Chapter 16. None
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By Hanae Armitage CHICAGO, ILLINOIS—Huntingtons disease, a neurological condition caused by brain-destroying mutant proteins, starts with mood swings and twitching and ends in dementia and death. The condition, which afflicts about 30,000 Americans, has no cure. But now, a new gene-editing method that many believe will lead to a Nobel Prize has been shown to effectively halt production of the defective proteins in mice, leading to hope that a potent therapy for Huntingtons is on the distant horizon. That new method is CRISPR, which uses RNA-guided enzymes to snip out or add segments of DNA to a cell. In the first time it has been applied to Huntingtons disease, CRISPR’s results are “remarkably encouraging,” says neuroscientist Nicole Déglon of the University of Lausanne in Switzerland, who led the mouse study, results of which she and her co-researcher Nicolas Merienne shared yesterday at the Society for Neuroscience Conference in Chicago, Illinois. As neurological diseases go, Huntingtons is an ideal candidate for CRISPR therapy, because the disease is determined by a single gene, Déglon notes. A mutation in the gene, which codes for a normally helpful brain protein called huntingtin, consists of different numbers of “tandem repeats,” repeating segments of DNA that cause the protein to fold into a shape that is toxic to the brain. Déglon and her team wondered whether CRISPR could halt production of this dangerous molecule. Using a virus as a delivery vehicle, the researchers infected two separate groups of healthy adult mice with a mutant huntingtin gene, but only one group received the therapy: a CRISPR “cassette,” which includes DNA for the gene-editing enzyme Cas9 and the RNA to target the huntingtin gene. © 2015 American Association for the Advancement of Science
Link ID: 21538 - Posted: 10.21.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
Link ID: 21537 - Posted: 10.21.2015
By WILLIAM GRIMES The first show at the Museum of Food and Drink’s new space in Brooklyn is “Flavor: Making It and Faking It,” and it wastes no time in getting to the point. “What makes your favorite food so delicious?” the text on a large free-standing panel near the entrance asks. The one-word answer: “Chemicals.” The word is deflating. It’s a little like being told that the human soul has a specific atomic weight. Chemicals? Yuck. But maybe not. Flavors come in two varieties, natural and artificial, but what do the words really mean? This is the looming question in an exhibition about food and culture that opens next Wednesday, in a museum that until now has been a free-floating idea rather than a building with an address. The show follows the history of lab-created flavors from the middle of the 19th century, when German scientists created artificial vanilla, to the present day, when the culinary spin doctors known as flavorists tweak and blend the myriad tastes found in virtually every food product on supermarket shelves. Flavor is a complex, beguiling subject. At one of several “smell machines” throughout the exhibition, where specific aromas are emitted through silver hoses at the push of a button, visitors learn that coffee gets a little lift — the je ne sais quoi that makes it irresistible in the morning — from a sulfur compound also found in skunk spray. Tiny edible pellets distributed from gumball machines send the message in tactile form. This is an exhibition that is not just hands-on, but tongue-on and nostrils-on. © 2015 The New York Times Company
Keyword: Chemical Senses (Smell & Taste)
Link ID: 21536 - Posted: 10.21.2015
Mark Easton Home editor An attempt by UN officials to get countries to decriminalise the possession and use of all drugs has been foiled, the BBC can reveal. A paper from the UN Office on Drugs and Crime (UNODC) has been withdrawn after pressure from at least one country. The document, which was leaked, recommends that UN members consider "decriminalising drug and possession for personal consumption". It argued "arrest and incarceration are disproportionate measures". The document was drawn up by Dr Monica Beg, chief of the HIV/AIDs section of the UNODC in Vienna. It was prepared for an international harm reduction conference currently being held in Kuala Lumpur. The UNODC oversees international drugs conventions and offers guidance on compliance. Sources within the UNODC have told the BBC the document was never sanctioned by the organisation as policy. One senior figure within the agency described Dr Beg as "a middle-ranking official" who was offering a professional viewpoint. The document, on headed agency notepaper, claims it "clarifies the position of UNODC to inform country responses to promote a health and human-rights approach to drug policy". "Treating drug use for non-medical purposes and possession for personal consumption as criminal offences has contributed to public health problems and induced negative consequences for safety, security, and human rights," the document states. © 2015 BBC.
Keyword: Drug Abuse
Link ID: 21535 - Posted: 10.21.2015
By BENEDICT CAREY More than two million people in the United States have a diagnosis of schizophrenia, and the treatment for most of them mainly involves strong doses of antipsychotic drugs that blunt hallucinations and delusions but can come with unbearable side effects, like severe weight gain or debilitating tremors. Stories from Our Advertisers Now, results of a landmark government-funded study call that approach into question. The findings, from by far the most rigorous trial to date conducted in the United States, concluded that schizophrenia patients who received smaller doses of antipsychotic medication and a bigger emphasis on one-on-one talk therapy and family support made greater strides in recovery over the first two years of treatment than patients who got the usual drug-focused care. The report, to be published on Tuesday in The American Journal of Psychiatry and funded by the National Institute of Mental Health, comes as Congress debates mental health reform and as interest in the effectiveness of treatments grows amid a debate over the possible role of mental illness in mass shootings. Its findings have already trickled out to government agencies: On Friday, the Centers for Medicare & Medicaid Services published in its influential guidelines a strong endorsement of the combined-therapy approach. Mental health reform bills now being circulated in Congress “mention the study by name,” said Dr. Robert K. Heinssen, the director of services and intervention research at the centers, who oversaw the research. In 2014, Congress awarded $25 million in block grants to the states to be set aside for early-intervention mental health programs. So far, 32 states have begun using those grants to fund combined-treatment services, Dr. Heinssen said. © 2015 The New York Times Company
Link ID: 21532 - Posted: 10.20.2015
Susan Gaidos CHICAGO — Teens like high-tech gadgets so much that they often use them all at once. While doing homework or playing video games, teens may listen to music or watch TV, all the while texting their friends. Some of these multitaskers think they are boosting their ability to attend to multiple activities, but in fact are more likely impairing their ability to focus, psychologist Mona Moisala of the University of Helsinki, reported October 18 at the annual meeting of the Society for Neuroscience. Moisala and colleagues tested 149 adolescents and young adults, ages 13 to 24, who regularly juggle multiple forms of media or play video games daily. Each participant had to focus attention on sentences (some logical, some illogical) under three conditions: without any distractions, while listening to distracting sounds, and while both listening to a sentence and reading another sentence. Using functional MRI to track brain activity, the researchers found that daily gaming had no effect on participants’ ability to focus. Those who juggle multiple forms of electronic media, however, had more trouble paying attention. Multitaskers performed lower overall, even when they weren’t being distracted. Brain images showed that the multitaskers also showed a higher level of activity in the right prefrontal cortex, an area of the brain implicated in problem solving and in processing complex thoughts and emotions. “Participants with the highest reported frequency of multimedia use showed the highest levels of brain activation in this area,” Moisala said. “In addition, these adolescents did worse on the task.” © Society for Science & the Public 2000 - 2015
Link ID: 21529 - Posted: 10.20.2015
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.
Link ID: 21528 - Posted: 10.20.2015
By Hanae Armitage About 70 million people worldwide stutter when they speak, and it turns out humans aren’t the only ones susceptible to verbal hiccups. Scientists at this year’s Society for Neuroscience Conference in Chicago, Illinois, show that mice, too, can stumble in their vocalizations. In humans, stuttering has long been linked to a mutation in the “housekeeping” gene Gnptab, which maintains basic levels of cellular function. To cement this curious genetic link, researchers decided to induce the Gnptab “stutter mutation” in mice. They suspected the change would trigger a mouse version of stammering. But deciphering stuttered squeaks is no easy task, so researchers set up a computerized model to register stutters through a statistical analysis of vocalizations. After applying the model to human speech, researchers boiled the verbal impediment down to two basic characteristics—fewer vocalizations in a given period of time and longer gaps in between each vocalization. For example, in 1 minute, stuttering humans made just 90 vocalizations compared with 125 for non-stutterers. Using these parameters to evaluate mouse vocalizations, researchers were able to identify stuttering mice over a 3.5-minute period. As expected, the mice carrying the mutated gene had far fewer vocalizations, with longer gaps between “speech” compared with their unmodified littermates—Gnptab mutant mice had about 80 vocalizations compared with 190 in the nonmutant mice. The findings not only supply evidence for Gnptab’s role in stuttering, but they also show that its function remains relatively consistent across multiple species. Scientists say the genetic parallel could help reveal the neural mechanisms behind stuttering, be it squeaking or speaking. © 2015 American Association for the Advancement of Science.
What if belief in God and prejudice against immigrants could be altered by magnetic energy? That’s the question researchers sought to explore in a study published Wednesday in the journal Social Cognitive and Affective Neuroscience. The “magnetic energy” comes in the form of transcranial magnetic stimulation (TMS), a noninvasive procedure that uses a metal coil to send pulses to the brain. By activating certain regions of the brain, doctors have used it for things like measuring the damage of a stroke or—increasingly—treating depression. These researchers sought to do the opposite—to temporarily disable one part of the brain (the part that responds to threats) and measure its effect on beliefs and prejudices connected to them. To do this, researchers from Britain’s University of York teamed up with UCLA to find 39 politically moderate college undergraduates who were divided into two groups. The first was given a “love-level sham” dose of TMS that had no effect on their brains. The second got a hit of magnetic energy strong enough to temporarily shut down their posterior medial frontal cortex. The pMFC, as this area near the forehead is known, is the part of the brain that identifies problems and—after measuring the level of threat—generates a response to them. Testing the effect of shutting down the part of the brain that forms judgments based on threats required first presenting threats. After receiving their respective doses of TMS, participants were asked to respond to questions about their own death. Previous studies have shown the threat of death is capable of directly affecting a person’s belief in religion. Therefore, shutting down the part of the brain that registers this threat—they theorized—would reduce the need to believe in God.
Link ID: 21525 - Posted: 10.17.2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored. The results, published in the journals Nature and NatureNeuroscience, provide a possible strategy for treating the two diseases. “This research shines a spotlight on the role of nuclear transport in the health of neurons,” said Amelie Gubitz, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “The results provide new insights into how this mutation derails an essential process in neurons and opens new avenues for therapy development.” Both ALS and FTD are caused by the death of specific neurons. In ALS, this leads to movement difficulties and eventually paralysis, while in FTD, patients experience problems with language and decision making. Past research has connected a specific mutation in the C9orf72 gene to 40 percent of inherited ALS cases and 25 percent of inherited FTD cases, as well as nearly 10 percent of non-inherited cases of each disorder. The recent experiments, conducted in yeast, fruit flies, and neurons from patients, found that the mutation prevents proteins and genetic material called RNA from moving between the nucleus and the cytoplasm that surrounds it. “At the end of the day, this culminates in a defect in the flow of genetic information, which leads to problems expressing genes in the right place at the right time,” said J. Paul Taylor, M.D., Ph.D., a researcher at St. Jude’s Children’s Research Hospital in Memphis, Tennessee, and the senior author of one of the papers.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21524 - Posted: 10.17.2015
By Anahad O'Connor For years, public health authorities have warned that smartphones, television screens and the hectic pace of modern life are disrupting natural sleep patterns, fueling an epidemic of sleep deprivation. By some estimates, Americans sleep two to three hours fewer today than they did before the industrial revolution. But now a new study is challenging that notion. It found that Americans on average sleep as much as people in three different hunter-gatherer societies where there is no electricity and the lifestyles have remained largely the same for thousands of years. If anything, the hunter-gatherer communities included in the new study — the Hadza and San tribes in Africa, and the Tsimané people in South America — tend to sleep even less than many Americans. The findings are striking because health authorities have long suggested that poor sleep is rampant in America, and that getting a minimum of seven hours on a consistent basis is a necessity for good health. Many studies suggest that lack of sleep, independent of other factors like physical activity, is associated with obesity and chronic disease. Yet the hunter-gatherers included in the new study, which was published in Current Biology, were relatively fit and healthy despite regularly sleeping amounts that are near the low end of those in industrialized societies. Previous research shows that their daily energy expenditure is about the same as most Americans, suggesting physical activity is not the reason for their relative good health. The prevailing notion in sleep medicine is that humans evolved to go to bed when the sun goes down, and that by and large we stay up much later than we should because we are flooded with artificial light, said Jerome Siegel, the lead author of the new study and a professor of psychiatry at the Semel Institute of Neuroscience and Human Behavior at U.C.L.A. © 2015 The New York Times Company
Link ID: 21523 - Posted: 10.17.2015
by Ben Cipollini Thanks to Ms. Amazing, it’s now cliche to say, but hey… I really love SfN. For the uninitiated SfN is a thirty thousand person international conference for neuroscience–a conference so large, only a few cities in the US can handle it. Yes, that’s a giant C-SPAN2 bus that's dwarfed by this small section of the “Great Room”. For many, SfN evokes fear and dread; it’s truly overwhelming in its size, breadth, and depth. For me, it was love at first “OM*G!!!”. Don’t believe me, scientists? Let’s review the data: I loathe running, but I actually do it at SfN. One needs wheels to get from talks to posters to talks again. We filled the New Orleans convention center in 2012; it’s so long you you can actually get directions from one end of it to the other on Google Maps. Yes, that map does say “1.0 kilometers”. I hate crowds, but I will fight through the poster session crowds like a salmon heading upstream to spawn, just to get to one more poster before the end of the session. SfN may have more human traffic jams than China has vehicle jams during Golden week… but that won’t stop me from finding out how callosal connections have properties similar to those of long-range lateral connections, or to understand how hemispherectomy affects functional organization. You’d better too; you never know when one of your research heroes might be presenting the poster, or you’ll find yourself standing in front of a poster that winds up in Science just a few months later.
Link ID: 21522 - Posted: 10.17.2015
Chris Samoray People in the postindustrial world don’t always get a sound night sleep. But they appear to spend a similar amount of time sleeping as do people in hunter-gatherer communities in Africa and South America, a new study finds. “It’s absolutely clear that they don’t sleep more than we do,” says Jerome Siegel, a UCLA sleep scientist. In fact, on average, hunter-gatherers may sleep a little less. Recommended nightly sleep for adults is typically seven to nine hours; a 2013 Gallup poll showed that most Americans get around 6.8 hours. On most nights, members of three hunter-gatherer groups — the Hadza of Tanzania, the Ju/’hoansi San of Namibia and the Tsimane of Bolivia — sleep 5.7 to 7.1 hours, Siegel and colleagues report online October 15 in Current Biology. That’s on the lower end of the sleep spectrum in postindustrial societies, the researchers say. Evidence from the new study also suggests that these groups experience less insomnia than sleepers in postindustrial societies. (The three hunter-gatherer languages even lack a word for insomnia.) Hunter-gatherer sleep patterns are closely tied to temperature, a new study shows. Among the Hadza of Tanzania, for instance, people fell asleep about three hours after sunset, on average, as ambient temperatures decreased. People then woke up about an hour before sunrise, when temperatures reached their lowest point. © Society for Science & the Public 2000 - 2015.
Link ID: 21520 - Posted: 10.16.2015
By Robert F. Service Prosthetic limbs may work wonders for restoring lost function in some amputees, but one thing they can’t do is restore an accurate sense of touch. Now, researchers report that one day in the not too distant future, those artificial arms and legs may have a sense of touch closely resembling the real thing. Using a two-ply of flexible, thin plastic, scientists have created novel electronic sensors that send signals to the brain tissue of mice that closely mimic the nerve messages of touch sensors in human skin. Multiple research teams have long worked on restoring touch to people with prosthetic limbs. 2 years ago, for example, a group at Case Western Reserve University in Cleveland, Ohio, reported giving people with prosthetic hands a sense of touch by wiring pressure sensors on the hands to peripheral nerves in their arms. Yet although these advances have restored a rudimentary sense of touch, the sensors and signals are very different from those sent by mechanoreceptors, natural touch sensors in the skin. For starters, natural mechanoreceptors put out what amounts to a digital signal. When they sense pressure, they fire a stream of nerve impulses; the more pressure, the higher the frequency of pulses. But previous tactile sensors have been analogue devices, where more pressure produces a stronger electrical signal, rather than a more frequent stream of pulses. The electrical signals must then be sent to another processing chip that converts the strength of the signals to a digital stream of pulses that is only then sent on to peripheral nerves or brain tissue. © 2015 American Association for the Advancement of Science.
Using a sensitive new technology called single-cell RNA-seq on cells from mice, scientists have created the first high-resolution gene expression map of the newborn mouse inner ear. The findings provide new insight into how epithelial cells in the inner ear develop and differentiate into specialized cells that serve critical functions for hearing and maintaining balance. Understanding how these important cells form may provide a foundation for the potential development of cell-based therapies for treating hearing loss and balance disorders. The research was conducted by scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health. In a companion study led by NIDCD-supported scientists at the University of Maryland School of Medicine and scientists at the Sackler School of Medicine at Tel Aviv University, researchers used a similar technique to identify a family of proteins critical for the development of inner ear cells. Both studies were published online on October 15 in the journal Nature Communications. “Age-related hearing loss occurs gradually in most of us as we grow older. It is one of the most common conditions among older adults, affecting half of people over age 75,” said James F. Battey, Jr., M.D., Ph.D., director of the NIDCD. “These new findings may lead to new regenerative treatments for this critical public health issue.” Specialized sensory epithelial cells in the inner ear include hair cells and supporting cells, which provide the hair cells with crucial structural and functional support. Hair cells and supporting cells located in the cochlea — the snail-shaped structure in the inner ear — work together to detect sound, thus enabling us to hear. In contrast, hair cells and supporting cells in the utricle, a fluid-filled pouch near the cochlea, play a critical role in helping us maintain our balance.
by Helen Thompson It's no secret that some plants lace their nectar with caffeine in an effort to attract more pollinators, and that buzz sticks around in a bee's memory. These caffeinated flowers lure naive honeybees to return over and over again — and bring their friends, researchers report October 15 in Current Biology. When feeding off caffeinated nectar (versus noncaffeinated nectar), honeybees increased their foraging activity and performed four times as many waggle dances to alert other workers to food sources. Though bees might be more persistent foragers while under the influence of caffeine, they focused mainly on caffeinated sources instead casting a broad search. Plants may also substitute caffeine for sugar, the researchers note, duping bees into gathering nectar that's less valuable for honey production. © Society for Science & the Public 2000 - 2015.
By Nicholas Bakalar Physical therapy may provide little relief for recent-onset low back pain, a small randomized trial has found. The study, published in JAMA, included 207 men and women, average age 37, with a score of 20 or higher on a widely used 100-point scale that quantifies disability from low back pain. The study included people with recent-onset pain who were assigned to one of two groups. The first received four sessions of exercise and manipulation under the guidance of a trained physical therapist. Those in the other group were told that low back pain usually gets better, and were advised to be as active as possible. There were no significant differences at any time in pain intensity, quality of life or the number of visits to health care providers. Compared with the usual care group, the physical therapy group did show significant improvement on the disability scale after three months. But after one year, there was no difference between the two groups in this measure either. “Most treatments that are effective have only modest effects,” said the lead author, Julie M. Fritz, a professor in the department of physical therapy at the University of Utah. “The pattern of low back pain is one of recurrence and remission, and changing that pattern is a real challenge. There are no magic answers.” © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21513 - Posted: 10.15.2015
By AUSTIN RAMZY HONG KONG — Australian officials have responded to criticism from animal rights activists and celebrities, including the former actress Brigitte Bardot and the singer Morrissey, that a government plan to protect threatened species by killing millions of feral cats is unnecessarily cruel. Gregory Andrews, Australia’s threatened species commissioner, has written open letters to Ms. Bardot and Morrissey saying that feral cats prey on more than 100 of the country’s threatened species and that they were a “major contributor” to the extinction of at least 27 mammal species in the country over the past 200 years. He called some of the extinct species, such as the lesser bilby, desert bandicoot, crescent nailtail wallaby and big-eared hopping mouse, “delightful creatures, rich in importance in Australian indigenous culture, and formerly playing important roles in the ecology of our country. We don’t want to lose any more species like these.” The Australian Department of the Environment says that feral cats are the biggest threat to the country’s mammals, ahead of foxes and habitat loss. The government plan would use poison and traps to kill the cats. In announcing the plan in July, Greg Hunt, the environment minister, said that he wanted two million feral cats culled by 2020. Australia has an estimated 20 million feral cats, which are an invasive species brought by European settlers. Calls to exterminate the cats have been floated before, including one in the 1990s that called for killing all feral cats by 2020. © 2015 The New York Times Company
Keyword: Animal Rights
Link ID: 21512 - Posted: 10.15.2015
by Bethany Brookshire It’s happened to all of us at one time or another: You’re walking through a crowd, and suddenly a face seems incredibly familiar — so much so that you do a double-take. Who is that? How do you know them? You have no idea, but something about their face nags at you. You know you’ve seen it before. The reason you know that face is in part because of your perirhinal cortex. This is an area of the brain that helps us to determine familiarity, or whether we have seen an object before. A new study of brain cells in this area finds that firing these neurons at one frequency makes the brain treat novel images as old hat. But firing these same neurons at another frequency can make the old new again. “Novelty and familiarity are both really important,” says study coauthor Rebecca Burwell, a neuroscientist at Brown University in Providence, R.I. “They are important for learning and memory and decision making.” Finding a cache of food and knowing it is new could be useful for an animal’s future. So is recognizing a familiar place where the pickings were good in the past. But knowing that something is familiar is not quite the same thing as knowing what that thing is. “You’re in a crowd and you see a familiar face, and there’s a feeling,” Burwell explains. “You can’t identify them, you don’t know where you met them, but there’s a sense of familiarity.” It’s different from recalling where you met the person, or even who the person is. This is a sense at the base of memory. And while scientists knew the perirhinal cortex was involved in this sense of familiarity, how that feeling of new or old was coded in the brain wasn’t fully understood. © Society for Science & the Public 2000 - 2015
Link ID: 21511 - Posted: 10.14.2015
Gene therapy preserved vision in a study involving dogs with naturally occurring, late-stage retinitis pigmentosa, according to research funded by the National Eye Institute (NEI), part of the National Institutes of Health. The findings contribute to the groundwork needed to move gene therapy forward into clinical trials for people with the blinding eye disorder, for which there is currently no cure. Scientists from the University of Pennsylvania and the University of Florida, Gainesville also determined for the first time that gene therapy may be of potential benefit even after there has been significant loss of cells in the eye. Up to this point, animal studies had shown benefits from gene therapy only when it was used in the earliest stages of the disease. “The study shows that a corrective gene can stop the loss of photoreceptors in the retina, and provides good proof of concept for gene therapy at the intermediate stage of the disease, thus widening the therapeutic window,” said Neeraj Agarwal, Ph.D., a program director at NEI. Retinitis pigmentosa is the most common inherited disease that causes degeneration of the retina, the light-sensitive tissue lining the back of the eye. Roughly 1 in 4,000 people are affected and about 10 to 20 percent have a particularly severe form called X-linked retinitis pigmentosa, which predominately affects males, causing night blindness by age 10 and progressive loss of the visual field by age 45. About 70 percent of people with the X-linked form carry mutations that cause loss of function of the retinitis pigmentosa GTPase Regulator (RPGR) gene, which encodes a protein important for maintaining the health of photoreceptors.
Link ID: 21510 - Posted: 10.14.2015