr. Giulio Tononi, also of the University of Wisconsin-Madison, introduced this synaptic homeostasis hypothesis (SHY) in 2003. © 2017 Scientific American
Carl Zimmer Over the years, scientists have come up with a lot of ideas about why we sleep. Some have argued that it’s a way to save energy. Others have suggested that slumber provides an opportunity to clear away the brain’s cellular waste. Still others have proposed that sleep simply forces animals to lie still, letting them hide from predators. A pair of papers published on Thursday in the journal Science offer evidence for another notion: We sleep to forget some of the things we learn each day. In order to learn, we have to grow connections, or synapses, between the neurons in our brains. These connections enable neurons to send signals to one another quickly and efficiently. We store new memories in these networks. In 2003, Giulio Tononi and Chiara Cirelli, biologists at the University of Wisconsin-Madison, proposed that synapses grew so exuberantly during the day that our brain circuits got “noisy.” When we sleep, the scientists argued, our brains pare back the connections to lift the signal over the noise. In the years since, Dr. Tononi and Dr. Cirelli, along with other researchers, have found a great deal of indirect evidence to support the so-called synaptic homeostasis hypothesis. It turns out, for example, that neurons can prune their synapses — at least in a dish. In laboratory experiments on clumps of neurons, scientists can give them a drug that spurs them to grow extra synapses. Afterward, the neurons pare back some of the growth. Other evidence comes from the electric waves released by the brain. During deep sleep, the waves slow down. Dr. Tononi and Dr. Cirelli have argued that shrinking synapses produce this change. © 2017 The New York Times Company
By CATHERINE SAINT LOUIS During her pregnancy, she never drank alcohol or had a cigarette. But nearly every day, Stacey, then 24, smoked marijuana. With her fiancé’s blessing, she began taking a few puffs in her first trimester to quell morning sickness before going to work at a sandwich shop. When sciatica made it unbearable to stand during her 12-hour shifts, she discreetly vaped marijuana oil on her lunch break. “I wouldn’t necessarily say, ‘Go smoke a pound of pot when you’re pregnant,’” said Stacey, now a stay-at-home mother in Deltona, Fla., who asked that her full name be withheld because street-bought marijuana is illegal in Florida. “In moderation, it’s O.K.” Many pregnant women, particularly younger ones, seem to agree, a recent federal survey shows. As states legalize marijuana or its medical use, expectant mothers are taking it up in increasing numbers — another example of the many ways in which acceptance of marijuana has outstripped scientific understanding of its effects on human health. Often pregnant women presume that cannabis has no consequences for developing infants. But preliminary research suggests otherwise: Marijuana’s main psychoactive ingredient — tetrahydrocannabinol, or THC — can cross the placenta to reach the fetus, experts say, potentially harming brain development, cognition and birth weight. THC can also be present in breast milk. “There is an increased perception of the safety of cannabis use, even in pregnancy, without data to say it’s actually safe,” said Dr. Torri Metz, an obstetrician at Denver Health Medical Center who specializes in high-risk pregnancies. Ten percent of her patients acknowledge recent marijuana use. © 2017 The New York Times Company
By Emma Hiolski Imagine cells that can move through your brain, hunting down cancer and destroying it before they themselves disappear without a trace. Scientists have just achieved that in mice, creating personalized tumor-homing cells from adult skin cells that can shrink brain tumors to 2% to 5% of their original size. Although the strategy has yet to be fully tested in people, the new method could one day give doctors a quick way to develop a custom treatment for aggressive cancers like glioblastoma, which kills most human patients in 12–15 months. It only took 4 days to create the tumor-homing cells for the mice. Glioblastomas are nasty: They spread roots and tendrils of cancerous cells through the brain, making them impossible to remove surgically. They, and other cancers, also exude a chemical signal that attracts stem cells—specialized cells that can produce multiple cell types in the body. Scientists think stem cells might detect tumors as a wound that needs healing and migrate to help fix the damage. But that gives scientists a secret weapon—if they can harness stem cells’ natural ability to “home” toward tumor cells, the stem cells could be manipulated to deliver cancer-killing drugs precisely where they are needed. Other research has already exploited this method using neural stem cells—which give rise to neurons and other brain cells—to hunt down brain cancer in mice and deliver tumor-eradicating drugs. But few have tried this in people, in part because getting those neural stem cells is hard, says Shawn Hingtgen, a stem cell biologist at the University of North Carolina in Chapel Hill. © 2017 American Association for the Advancement of Science.
New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”
Homa Khaleeli The old saying, “If at first you don’t succeed: try, try again”, might need rewriting. Because, according to new research, even if you do succeed, you should still try, try again. “Overlearning”, scientists say, could be the key to remembering what you have learned. In a study of 183 volunteers, participants were asked to spot the orientation of a pattern in an image. It is a task that took eight 20-minute rounds of training to master. Some volunteers, however, were asked to carry on for a further 16 20-minute blocks to “overlearn” before being moved on to another task. When tested the next day, they had retained the ability better than those who had mastered it and then stopped learning. Primary school encourages pupils to wear slippers in class Read more The lead author of the paper, Takeo Watanabe, a professor of cognitive linguistic and psychological sciences, pointed out that: “If you do overlearning, you may be able to increase the chance that what you learn will not be gone.” But what other tricks can help us learn better? According to researchers at Bournemouth University, children who don’t wear shoes in the classroom not only learn, but behave better. Pupils feel more relaxed when they can kick their shoes off at the door says lead researcher Stephen Heppell, which means they are more engaged in lessons. © 2017 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 23173 - Posted: 02.01.2017
By SHERI FINK, STEVE EDER and MATTHEW GOLDSTEIN A group of brain performance centers backed by Betsy DeVos, the nominee for education secretary, promotes results that are nothing short of stunning: improvements reported by 91 percent of patients with depression, 90 percent with attention deficit disorder, 90 percent with anxiety. The treatment offered by Neurocore, a business in which Ms. DeVos and her husband, Dick, are the chief investors, consists of showing movies to patients and interrupting them when the viewers become distracted, in an effort to retrain their brains. With eight centers in Michigan and Florida and plans to expand, Neurocore says it has assessed about 10,000 people for health problems that often require medication. “Is it time for a mind makeover?” the company asks in its advertising. “All it takes is science.” But a review of Neurocore’s claims and interviews with medical experts suggest its conclusions are unproven and its methods questionable. Neurocore has not published its results in peer-reviewed medical literature. Its techniques — including mapping brain waves to diagnose problems and using neurofeedback, a form of biofeedback, to treat them — are not considered standards of care for the majority of the disorders it treats, including autism. Social workers, not doctors, perform assessments, and low-paid technicians with little training apply the methods to patients, including children with complex problems. In interviews, nearly a dozen child psychiatrists and psychologists with expertise in autism and attention deficit hyperactivity disorder, or A.D.H.D., expressed caution regarding some of Neurocore’s assertions, advertising and methods. “This causes real harm to children because it diverts attention, hope and resources,” said Dr. Matthew Siegel, a child psychiatrist at Maine Behavioral Healthcare and associate professor at Tufts School of Medicine, who co-wrote autism practice standards for the American Academy of Child and Adolescent Psychiatry. “If there were something out there that was uniquely powerful and wonderful, we’d all be using it.” © 2017 The New York Times Company
Keyword: Learning & Memory
Link ID: 23171 - Posted: 01.31.2017
James Gorman What fly is famous on TV? Think corpses and detectives wanting to know how long that body has been in a storage locker or suitcase. It’s the blowfly, of course. Its larvae, a.k.a. maggots, feed on rotting flesh, which could be that spouse or business partner who got in the way. Or, in a good police procedural, both the spouse and the business partner, sent to the great beyond together for their transgressions. By seeing whether the eggs have hatched and how big the larvae are, forensic scientists can get an idea of how much time has passed since the victims met their end and began the final chapter in the way of all flesh. By the way, if you have a problem with a spouse or business partner, it’s worth keeping in mind that the flies can indeed get into a suitcase. They stick their ovipositor through the gaps in the zipper. Or the newly hatched larvae themselves can sneak through. But there are aspects of the maggot’s life that have remained somewhat obscure. Martin Hall, a forensic entomologist at the Natural History Museum in London, thought that one part of the fly’s development in particular needed further study. The maggots are a bit like caterpillars in that at a certain point in their development they wrap themselves up in a case and go through one of the most astonishing events in the natural world: metamorphosis. In 10 days, the maggot, which has no legs or eyes and is something like “an animated sock,” Dr. Hall said, turns into the extraordinarily complex blowfly. No doubt blowflies are not as appealing as butterflies to most people, but chalk that up to a human bias for pretty fluttery things that land on flowers. It’s certainly not the fly’s fault. Any close-up image of its multifaceted, jewel-like eye shows that it is marvelous in its own way, even if it does feed on the dead. Science Times © 2017 The New York Times Company
Keyword: Development of the Brain
Link ID: 23169 - Posted: 01.31.2017
By Andrew Joseph, Public health officials on Thursday said they had detected a bizarre cluster of cases in which patients in Massachusetts developed amnesia over the past few years — a highly unusual syndrome that could be connected to opioid use. The officials have identified only 14 cases so far. But officials said it’s possible that clinicians have simply missed other cases. The patients were all relatively young — they ranged in age from 19 to 52. Thirteen of the 14 patients identified had a substance use disorder, and the 14th patient tested positive for opioids and cocaine on a toxicology screen. “What we’re concerned about is maybe a contaminant or something else added to the drug might be triggering this,” said Dr. Alfred DeMaria, the state epidemiologist at the Massachusetts Department of Public Health and an author of the new report. “Traditionally there’s no evidence that the drugs themselves can do this.” The pattern emerged when Dr. Jed Barash, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., reported four of the amnesia cases to the state’s public health department. The department then sent out an alert to specialists, including neurologists and emergency physicians, asking about similar cases, ultimately identifying 10 more from 2012 to 2016 at hospitals in eastern Massachusetts. (The patients included one person who lived in New Hampshire and one person who was visiting Massachusetts from Washington state.) © 2017 Scientific American,
By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.
By Anil Ananthaswamy People with post-traumatic stress disorder often get flashbacks that can be triggered by an innocuous smell or sound. Now a study that linked unrelated memories and separated them again, suggests that one day we may be able to decouple memories and prevent flashbacks in people with PTSD. Individual memories are stored in groups of neurons – an idea first proposed by psychologist Donald Hebb in 1949. Only now are we developing sophisticated techniques for examining these ensembles of neurons. To see whether two independent memories can become linked, Kaoru Inokuchi at the University of Toyama in Japan, and colleagues used a standard method for creating memories in mice. When mice are exposed to pain, they can learn to link this with associated stimuli, a taste, for example. The team trained mice to form two separate fear memories. First, the mice learned to avoid the sugary taste of saccharine. Whenever they licked a bottle filled with saccharine solution, they were injected with lithium chloride, which induces nausea. Disconnecting memories A few days later, the same mice were taught to associate a tone with a mild electric shock. This caused the mice to freeze whenever they heard it, even if it wasn’t followed with a shock. They remembered the tone as a traumatic experience. © Copyright Reed Business Information Ltd.
By Meredith Wadman Many children with congenital heart disease (CHD)—the most common major birth defect in the United States—sustain brain damage that often leads to problems with behavior, thinking, and learning. Now, for the first time, researchers have described how the lack of brain oxygen that results from heart malformations might stunt the brains of newborns, opening avenues to potential therapies that could be used even before babies are born. The results are “incredibly exciting,” says Caitlin Rollins, a child neurologist at Boston Children’s Hospital. “This kind of study allows us to start understanding the cellular mechanisms” behind the brain damage, she says. In the future, she adds, “we might be able to alter the course of brain development” with drugs targeted at the cellular anomalies and delivered during pregnancy. CHD reduces oxygen delivery to the brain at a time when the fetus most needs it. This lack of oxygen is thought to be a primary cause of the brain aberrations, which first become visible on MRI scans in the third trimester of pregnancy. (The heart anomalies themselves are commonly identified in the second trimester, on routine ultrasound scans.) Yet until now, scientists have been unclear about the underlying cellular process causing the brain problems. So a research team led by scientists at Children’s National Health System in Washington, D.C., delivered subpar levels of oxygen to newborn piglets, whose course of brain development and whose highly evolved brain structure mirrors in many respects those of humans. © 2017 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 23150 - Posted: 01.26.2017
By Andy Coghlan NEW drug will finally cure Alzheimer’s! Sound familiar? Seemingly every other week, the results of one preliminary trial or another promise that a game-changing drug for Alzheimer’s disease is just around the corner. Check back a few months later, though, and all mention of the drug has vanished, save perhaps for a terse story about a failed trial. Almost all clinical trials of new drugs to combat Alzheimer’s fail. No drug has bucked the trend in 20 years, but you wouldn’t know it from the constant promises of a breakthrough. Last November, after the failure of a particularly high-profile trial, for some the jig was up. “There are no treatments that can slow or reverse this devastating condition,” says Bryce Vissel at the University of Technology in Sydney, Australia. “There is no question that we have to look at Alzheimer’s in a different way.” So are we heading in the right direction, or do we need to rip up all the textbooks and start over? Alzheimer’s is the most common cause of dementia, and by some metrics its prevalence is rising. Alzheimer’s Disease International estimates that in 2015, 46.8 million people worldwide had dementia, a number that is set to double every 20 years, mostly because of an increasing number of older people in developing countries like India and China, leading to a global healthcare crisis. © Copyright Reed Business Information Ltd.
Link ID: 23149 - Posted: 01.26.2017
Sarah DeVos Targeting tangles of tau protein in mice with Alzheimer’s-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer’s disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer’s have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. “Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial,” says Tim Miller of Washington University in St Louis, Missouri. Now Miller’s team has purged tau tangles from the brains of Alzheimer’s-like mice for the first time. They used fragments of RNA called antisense oligonucleotides to sabotage the gene that makes tau, preventing it from being fully translated into protein. Once a day for four weeks, the team injected the antisense treatment, named Tau-ASO12, into the fluid at the base of each mouse’s spine. The mice had been genetically engineered to make a rogue form of tau similar to what is seen in people with Alzheimer’s, predisposing the mice to developing tau-related brain problems. The drug successfully spread throughout the brain, and was linked to a reduction in levels of tau that was made. It also seemed to destroy existing tau tangles, and prevent tau from spreading around the brain in older mice. © Copyright Reed Business Information Ltd.
Link ID: 23148 - Posted: 01.26.2017