Chapter 7. Life-Span Development of the Brain and Behavior
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Linda Geddes Jack struggled in regular school. Diagnosed with dyslexia and the mathematical equivalent, dyscalculia, as well as the movement disorder dyspraxia, Jack (not his real name) often misbehaved and played the class clown. So the boy’s parents were relieved when he was offered a place at Fairley House in London, which specializes in helping children with learning difficulties. Fairley is also possibly the first school in the world to have offered pupils the chance to undergo electrical brain stimulation. The stimulation was done as part of an experiment in which twelve eight- to ten-year-olds, including Jack, wore an electrode-equipped cap while they played a video game. Neuroscientist Roi Cohen Kadosh of the University of Oxford, UK, who led the pilot study in 2013, is one of a handful of researchers across the world who are investigating whether small, specific areas of a child’s brain can be safely stimulated to overcome learning difficulties. “It would be great to be able to understand how to deliver effective doses of brain stimulation to kids’ brains, so that we can get ahead of developmental conditions before they really start to hold children back in their learning,” says psychologist Nick Davis of Swansea University, UK. The idea of using magnets or electric currents to treat psychiatric or learning disorders — or just to enhance cognition — has generated a flurry of excitement over the past ten years. The technique is thought to work by activating neural circuits or by making it easier for neurons to fire. The research is still in its infancy, but at least 10,000 adults have undergone such stimulation, and it seems to be safe — at least in the short term. One version of the technology, called transcranial magnetic stimulation (TMS), has been approved by the US Food and Drug Administration to treat migraine and depression in adults. © 2015 Nature Publishing Group,
Claudia Dreifus Cornelia Bargmann, a neurobiologist at Rockefeller University in New York, studies how genes interact with neurons to create behavior. Two years ago, President Obama named Dr. Bargmann, who is known as Cori, a co-chairwoman of the advisory commission for the Brain Initiative, which he has described as “giving scientists the tools they need to get a dynamic picture of the brain in action.” I spoke with Dr. Bargmann, 53, for two hours at the Manhattan apartment she shares with her husband, Dr. Richard Axel, a neuroscientist at Columbia University. Our interview has been edited and condensed. Q. As an M.I.T. graduate student, you made a discovery that ultimately led to the breast cancer drug Herceptin. How did it happen? A. What I did was discover a mutated gene that triggered an obscure cancer in rats. Afterwards, it was discovered — by others — that this same gene is also altered in human breast cancers. Since our work in the rat cancer showed that the immune system could attack the product of this gene, Genentech developed a way to deploy the immune system. That’s Herceptin. It is an antibody against the gene that sits on the surface of a cancer cell. It can attack the cancer cell growing because of that gene. Currently, you spend your time trying to understand the nervous system of a tiny worm, C. elegans. Why do you study this worm? Well, the reason is this: Understanding the human brain is a great and complex problem. To solve the brain’s mysteries, you often have to break a problem down to a simpler form. Your brain has 86 billion nerve cells, and in any mental process, millions of them are engaged. Information is sweeping across these millions of neurons. With present technology, it’s impossible to study that process at the level of detail and speed you would want. © 2015 The New York Times Company
by Laura Sanders Like every other person who carries around a smartphone, I take a lot of pictures, mostly of my kids. I thought I was bad with a few thousand snaps filling my phone’s memory. But then I talked to MIT researcher Deb Roy. For three years, Roy and a small group of researchers recorded every waking moment of Roy’s son’s life at home, amassing over 200,000 hours of video and audio recordings. Roy’s intention wasn’t to prove he was the proudest parent of all time. Instead, he wanted to study how babies learn to say words. As a communication and machine learning expert, Roy and his wife Rupal Patel, also a speech researcher, recognized that having a child would be a golden research opportunity. The idea to amass this gigantic dataset “was kicking around and something we thought about for years,” Roy says. So after a pregnancy announcement and lots of talking and planning and “fascinating conversations” with the university administration in charge of approving human experiments, the researchers decided to go for it. To the delight of his parents, a baby boy arrived in 2005. When Roy and Patel brought their newborn home, the happy family was greeted by 11 cameras and 14 microphones, tucked up into the ceiling. From that point on, cameras rolled whenever the baby was awake. © Society for Science & the Public 2000 - 2015
Steve Connor A painkiller widely used to treat rheumatoid arthritis has been shown to reverse the symptoms of dementia in the brains of laboratory mice, raising hope that there may soon be an effective treatment for Alzheimer’s disease, scientists have said. The drug, salsalate, is a licensed pain killer but in mice with a form of dementia similar to Alzheimer’s it reversed the changes to a key protein in the brain that builds up in patients with the debilitating neurological disease, they found. The researchers said it is the first time any drug has been shown to have an effect on the “tau” protein that accumulates in the brain of people with Alzheimer’s and a range of similar dementias known as “tauopathies”. It could lead to an effective therapy even for patients in the later stages of disease, the researchers said. “We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity," said Li Gan, PhD of the Gladstone Institutes, a non-profit research organisation affiliated with the University of California, San Francisco. “Remarkably, the profound protective effects of salsalate were achieved even though it was administered after disease onset, indicating that it may be an effective treatment option,” said Dr Gan a senior co-author of the study published in the journal Nature Medicine. As many as 800,000 people in Britain are already affected by Alzheimer’s disease and a new study has suggested that as many as one in three babies born this year will get dementia in their lifetime, largely as a result of people living longer. Age is the biggest risk factor for the disease. © independent.co.uk
Link ID: 21428 - Posted: 09.22.2015
By John Pavlus The “brain in a vat” has long been a staple of philosophical thought experiments and science fiction. Now scientists are one step closer to creating the real thing, which could enable groundbreaking experiments of a much more empirical kind. Research teams at Stanford University and the RIKEN Center for Developmental Biology in Japan have each discovered methods for coaxing human stem cells to form three-dimensional neural structures that display activity associated with that of an adult brain. By applying a variety of chemical growth factors, the RIKEN researchers transformed human embryonic stem cells into neurons that self-organized in patterns unique to the cerebellum, a region of the brain that coordinates movement. The Stanford team worked with induced pluripotent stem cells derived from skin cells and chemically nudged them to become neurons that spontaneously wired up into networks of 3-D circuits, much like the ones found in the cerebral cortex—the wrinkled gray matter of the brain that supports attention, memory and self-awareness in humans. “For years people have used mouse embryonic stem cells to generate teratomas—things that look like they could be organs,” says David Panchision, a neuroscientist at the National Institutes of Health, which supported the Stanford research. “But it's not organized and systematic, the way a developing brain needs to be to function.” In contrast, the Stanford team's neural structures not only self-assembled as cortexlike tissue, the neurons also sent signals to one another in coordinated patterns—just as they would in a brain. The cerebellar tissue generated by the Japanese scientists did, too. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 21427 - Posted: 09.21.2015
Mo Costandi The human brain is often said to be the most complex object in the known universe, and there’s good reason to believe that this old cliché is true. Even the apparently simple task of compiling a census of the different types of cells it contains has proven to be extremely difficult. Researchers still can’t agree on the best way to classify the numerous sub-types of neurons, and different methods produce different results, so estimates range from several hundred to over a thousand. Basket cells illustrate this neuronal identity crisis perfectly. They are currently sub-divided into multiple different types, according to their shape, electrical properties, and molecular profiles. After nearly ten years of detective work, researchers at King’s College London now reveal them to be masters of disguise. In a surprising new study, they show that these cells can dynamically switch from one identity to another in response to neuronal network activity. Basket cells are a type of interneuron, which are found scattered throughout the cerebral cortex, hippocampus, and cerebellum, and make up about 5% of the total number of cells in these brain regions. They form local circuits with each other and with pyramidal neurons, the much larger and more numerous cells that transmit information to distant parts of the brain, and synthesize the inhibitory neurotransmitter GABA, which dampens pyramidal cell activity when released. These enigmatic cells are thought to exist in more than twenty different types, the best known being the fast-spiking ones, which respond rapidly to incoming signals, and slower ones, which respond after a delay. During brain development, immature forms of all types of basket cells are created in a structure called the medial ganglionic eminence, along with various other types of brain cells. They then migrate into the developing cerebral cortex, before going on to form synaptic connections with other cells. © 2015 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21423 - Posted: 09.20.2015
By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company
Nancy Shute There have been suggestions that low levels of vitamin D might be a factor in cognitive decline and Alzheimer's disease, but there's no proof that the lack of D is actually causing the problems. A study published Monday doesn't prove that link, but it does find that people with low levels of vitamin D lost key thinking skills more quickly than people with enough. The study is notable because of the diversity of the participants: 62 percent were women, 30 percent were African-American, 25 percent Hispanic and 41 percent white. Most earlier studies looking at cognitive decline and vitamin D were in white people. The participants lived in California's Sacramento Valley and were mostly in their 70s when they entered the study. The researchers followed up with them for about five years, having them take annual neurological exams and neuropsychological testing at the University of California, Davis, Alzheimer's Disease Center. Most of the 382 people in the study were low on vitamin D, tested by measuring 25-hydroxyvitamin D in the blood. One-quarter of the participants were deficient in vitamin D, and 35 percent had levels deemed insufficient. That's not a surprise — most older people are below the "adequate" level of 20 to less than 50 ng/ml, often because they're not outside much. And most of the people in the study weren't getting the recommended three servings of dairy foods daily that could help. © 2015 NPR
By CLYDE HABERMAN Perhaps no crime staggers the mind, or turns the stomach, more than the murder of a baby, and so it is not a surprise when law enforcement comes down hard on the presumed killers. Often enough, these are men and women accused of having succumbed to sudden rage or simmering frustration and literally shaken the life out of a helpless infant who would not stop crying or would not fall asleep. Shaken baby syndrome has been a recognized diagnosis for several decades, though many medical professionals now prefer the term abusive head trauma. It is defined by a constellation of symptoms known as the triad: brain swelling, bleeding on the surface of the brain and bleeding behind the eyes. For years, those three symptoms by themselves were uniformly accepted as evidence that a crime had been committed, even in the absence of bruises, broken bones or other signs of abuse. While many doctors, maybe most, still swear by the diagnosis, a growing number have lost faith. Not that they doubt that some babies have been abused. But these skeptics assert that factors other than shaking, and having nothing to do with criminal behavior, may sometimes explain the triad. Has the syndrome been diagnosed too liberally? Are some innocent parents and other caretakers being wrongly sent to prison? Those questions, at the complex intersection of medicine and the law, can stir strong emotions among doctors, parents and prosecutors. They shape this first installment in a new series of Retro Report, video documentaries that explore major news stories of the past and their enduring consequences. The video’s starting point is a Massachusetts criminal case that introduced the concept of shaken baby syndrome to many Americans: the 1997 murder trial of Louise Woodward, an 18-year-old British au pair accused of having shaken an 8-month-old boy, Matthew Eappen, so aggressively that he died. Matthew also had injuries that may have predated Ms. Woodward’s joining the Eappen family in Newton, outside Boston. The focus, however, was on the triad of symptoms. To prosecution witnesses, they proved that the baby had been shaken violently, his head hitting some hard surface. © 2015 The New York Times Company
A study suggests that a chemical in dark chocolate and red wine can slow the progression of Alzheimer’s disease. But how conclusive is the data, and does this mean we should all drink more wine? New Scientist looks at the evidence. What is resveratrol? Found in grapes, red wine and dark chocolate, many claims have been made about resveratrol. It has been touted as a potential panacea for a range of age-related disorders, including cancer, diabetes and neurological problems, but so far most of the data supporting these claims has come from lab studies and work in animals. There have been only a few, small studies in humans. How might resveratrol protect us from age-related illness? Extremely calorie-restricted diets greatly reduce age-related diseases in lab animals. This is thought to happen through the activation of a group of enzymes called sirtuins, which seem to affect gene expression and protect against the effects of stress, including a poor diet. The hope is that resveratrol activates sirtuins to get the same benefits – like preventing the onset of age-related diseases, including Alzheimer’s – without having to stick to such a low-energy diet. But some experiments have suggested slowed ageing from caloric restriction may not be down to sirtuins after all. What does the latest study show? To see if resveratrol could delay the progression of Alzheimer’s disease in people , Scott Turner at Georgetown University Medical Centre in Washington DC and his team gave 119 people with mild to moderate symptoms of the disease either a gram of synthesised resveratrol twice a day in pills for a year, or a placebo. © Copyright Reed Business Information Ltd.
Link ID: 21404 - Posted: 09.14.2015
By Elizabeth Landau Ask a physician what the hormone vasopressin is good for, and she will explain that it regulates the volume of water in your body and also affects blood pressure. But since the 1990s, vasopressin has been a hot topic in a very different field: social behavior. And recently it has emerged as a possible target for treating autism spectrum disorders (ASD), which are characterized by social, behavioral and communication impairments. The research is still in early stages, however, and has yielded more questions than answers. Given that one out of 68 children in the U.S. has an autism spectrum disorder, researchers are scrambling to figure out what in the brain might be related to the symptoms, and how they might design an effective treatment. Vasopressin may be a key player in the disorder. But scientists do not yet know whether too much or too little of the hormone—or perhaps some combination of both—is tied to autism. New clinical trials may yield insights. “I think that the work is exciting and important” says Suma Jacob, who leads an autism research laboratory at the University of Minnesota. “I also think we still have a lot more work to do in this field as a whole.” Previous research has shown that vasopressin, like the hormone oxytocin, is associated with parenting behavior and social bonding, including falling in love. In fact, the two hormones are structurally very similar, and there are receptors in the brain that interact with both of them. But high levels of vasopressin are also associated with anxiety and aggression. Intriguingly, some animal studies have found that higher levels of vasopressin increased aggression specifically in males. © 2015 Scientific American
Alison Abbott Only a decade ago, the idea that Alzheimer’s disease might be transmissible between people would have been laughed off the stage. But scientists have since shown that tissues can transmit symptoms of the disease between animals — and new results imply that humans, at least in one unusual circumstance, may not be an exception. The findings, published in this issue of Nature, emerged during autopsy studies of the brains of eight people who had died of the rare but deadly Creutzfeldt–Jakob disease (CJD; Z. Jaunmuktane et al. Nature 525, 247–250; 2015). They contracted it decades after treatment with contaminated batches of growth hormone that had been extracted from the pituitary glands of human cadavers. Six of the brains, in addition to the damage caused by CJD, harboured the tell-tale amyloid pathology that is associated with Alzheimer’s disease. “This is the first evidence of real-world transmission of amyloid pathology,” says molecular neuroscientist John Hardy of University College London (UCL). “It is potentially concerning.” If confirmed, the findings raise the spectre that tens of thousands of other people treated with the human growth-hormone (hGH) extracts might be at risk of Alzheimer’s. And although there is no suggestion that Alzheimer’s could be contracted through normal contact with patients, some scientists worry that the findings may have broader implications: that Alzheimer’s could be passed on by other routes through which CJD can be transmitted, such as blood transfusions or contaminated surgical instruments. © 2015 Nature Publishing Group
By Siri Carpenter Alex, age 10, bounds onto his bed to pose with his Aaron Rodgers poster, grinning as proudly as if he had recruited the Green Bay Packers’ quarterback himself. Continuing the tour of his suburban New York bedroom, he points out his Packers-themed alarm clock, his soccer trophy, his Boy Scout trophy, and then the big reveal: a homemade foam box in Packers green and gold. “Mmm, very nice,” I say. Alex grins—part shy, part sly—as he turns it around to show me the message on the back: “Jets stink.” Even though he seems to be an entirely ordinary boy, there’s something unusual about Alex: He once had autism, and now he does not. There was a time when Alex’s parents didn’t know if he would ever speak in full sentences, let alone joke around with a stranger. His autism, they suspected, might prevent any such future. Alex’s parents began to worry about him before he was even a year old. He wasn’t learning to sit, crawl, or stand as his fraternal twin brother was. Even more striking was how much less social he was than his brother. “Alex was an expressionless child,” says his mother, Amy. (Alex’s and Amy’s names have been changed to protect their privacy.) She remembers a friend trying in vain to get Alex to laugh—jumping up and down, gesturing wildly, making silly faces. “His brother would be in belly laughs, and Alex would be just glazed over,” Amy says. © 2015 The Slate Group LLC.
Link ID: 21393 - Posted: 09.10.2015
By Nicholas Bakalar Being obese at age 50 may be tied to an increased risk of developing Alzheimer’s disease at a younger age. Previous studies have shown that being overweight at midlife is associated with an increased risk of developing Alzheimer’s. Now researchers have found that it also predicts occurrence at a younger age. Scientists studied 1,394 cognitively normal people, average age around 60, following them for an average of 14 years. During the study, 142 developed Alzheimer’s. After controlling for age, race, level of education and cardiovascular risk factors, they found that each unit increase in B.M.I., or body mass index, at age 50 was associated with a 6.7-month decrease in the age of onset of Alzheimer’s. The study, in Molecular Psychiatry, also found an association of higher B.M.I. with larger deposits of neurofibrillary tangles on autopsy, one of the characteristics of brain damage in Alzheimer’s disease. “Age of onset is not as well studied as risk,” said the senior author, Dr. Madhav Thambisetty, a neurologist at the National Institute on Aging. “As we try to cure Alzheimer’s disease, we also want to delay the onset of symptoms. Until we know what factors accelerate onset, we won’t be able to test any potential interventions. And that is perhaps as important as the search for treatment.” © 2015 The New York Times Company
By Melinda Wenner Moyer A worrisome new study caught my eye last week as I perused the website of the journal Pediatrics. It was titled “Cognition and Brain Structure Following Early Childhood Surgery With Anesthesia.” Considering that my now 4-year-old underwent general anesthesia for a minor procedure when he was 2 and that my 14-month-old may be a candidate for ear tube surgery, my interest was immediately piqued. I clicked through and came face to face with a whole lot of yuck. The first sentence alone made me gasp: “Anesthetics induce widespread cell death, permanent neuronal deletion, and neurocognitive impairment in immature animals, raising substantial concerns about similar effects occurring in young children.” Wait, so anesthesia causes brain damage? Why didn’t anyone tell me? I thought. Obviously, I needed to know more. Considering that 6 million American children—including 1.5 million babies under the age of 1—undergo general anesthesia each year, this seemed like a pretty serious issue to delve into. Twenty studies and several phone calls later, I’m feeling a lot better about my kids’ brains. There are still many things scientists don’t know about how anesthesia affects the nervous system, in part because they can’t ethically do the types of experiments that would provide clear answers, like unnecessarily exposing kids to anesthesia. But based on the research that does exist, there’s really no need for parents to freak out. If “going under” has an effect on the developing brain, it’s likely to be very small. Even Andreas Loepke, the pediatric anesthesiologist at Cincinnati Children’s Hospital Medical Center who co-authored the Pediatrics paper, was reassuring to me over the phone. “These are theoretical concerns,” he said. © 2015 The Slate Group LLC.
In 1938, an Austrian pediatrician named Hans Asperger gave the first public talk on autism in history. Asperger was speaking to an audience of Nazis, and he feared that his patients — children who fell onto what we now call the autism spectrum — were in danger of being sent to Nazi extermination camps. As Asperger spoke, he highlighted his "most promising" patients, a notion that would stick with the autistic spectrum for decades to come. "That is where the idea of so-called high-functioning versus low-functioning autistic people comes from really — it comes from Asperger's attempt to save the lives of the children in his clinic," science writer Steve Silberman tells Fresh Air's Terry Gross. Silberman chronicles the history of autism and examines some of the myths surrounding our current understanding of the condition in his new book, NeuroTribes. Along the way, he revisits Asperger's calculated efforts to save his patients. Steve Silberman's articles have been published in Wired, The New Yorker, Nature and Salon. Silberman shies away from using the terms high-functioning and low-functioning, because "both of those terms can be off base," he says. But he praises Asperger's courage in speaking to the Nazis. "I would literally weep while I was writing that chapter," he says. NeuroTribes also explores how a 1987 expansion of the medical definition of autism (which was previously much narrower and led to less frequent diagnoses) contributed to the perception that there was an autism epidemic. © 2015 NPR
Link ID: 21378 - Posted: 09.03.2015
By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.
Aftab Ali People who were born prematurely are less intelligent later on in life and earn less money as a result, according to a new study by the University of Warwick. Researchers at the Coventry-based institution said they found a link which connects pre-term birth with low reading and, in particular, maths skills which affect the amount of wealth accumulated as adults. Funded by the Nuffield Foundation, the researchers examined data from two other large studies, following children born more than a decade apart, with one group from 1958 and the other from 1970. In total, more than 15,000 individuals were surveyed – which recruited all children born in a single week in England, Scotland, and Wales. Data were examined for all individuals who were born at between 28 and 42 weeks gestational age, and who had available wealth information at the age of 42. Those participants who were born pre-term – at less than 37 weeks – were compared with those who were born full-term to find both groups’ mathematical ability in childhood had a direct effect on how much they earned as an adult, regardless of later educational qualifications. In order to measure adult wealth, the researchers looked at factors including: family income and social class, housing and employment status, and their own perceptions of their financial situation. In regards to academic abilities, they examined: validated measures for mathematics, reading, and intelligence, along with ratings from teachers and parents. © independent.co.uk
By Gretchen Reynolds At the age of 93, Olga Kotelko — one of the most successful and acclaimed nonagenarian track-and-field athletes in history — traveled to the University of Illinois to let scientists study her brain. Ms. Kotelko held a number of world records and had won hundreds of gold medals in masters events. But she was of particular interest to the scientific community because she hadn’t begun serious athletic training until age 77. So scanning her brain could potentially show scientists what late-life exercise might do for brains. Ms. Kotelko died last year at the age of 95, but the results of that summer brain scan were published last month in Neurocase. And indeed, Ms. Kotelko’s brain looked quite different from those of other volunteers aged 90-plus who participated in the study, the scans showed. The white matter of her brain — the cells that connect neurons and help to transmit messages from one part of the brain to another — showed fewer abnormalities than the brains of other people her age. And her hippocampus, a portion of the brain involved in memory, was larger than that of similarly aged volunteers (although it was somewhat shrunken in comparison to the brains of volunteers decades younger than her). Over all, her brain seemed younger than her age. But because the scientists didn’t have a scan showing Ms. Kotelko’s brain before she began training, it’s impossible to know whether becoming an athlete late in life improved her brain’s health or whether her naturally healthy brain allowed her to become a stellar masters athlete. © 2015 The New York Times Company
An experimental gene therapy reduces the rate at which nerve cells in the brains of Alzheimer’s patients degenerate and die, according to new results from a small clinical trial, published in the current issue of the journal JAMA Neurology. Targeted injection of the Nerve Growth Factor gene into the patients’ brains rescued dying cells around the injection site, enhancing their growth and inducing them to sprout new fibres. In some cases, these beneficial effects persisted for 10 years after the therapy was first delivered. Alzheimer’s is the world’s leading form of dementia, affecting an estimated 47 million people worldwide. This figure is predicted to almost double every 20 years, with much of this increase is likely to be in the developing world. And despite the huge amounts of time, effort, and money devoted to developing an effective cure, the vast majority of new drugs have failed in clinical trials. The new results are preliminary findings from the very first human trials designed to test the potential benefits of nerve growth factor (NGF) gene therapy for Alzheimer’s patients. NGF was discovered in the 1940s by Rita Levi-Montalcini, who convincingly demonstrated that the small protein promotes the survival of certain sub-types of sensory neurons during development of the nervous system. Since then, others have shown that it also promotes the survival of acetylcholine-producing cells in the basal forebrain, which die off in Alzheimer’s. © 2015 Guardian News and Media Limited