By James Gorman Carpenter ants follow trails. Just watch them wandering about on your wooden porch until they strike a trail of pheromones (chemicals ants use for communication) that another ant has laid down. Ants don’t have noses, so they wave their antennas around to pick up the trail, then off they go on the road to ruin. (Carpenter ants destroy houses.) Scientists know plenty about ants, including their ability to follow scent trails, but researchers at Harvard wanted to get a more detailed understanding of how exactly ants sniff, or taste, the pheromone-marked path. First, some basics: Ants use their antennas to pick up chemical cues left by other ants. And the chemical sense of ants, call it smell or taste or chemo-reception, enables them to follow straight trails, curved trails, even zigzags. To see how ants do it, the scientists mixed ink and ant pheromones and used the result to paint trails on paper. They set ants out on trails and recorded dozens of hours of ant movement. They analyzed the video and tried out different computer models of the ants’ behavior. What Ryan W. Dash and his adviser, Venkatesh N. Murthy, and other researchers found was that the ants had several strategies for path-following. The scientists published their results in the Journal of Experimental Biology. All the ants used their antennas to sweep the trail side to side. One strategy they used was probing. A probing ant moved slowly, keeping its antennas close together. The researchers termed another strategy exploratory: Ants still moved slowly, but they took winding paths moving away from and back to a trail. When they were locked into a pheromone trail, they moved along more quickly, keeping their antennas on either side of the path. They kept one antenna closer to the path, but which antenna varied from ant to ant. In other words, some were lefties and others were righties. © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 25891 - Posted: 01.22.2019

John Bergeron During the first weeks of the new year, resolutions are often accompanied by attempts to learn new behaviours that improve health. We hope that old bad habits will disappear and new healthy habits will become automatic. But how can our brain be reprogrammed to assure that a new health habit can be learned and retained? In 1949, Canadian psychologist Donald Hebb proposed the theory of Hebbian learning to explain how a learning task is transformed into a long-term memory. In this way, healthy habits become automatically retained after their continual repetition. Synapses transmit electrical signals. Svitlana Pavliuk Learning and memory are a consequence of how our brain cells (neurons) communicate with each other. When we learn, neurons communicate through molecular transmissions which hop across synapses producing a memory circuit. Known as long-term potentiation (LTP), the more often a learning task is repeated, the more often transmission continues and the stronger a memory circuit becomes. It is this unique ability of neurons to create and strengthen synaptic connections by repeated activation that leads to Hebbian learning. Understanding the brain requires investigation through different approaches and from a variety of specialities. The field of cognitive neuroscience initially developed through a small number of pioneers. Their experimental designs and observations led to the foundation for how we understand learning and memory today. © 2010–2019, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 25890 - Posted: 01.22.2019

Alison Abbott Neuroscientists have for the first time discovered differences between the ‘software’ of humans and monkey brains, using a technique that tracks single neurons. They found that human brains trade off ‘robustness’ — a measure of how synchronized neuron signals are — for greater efficiency in information processing. The researchers hypothesize that the results might help to explain humans’ unique intelligence, as well as their susceptibility to psychiatric disorders. The findings were published in Cell1 on 17 January. Scientists say that this type of unusual study could help them to better translate research in animal models of psychiatric diseases into the clinic. The research exploited a rare set of data on the activity of single neurons collected deep in the brains of people with epilepsy who were undergoing neurosurgery to identify the origin of their condition. The technique is so difficult that only a handful of clinics around the world can participate in this type of research. The study also used similar, existing data from three monkeys and collected neuron information from two more. Over the decades, neuroscientists have discovered many subtle and significant differences in the anatomy — the hardware — of the brains of humans and other primates. But the latest study looked instead at differences in brain signals. © 2019 Springer Nature Publishing AG

Keyword: Schizophrenia; Epilepsy
Link ID: 25889 - Posted: 01.21.2019

By Scott Barry Kaufman Robert Plomin is a legend. For over 40 years he has been on the forefront of our understanding of the genetic and environmental influences on human behavior. Based on his groundbreaking work on twins, he showed that genes really do have a substantial influence on our psychological traits-- we are not born a lump of clay. Plomin coined the phrase "non-shared environment," and he was ranked as the 71st most "eminent psychologists of the 20th century." When I taught a course on human intelligence at NYU, I repeatedly cited his research and quoted his measured language and caution surrounding the interpretation of his findings. All of this makes it rather bewildering that, ever since his book Blueprint: How DNA Makes Us Who We Are came out, he has been spreading a lot of outdated misinformation in the media that is not supported by the latest science of genetics, including his own work. Also, many of his statements have been riddled with contradictions and logical non sequiturs, and some of his more exaggerated rhetoric is even potentially dangerous if actually applied to educational selection. Don't get me wrong: I am excited about the rapid progress scientists are making in using information about DNA to predict individual differences in intellectual functioning and personality. But I firmly believe we need to be more thoughtful in determining what relevance these rapidly emerging findings have for the actual individual human beings who are inhabited by the DNA.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 25888 - Posted: 01.21.2019

By Perri Klass, M.D. Acute pain that calls out to warn you — “Hey, don’t walk on this broken leg!” — may be unpleasant, but it’s also protective. That acute pain is letting you know that a part of your body needs to heal, or in some other way needs extra attention, said Dr. Neil Schechter, the director of the chronic pain clinic at Boston Children’s Hospital. That’s very different, he said, from chronic pain that goes on over the course of months, whether abdominal pain or headache or musculoskeletal — it may persist and be incapacitating, because “the pain has become the disease.” That doesn’t mean the pain is any less painful for the person experiencing it. “There is really strong evidence supporting the psychological treatment for chronic pain, and that doesn’t imply that the pain itself is a psychological problem,” said Rachael Coakley, a psychologist who is the director of clinical innovation and outreach in pain medicine at Boston Children’s Hospital. Her book, “When Your Child Hurts,” is an excellent resource for parents. “When you’re a kid and you’ve had pain for a really long time, a lot of that is an experience of not having control over what’s happening in your body,” said Anna C. Wilson, a pediatric pain psychologist at Oregon Health and Science University. “Relaxation and other biobehavioral techniques help kids gain a sense of control.” She tells patients, “Your pain is absolutely real, and chronic pain in particular is a neurologic problem.” She recommended TED Talks by Dr. Elliot Krane, an anesthesiologist, and Lorimer Moseley, a neuroscience professor, to help explain chronic pain. Chronic pain develops, Dr. Schechter said, when there is an underlying biological vulnerability, either inherited or resulting from stressors like infections or procedures or traumas, and then a triggering event, such as a gastrointestinal infection or an injury. © 2019 The New York Times Company

Keyword: Pain & Touch; Development of the Brain
Link ID: 25887 - Posted: 01.21.2019

By David Grossman The brain remains famously remains one of the most mysterious parts of the human body. The challenges of neuroscience are among the most daunting in the medical field. Expansion microscopy is a crucial element of that study, a chemical technique that expands a small specimen to make it more observable at the molecular level. A new technique allows scientists to expand microscopy so instead of focusing a single sell, it can explore full neural circuits, at a speed around 1,000 times faster than before. A struggle in studying live cells is watching them without altering their actions. Scientists work around this problem by using thin sheets of light to illuminate cells with a piece of complex technology called a lattice light sheet microscope. By combining this microscope with expansion microscopy, scientists at the Howard Hughes Medical Institute (HHMI) were able to expand the possibility of how they could study insect brains. “I thought they were full of it,” says Eric Betzig, now an HHMI investigator at the University of California, Berkeley, in a press statement. "They" refers to Ruixuan Gao and Shoh Asano of MIT, who wanted to use Betzig's lab to attempt their combining of the two practices. While a complex procedure involving high-end scientific equipment, at its heart “the idea does sound a bit crude,” Gao says. “We’re stretching tissues apart." When the experiment was over, Betzig says, “I couldn’t believe the quality of the data I was seeing. You could have knocked me over with a feather.” ©2019 Hearst Magazine Media, Inc

Keyword: Brain imaging
Link ID: 25886 - Posted: 01.21.2019

By John Horgan In my freshman humanities class, I make students ponder the pros and cons of knowledge. We talk about Plato’s parable, in which people imprisoned in a cave mistake shadows projected on a wall for reality. I ask, Assuming we’re in the cave, how many of you want to escape? Most students dutifully raise their hands, because of course truth is good and ignorance is bad. Then I ask, What if the cave is comfy and the outside world nasty? I bring up The Matrix, in which humans live in a computer simulation, called the Matrix, constructed by evil machines. A band of rebels who have escaped this digital cave is trying to liberate other humans. A rebel named Cypher gives Agent Smith, nasty sentient software created by the machines, information to help him capture the rebels. Agent Smith asks Cypher what he wants for betraying his comrades, and Cypher says he doesn't want to live in reality any more. It’s ugly and stressful, and he hates being bossed around by the rebel leader. Cypher asks for a happy simulated life in the Matrix. Here is an excerpt from his dialogue with Agent Smith, which takes place in a virtual restaurant: Cypher: You know, I know this steak doesn't exist. I know that when I put it in my mouth, the Matrix is telling my brain that it is juicy and delicious. After nine years, you know what I realize? Ignorance is bliss. Agent Smith: Then we have a deal? Cypher: I don't want to remember nothing. Nothing. You understand? And I want to be rich. You know, someone important, like an actor. Agent Smith: Whatever you want.

Keyword: Alzheimers; Consciousness
Link ID: 25885 - Posted: 01.21.2019

Jonathan Lambert Pain is a complicated experience. Our skin and muscles sense it, just like they sense softness or warmth. But unlike other sensations, the experience of pain is distinctly unpleasant. Pain has to hurt for us to pay attention to it, and avoid hurting ourselves further. But for people in chronic pain, the pain has largely lost its purpose. It just hurts. While it has long been understood how nerves signal pain to the brain, scientists haven't known how the brain adds a layer of unpleasantness. Findings of a study published Thursday in Science offer an answer. A research team from Stanford University pinpointed the neurons in mouse brains that make pain hurt and were able to alter these neurons in a way that reduced the unpleasantness of pain without eliminating the sensation. The study lays the groundwork for future research into more targeted pain treatments. "This study is a major advance," says Irene Tracey, a pain neuroscientist at Oxford University who wasn't involved in the study. "It was a tour de force and a welcome addition to understanding this complex and major problem." Stanford neuroscientist Grégory Scherrer, who co-led the study, started the search for pain neurons in the amygdala — the slim, almond-shaped region scientists know regulates many emotions. The challenge for Scherrer was to sift through the tangle of neurons there and identify the ones associated with pain. © 2019 npr

Keyword: Pain & Touch
Link ID: 25884 - Posted: 01.19.2019

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Keyword: Parkinsons
Link ID: 25883 - Posted: 01.19.2019

Aimee Cunningham As public health officials tackle opioid addiction and overdoses, another class of prescription drugs has been contributing to a growing number of deaths across the United States. Benzodiazepines, such as Valium and Xanax, are commonly prescribed for anxiety and insomnia. The drugs are also highly addictive and can be fatal, especially when combined with alcohol or opioids. In the latest sign of the drug’s impact, the number of overdose deaths involving “benzos” rose from 0.54 per 100,000 in 1999 to 5.02 per 100,000 in 2017 among women aged 30 to 64, researchers report January 11 in the Morbidity and Mortality Weekly Report. That’s a spike of 830 percent, surpassed only by increases seen in overdose deaths involving synthetic opioids or heroin. Overall, there were 10,684 overdose deaths involving benzodiazepines in the United States in 2016, according to the National Institute on Drug Abuse. In 1999, the total was 1,135. Benzodiazepines have a sedating effect, and are particularly dangerous when used with other drugs that slow breathing, such as opioids and alcohol. In combination, the substances can “cause people to fall asleep and essentially never wake up again,” says Anna Lembke, an addiction psychiatrist at Stanford University School of Medicine. Benzos and opioids are often prescribed together, and opioids contribute to 75 percent of overdose deaths involving benzos. The rising number of deaths involving benzos hasn’t stopped the flow of prescriptions. The number of U.S. adults who filled a prescription for benzos rose from 8.1 million in 1996 to 13.5 million in 2013, a jump of 67 percent, a study in the American Journal of Public Health in 2016 found. The quantity of benzos acquired more than tripled over the same time. |© Society for Science & the Public 2000 - 2019.

Keyword: Drug Abuse; Stress
Link ID: 25882 - Posted: 01.19.2019

By Abby Goodnough WASHINGTON — A new study offers some of the strongest evidence yet of the connection between the marketing of opioids to doctors and the nation’s addiction epidemic. It found that counties where opioid manufacturers offered a large number of gifts and payments to doctors had more overdose deaths involving the drugs than counties where direct-to-physician marketing was less aggressive. The study, published Friday in JAMA Network Open, said the industry spent about $40 million promoting opioid medications to nearly 68,000 doctors from 2013 through 2015, including by paying for meals, trips and consulting fees. And it found that for every three additional payments that companies made to doctors per 100,000 people in a county, overdose deaths involving prescription opioids there a year later were 18 percent higher. Even as the opioid epidemic was killing more and more Americans, such marketing practices remained widespread. From 2013 through 2015, roughly 1 in 12 doctors received opioid-related marketing, according to the study, including 1 in 5 family practice doctors. The authors, from Boston Medical Center and New York University School of Medicine, found that counties where doctors received more industry marketing subsequently saw an increase in both the number of opioids prescribed and opioid-related overdose deaths. In response to the study, Dr. John Cullen, president of the American Academy of Family Physicians, said, “A limitation of the study, as acknowledged by the authors, is the many unknown variables that prevent drawing a direct causal link between pharmaceutical marketing and opioid-related deaths.” He added, “We’re very much aware of the critical and devastating impact of the opioid epidemic and work every day, with every patient interaction, to fight it. At the same time, we must protect the physician’s ability to provide adequate pain management.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 25881 - Posted: 01.19.2019

By Diana Kwon o For the longest time the cerebellum, a dense, fist-size formation located at the base of the brain, never got much respect from neuroscientists. For about two centuries the scientific community believed the cerebellum (Latin for “little brain”), which contains approximately half of the brain’s neurons, was dedicated solely to the control of movement. In recent decades, however, the tide has started to turn, as researchers have revealed details of the structure’s role in cognition, emotional processing and social behavior. The longstanding interest in the cerebellum can be seen in the work of French physiologist Marie Jean Pierre Flourens—(1794–1867). Flourens removed the cerebella of pigeons and found the birds became unbalanced, although they could still move. Based on these observations, he concluded the cerebellum was responsible for coordinating movements. “[This] set the dogma that the cerebellum was involved in motor coordination,” says Kamran Khodakhah, a neuroscientist at Albert Einstein College of Medicine, adding: “For many years, we ignored the signs that suggested it was involved in other things.” One of the strongest pieces of evidence for the cerebellum’s broader repertoire emerged around two decades ago, when Jeremy Schmahmann, a neurologist at Massachusetts General Hospital, described cerebellar cognitive affective syndrome after discovering behavioral changes such as impairments in abstract reasoning and regulating emotion in individuals whose cerebella had been damaged. Since then this line of study has expanded. There has been human neuroimaging work showing the cerebellum is involved in cognitive processing and emotional control—and investigations in animals have revealed, among other things, that the structure is important for the normal development of social and cognitive capacities. Researchers have also linked altered cerebellar function to addiction, autism and schizophrenia.

Keyword: Drug Abuse; Emotions
Link ID: 25880 - Posted: 01.19.2019

Rachel Zamzow Patterns of brain activity in people with autism are unusually consistent over seconds—and even years, two new studies suggest. One study shows that patterns of connectivity remain stable in autistic adolescents, whereas they tend to change and specialize in controls. The other study found that connections remain fixed longer in people with autism than in controls. Both focused on so-called “functional connectivity,” the extent to which the activity of pairs of brain areas is synchronized. Together, the studies may help untangle seemingly contradictory findings on connectivity in autism: reports of both underconnectivity and overconnectivity in the brain. “Maybe the primary abnormality isn’t just that things are too weakly or strongly connected, that it has more to do with the timing of brain connections,” says Jeff Anderson, professor of radiology at the University of Utah, who led the second study. The studies also highlight the importance of measuring brain activity over varying time periods and at different ages. Researchers who home in on a single age may overlook differences that appear over time, says Mirella Dapretto, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, and lead researcher on the adolescent study. “You miss some of the bigger picture.” Studying brain activity over time provides a rare window into the development of connectivity. © 1986 - 2019 The Scientist

Keyword: Autism; Development of the Brain
Link ID: 25879 - Posted: 01.19.2019

Laura Sanders Using laser light, ballooning tissue and innovative genetic tricks, scientists are starting to force brains to give up their secrets. By mixing and matching powerful advances in microscopy and cell biology, researchers have imaged intricate details of individual nerve cells in fruit flies and mice, and even controlled small groups of nerve cells in living mice. The techniques, published in two new studies, represent big steps forward for understanding how the brain operates, says molecular neuroscientist Hongkui Zeng of the Allen Institute for Brain Science in Seattle. “Without this kind of technology, we were only able to look at the soup level,” in which diverse nerve cells, or neurons, are grouped and analyzed together, she says. But the new studies show that nerve cells can be studied individually. That zoomed-in approach will begin to uncover the tremendous diversity that’s known to exist among cells, says Zeng, who was not involved in the research. “That is where the field is going. It’s very exciting to see that technologies are now enabling us to do that,” she says. These novel abilities came from multiple tools. At Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va., physicist Eric Betzig and his colleagues had developed a powerful microscope that can quickly peer deep into layers of brain tissue. Called a lattice light sheet microscope, the rig sweeps a thin sheet of laser light down through the brain, revealing cells’ structures. But like any microscope, it hits a wall when structures get really small, unable to resolve the most minute aspects of the scene. |© Society for Science & the Public 2000 - 2019.

Keyword: Brain imaging
Link ID: 25878 - Posted: 01.18.2019

By: Brenna Hassinger-Das, Ph.D., and Kathryn Hirsh-Pasek, Ph.D. In 1954, Walt Disney was the first to envision a new form of entertainment that melded traditional fun and education—a form that he dubbed “edutainment.” By the latter part of the 20th century, this form had morphed into educational toys and games, a multi-billion-dollar industry that is projected to capture a full 36 percent of the global toy market share by 2022. Nowhere is this trend more apparent than in the explosion of digital apps: of the 2.2 million apps available in the Apple Store, roughly 176,000—8.5 percent—are loosely designated as “ educational. ” Their growth continues, with annual increases of 10 percent expected through 2021. Whether called edutainment, educational toys, or the digital learning revolution, this trend shares the implicit philosophy that mixing fun and learning will offer a kind of “brain training” that will enhance children’s thinking and amplify their learning potential. But there are many questions before us. What do manufacturers and marketers mean when they designate a product “ educational? ” What relevant research in the science of learning has been done? Is there a standard definition of educational value that guides the field? Indeed, a framework we use highlights when toys might sculpt mental muscle and when products are likely to be total imposters. This framework helps us elucidate which educational and digital toys are likely to confer benefits for children.

Keyword: Learning & Memory; Development of the Brain
Link ID: 25877 - Posted: 01.18.2019

A new study in rodents has shown that the brain’s cerebellum—known to play a role in motor coordination—also helps control the brain’s reward circuitry. Researchers found a direct neural connection from the cerebellum to the ventral tegmental area (VTA) of the brain, which is an area long known to been involved in reward processing and encoding. These findings, published in Science, demonstrate for the first time that the brain’s cerebellum plays a role in controlling reward and social preference behavior, and sheds new light on the brain circuits critical to the affective and social dysfunction seen across multiple psychiatric disorders. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. “This type of research is fundamental to deepening our understanding of how brain circuit activity relates to mental illnesses,” said Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Findings like the ones described in this paper help us learn more about how the brain works, a key first step on the path towards developing new treatments.” The cerebellum plays a well-recognized role in the coordination and regulation of motor activity. However, research has also suggested that this brain area contributes to a host of non-motor functions. For example, abnormalities in the cerebellum have been linked to autism, schizophrenia, and substance use disorders, and brain activation in the cerebellum has been linked to motivation, social and emotional behaviors, and reward learning, each of which can be disrupted in psychiatric disorders.

Keyword: Drug Abuse; Emotions
Link ID: 25876 - Posted: 01.18.2019

By Benedict Carey Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone. Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient. The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science. Can cannabis use cause psychosis? Yes, but so can overuse of caffeine, nicotine, alcohol, stimulants and hallucinogens. Psychosis is a symptom: a temporary disorientation that resembles a waking dream, with odd, imagined sights and sounds, often accompanied by paranoia or an ominous sensation. The vast majority of people who have this kind of psychotic experience do not go on to develop a persistent condition such as schizophrenia, which is characterized by episodes of psychosis that recur for years, as well as cognitive problems and social withdrawal. © 2019 The New York Times Company

Keyword: Drug Abuse; Schizophrenia
Link ID: 25875 - Posted: 01.18.2019

By Elie Dolgin The compound eyes of the common fruit fly are normally brick red. But in neurologist Tom Lloyd's lab at Johns Hopkins University School of Medicine in Baltimore, Maryland, many of the fly eyes are pocked with white and black specks, a sign that neurons in each of their 800-odd eye units are shriveling away and dying. Those flies have the genetic equivalent of amyotrophic lateral sclerosis (ALS), the debilitating neurodegenerative disorder also known as Lou Gehrig's disease, and their eyes offer a window into the soul of the disease process. By measuring the extent of damage to each insect's eyes, researchers can quickly gauge whether a drug, genetic modification, or some other therapeutic intervention helps stop neuronal loss. Those eyes have also offered an answer to the central mystery of ALS: just what kills neurons—and, ultimately, the patient. The flies carry a mutation found in about 40% of ALS patients who have a family history of the disease, and in about 10% of sporadic cases. The mutation, in a gene called C9orf72, consists of hundreds or thousands of extra copies of a short DNA sequence, just six bases long. They lead to unusually large strands of RNA that glom onto hundreds of proteins in the cell nucleus, putting them out of action. Some of those RNA-ensnared proteins, Lloyd and his Hopkins colleague Jeffrey Rothstein hypothesized, might hold the key to ALS. © 2018 American Association for the Advancement of Science

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25874 - Posted: 01.17.2019

Using a novel patient-specific stem cell-based therapy, researchers at the National Eye Institute (NEI) prevented blindness in animal models of geographic atrophy, the advanced "dry" form of age-related macular degeneration (AMD), which is a leading cause of vision loss among people age 65 and older. The protocols established by the animal study, published January 16 in Science Translational Medicine (STM), set the stage for a first-in-human clinical trial testing the therapy in people with geographic atrophy, for which there is currently no treatment. "If the clinical trial moves forward, it would be the first ever to test a stem cell-based therapy derived from induced pluripotent stem cells (iPSC) for treating a disease," said Kapil Bharti, Ph.D., a Stadtman Investigator and head of the NEI Unit on Ocular and Stem Cell Translational Research. Bharti was the lead investigator for the animal-model study published in STM. The NEI is part of the National Institutes of Health. The therapy involves taking a patient’s blood cells and, in a lab, converting them into iPS cells, which can become any type of cell in the body. The iPS cells are programmed to become retinal pigment epithelial cells, the type of cell that dies early in the geographic atrophy stage of macular degeneration. RPE cells nurture photoreceptors, the light-sensing cells in the retina. In geographic atrophy, once RPE cells die, photoreceptors eventually also die, resulting in blindness. The therapy is an attempt to shore up the health of remaining photoreceptors by replacing dying RPE with iPSC-derived RPE.

Keyword: Vision
Link ID: 25873 - Posted: 01.17.2019

Nicola Davis Moving more might help to keep people’s brains sharp as they age – even in the face of dementia, researchers have said. Scientists have found older adults fared better when it came to cognitive tasks if they clocked up higher levels of daily activity on a wrist-based tracker – something the researchers said picked up everything from exercising to mundane tasks like chopping onions. What’s more, the benefits of movement remained even when the team took into account the level of tell-tale signs of Alzheimer’s and other dementia-related diseases in the brain. Co-author of the Rush University study, Dr Aron Buchman, said the results showed that “even though we don’t have a treatment for Alzheimer’s disease pathology, and we know people are accumulating it, you can mitigate the deleterious effects … by having more activity.” But it’s not only moving more which is linked to better scores for traits like thinking, comprehension and and memory: the team found better motor abilities, as measured through tasks like the strength in gripping items or speed of turning on the spot, also seemed to offer protection when it comes to cognitive prowess. The team say previous work has shown that moving more is linked to a lower risk of dementia, and slows the decline in thinking and memory skills in older adults as they age – but the latest research goes further. © 2019 Guardian News and Media Limited

Keyword: Alzheimers
Link ID: 25872 - Posted: 01.17.2019