Chapter 13. Memory, Learning, and Development
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By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © Copyright Reed Business Information Ltd.
Link ID: 22588 - Posted: 08.23.2016
By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company
By Virginia Morell Scientists have long worried whether animals can respond to the planet’s changing climate. Now, a new study reports that at least one species of songbird—and likely many more—already knows how to prep its chicks for a warming world. They do so by emitting special calls to the embryos inside their eggs, which can hear and learn external sounds. This is the first time scientists have found animals using sound to affect the growth, development, behavior, and reproductive success of their offspring, and adds to a growing body of research revealing that birds can “doctor” their eggs. “The study is novel, surprising, and fascinating, and is sure to lead to much more work on parent-embryo communication,” says Robert Magrath, a behavioral ecologist at the Australian National University in Canberra who was not involved in the study. The idea that the zebra finch (Taeniopygia guttata) parents were “talking to their eggs” occurred to Mylene Mariette, a behavioral ecologist at Deakin University in Waurn Ponds, Australia, while recording the birds’ sounds at an outdoor aviary. She noticed that sometimes when a parent was alone, it would make a rapid, high-pitched series of calls while sitting on the eggs. Mariette and her co-author, Katherine Buchanan, recorded the incubation calls of 61 female and 61 male finches inside the aviary. They found that parents of both sexes uttered these calls only during the end of the incubation period and when the maximum daily temperature rose above 26°C (78.8°F). © 2016 American Association for the Advancement of Scienc
By Emily Underwood In 2010, neurobiologist Beth Stevens had completed a remarkable rise from laboratory technician to star researcher. Then 40, she was in her second year as a principal investigator at Boston Children’s Hospital with a joint faculty position at Harvard Medical School. She had a sleek, newly built lab and a team of eager postdoctoral investigators. Her credentials were impeccable, with high-profile collaborators and her name on an impressive number of papers in well-respected journals. But like many young researchers, Stevens feared she was on the brink of scientific failure. Rather than choosing a small, manageable project, she had set her sights on tackling an ambitious, unifying hypothesis linking the brain and the immune system to explain both normal brain development and disease. Although the preliminary data she’d gathered as a postdoc at Stanford University in Palo Alto, California, were promising, their implications were still murky. “I thought, ‘What if my model is just a model, and I let all these people down?’” she says. Stevens, along with her mentor at Stanford, Ben Barres, had proposed that brain cells called microglia prune neuronal connections during embryonic and later development in response to a signal from a branch of the immune system known as the classical complement pathway. If a glitch in the complement system causes microglia to prune too many or too few connections, called synapses, they’d hypothesized, it could lead to both developmental and degenerative disorders. © 2016 American Association for the Advancement of Science.
Meghan Rosen Zika may harm grown-up brains. The virus, which can cause brain damage in infants infected in the womb, kills stem cells and stunts their numbers in the brains of adult mice, researchers report August 18 in Cell Stem Cell. Though scientists have considered Zika primarily a threat to unborn babies, the new findings suggest that the virus may cause unknown — and potentially long-term — damage to adults as well. In adults, Zika has been linked to Guillain-Barré syndrome, a rare neurological disorder (SN: 4/2/16, p. 29). But for most people, infection is typically mild: a headache, fever and rash lasting up to a week, or no symptoms at all. In pregnant women, though, the virus can lodge in the brain of a fetus and kill off newly developing cells (SN: 4/13/16). If Zika targets newborn brain cells, adults may be at risk, too, reasoned neuroscientist Joseph Gleeson of Rockefeller University in New York City and colleagues. Parts of the forebrain and the hippocampus, which plays a crucial role in learning and memory, continue to generate nerve cells in adult brains. In mice infected with Zika, the virus hit these brain regions hard. Nerve cells died and the regions generated one-fifth to one-half as many new cells compared with those of uninfected mice. The results might not translate to humans; the mice were genetically engineered to have weak immune systems, making them susceptible to Zika. But Zika could potentially harm immunocompromised people and perhaps even healthy people in a similar way, the authors write. © Society for Science & the Public 2000 - 2016.
Keyword: Development of the Brain
Link ID: 22575 - Posted: 08.20.2016
By Nicholas Bakalar Taking antipsychotic medicines during pregnancy does not increase the risk for birth defects, a large new study has found. Antipsychotics are used to treat schizophrenia, bipolar disorder, depression and other psychiatric disorders. Previous studies of their use during pregnancy have been small and have had mixed results. This study, in JAMA Psychiatry, reviewed records of 1,341,715 pregnant women, of whom 9,258 filled prescriptions for the newer atypical antipsychotics like quetiapine (Seroquel) or aripiprazole (Abilify), and 733 for older typical antipsychotics such as haloperidol (Haldol). All prescriptions were filled in the first trimester of pregnancy. After controlling for race, number of pregnancies, smoking, alcohol use, psychiatric conditions, additional medications and other variables, there was no difference in the risk for birth defects between those who took the drugs and those who did not. One possible exception was a marginal increase in risk with one drug, risperidone (Risperdal), which the authors said will require further study. “These findings suggest that the use of antipsychotics during the first trimester does not seem to increase congenital malformation,” or birth defects, said the lead author, Krista F. Huybrechts, an assistant professor of medicine at Harvard. But, she added, “we only looked at congenital malformation, not other possible negative outcomes for women and their children.” © 2016 The New York Times Company
By Jessica Hamzelou Feel like you’ve read this before? Most of us have experienced the eerie familiarity of déjà vu, and now the first brain scans of this phenomenon have revealed why – it’s a sign of our brain checking its memory. Déjà vu was thought to be caused by the brain making false memories, but research by Akira O’Connor at the University of St Andrews, UK, and his team now suggests this is wrong. Exactly how déjà vu works has long been a mystery, partly because its fleeting and unpredictable nature makes it difficult to study. To get around this, O’Connor and his colleagues developed a way to trigger the sensation of déjà vu in the lab. The team’s technique uses a standard method to trigger false memories. It involves telling a person a list of related words – such as bed, pillow, night, dream – but not the key word linking them together, in this case, sleep. When the person is later quizzed on the words they’ve heard, they tend to believe they have also heard “sleep” – a false memory. To create the feeling of déjà vu, O’ Connor’s team first asked people if they had heard any words beginning with the letter “s”. The volunteers replied that they hadn’t. This meant that when they were later asked if they had heard the word sleep, they were able to remember that they couldn’t have, but at the same time, the word felt familiar. “They report having this strange experience of déjà vu,” says O’Connor. © Copyright Reed Business Information Ltd.
By Roni Caryn Rabin Dementia is a general term for a set of symptoms that includes severe memory loss, a significant decline in reasoning and severely impaired communication skills; it most commonly strikes elderly people and used to be referred to as “senility.” Alzheimer’s disease is a specific illness that is the most common cause of dementia. Though many diseases can cause dementia, Alzheimer’s accounts for 60 percent to 80 percent of dementia cases, “which is why you’ll often hear the terms used interchangeably,” said Heather Snyder, the senior director of medical and scientific operations for the Alzheimer’s Association. She said the question comes up frequently because patients may receive an initial diagnosis of dementia followed by an evaluation that yields the more specific diagnosis of Alzheimer’s disease, and they may be confused. The second most common form of dementia is vascular dementia, which is caused by a stroke or poor blood flow to the brain. Other diseases that can lead to dementia include Huntington’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Some patients may have more than one form of dementia. Dementia is caused by damage to brain cells. In the case of Alzheimer’s disease, that damage is characterized by telltale protein fragments or plaques that accumulate in the space between nerve cells and twisted tangles of another protein that build up inside cells. In Alzheimer’s disease, dementia gets progressively worse to the point where patients cannot carry out daily activities and cannot speak, respond to their environment, swallow or walk. Although some treatments may temporarily ease symptoms, the downward progression of disease continues and it is not curable. © 2016 The New York Times Company
Link ID: 22559 - Posted: 08.16.2016
By Anna Azvolinsky Sets of neurons in the brain that behave together—firing synchronously in response to sensory or motor stimuli—are thought to be functionally and physiologically connected. These naturally occurring ensembles of neurons are one of the ways memories may be programmed in the brain. Now, in a paper published today (August 11) in Science, researchers at Columbia University and their colleagues show that it is possible to stimulate visual cortex neurons in living, awake mice and induce a new ensemble of neurons that behave as a group and maintain their concerted firing for several days. “This work takes the concept of correlated [neuronal] firing patterns in a new and important causal direction,” David Kleinfeld, a neurophysicist at the University of California, San Diego, who was not involved in the work told The Scientist. “In a sense, [the researchers] created a memory for a visual feature that does not exist in the physical world as a proof of principal of how real visual memories are formed.” “Researchers have previously related optogenetic stimulation to behavior [in animals], but this study breaks new ground by investigating the dynamics of neural activity in relation to the ensemble to which these neurons belong,” said Sebastian Seung, a computational neuroscientist at the Princeton Neuroscience Institute in New Jersey who also was not involved in the study. Columbia’s Rafael Yuste and colleagues stimulated randomly selected sets of individual neurons in the visual cortices of living mice using two-photon stimulation while the animals ran on a treadmill. © 1986-2016 The Scientist
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Ed Yong At the age of seven, Henry Gustav Molaison was involved in an accident that left him with severe epilepsy. Twenty years later, a surgeon named William Scoville tried to cure him by removing parts of his brain. It worked, but the procedure left Molaison unable to make new long-term memories. Everyone he met, every conversation he had, everything that happened to him would just evaporate from his mind. These problems revolutionized our understanding of how memory works, and transformed Molaison into “Patient H.M.”—arguably the most famous and studied patient in the history of neuroscience. That’s the familiar version of the story, but the one presented in Luke Dittrich’s new book Patient H.M.: A Story of Memory, Madness, and Family Secrets is deeper and darker. As revealed through Dittrich’s extensive reporting and poetic prose, Molaison’s tale is one of ethical dilemmas that not only influenced his famous surgery but persisted well beyond his death in 2008. It’s a story about more than just the life of one man or the root of memory; it’s also about how far people are willing to go for scientific advancement, and the human cost of that progress. And Dittrich is uniquely placed to consider these issues. Scoville was his grandfather. Suzanne Corkin, the scientist who worked with Molaison most extensively after his surgery, was an old friend of his mother’s. I spoke to him about the book and the challenges of reporting a story that he was so deeply entwined in. Most of this interview was conducted on July 19th. Following a New York Times excerpt published on August 7th, and the book’s release two weeks later, many neuroscientists have expressed “outrage” at Dittrich’s portrayal of Corkin. The controversy culminated in a statement from MIT, where Corkin was based, rebutting three allegations in the book. Dittrich has himself responded to the rebuttals, and at the end of this interview, I talk to him about the debate. © 2016 by The Atlantic Monthly Group.
Keyword: Learning & Memory
Link ID: 22552 - Posted: 08.13.2016
Like many students of neuroscience, I first learned of patient HM in a college lecture. His case was so strange yet so illuminating, and I was immediately transfixed. HM was unable to form new memories, my professor explained, because a surgeon had removed a specific part of his brain. The surgery froze him in time. HM—or Henry Molaison, as his name was revealed to be after his death in 2008—might be the most famous patient in the history of brain research. He is now the subject of the new book, Patient HM: A Story of Memory, Madness, and Family Secrets. An excerpt from the book in the New York Times Magazine, which details MIT neuroscientist Sue Corkin’s custody fight over HM’s brain after his death, has since sparked a backlash. Should you wish to go down that particular rabbit hole, you can read MIT’s response, the book author’s response to the response, and summaries of the back and forth. Why HM’s brain was worth fighting over should be obvious; he was probably the most studied individual in neuroscience while alive. But in the seven years since scientists sectioned HM’s brain into 2,401 slices, it has yielded surprisingly little research. Only two papers examining his brain have come out, and so far, physical examinations have led to no major insights. HM’s scientific potential remains unfulfilled—thanks to delays from the custody fight and the limitations of current neuroscience itself. Corkin, who made her career studying HM, confronted her complicated emotions about his death in her own 2013 book. She describes being “ecstatic to see his brain removed expertly from his skull.” Corkin passed away earlier this year.
Keyword: Learning & Memory
Link ID: 22551 - Posted: 08.13.2016
Cassie Martin Understanding sea anemones’ exceptional healing abilities may help scientists figure out how to restore hearing. Proteins that the marine invertebrates use to repair damaged cells can also repair mice’s sound-sensing cells, a new study shows. The findings provide insights into the mechanics of hearing and could lead to future treatments for traumatic hearing loss, researchers report in the Aug. 1 Journal of Experimental Biology. “This is a preliminary step, but it’s a very useful step in looking at restoring the structure and function of these damaged cells,” says Lavinia Sheets, a hearing researcher at Harvard Medical School who was not involved in the study. Tentacles of starlet sea anemones (Nematostella vectensis) are covered in tiny hairlike cells that sense vibrations in the water from prey swimming nearby.The cells are similar to sound-sensing cells found in the ears of humans and other mammals. When loud noises damage or kill these hair cells, the result can range from temporary to permanent hearing loss. Anemones’ repair proteins restore their damaged hairlike cells, but landlubbing creatures aren’t as lucky. Glen Watson, a biologist at the University of Louisiana at Lafayette, wondered if anemones’ proteins — which have previously been shown to mend similar cells in blind cave fish — might also work in mammals. |© Society for Science & the Public 2000 - 2016.
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
By Sharon Begley, The Massachusetts Institute of Technology brain sciences department and, separately, a group of some 200 neuroscientists from around the world have written letters to The New York Times claiming that a book excerpt in the newspaper’s Sunday magazine this week contains important errors, misinterpretations of scientific disputes, and unfair characterizations of an MIT neuroscientist who did groundbreaking research on human memory. In particular, the excerpt contains a 36-volley verbatim exchange between author Luke Dittrich and MIT’s Suzanne Corkin in which she says that key documents from historic experiments were “shredded.” “Most of it has gone, is in the trash, was shredded,” Corkin is quoted as telling Dittrich before she died in May, explaining, “there’s no place to preserve it.” Destroying files related to historic scientific research would raise eyebrows, but Corkin’s colleagues say it never happened. “We believe that no records were destroyed and, to the contrary, that professor Corkin worked in her final days to organize and preserve all records,” said the letter that Dr. James DiCarlo, head of the MIT Department of Brain and Cognitive Sciences, sent to the Times late Tuesday. Even as Corkin fought advanced liver cancer, he wrote, “she instructed her assistant to continue to organize, label, and maintain all records” related to the research, and “the records currently remain within our department.” © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22546 - Posted: 08.11.2016
By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.
Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited
By Robert Lavine Just the briefest eye contact can heighten empathetic feelings, giving people a sense of being drawn together. But patients who suffer from autism, even in its most high-functioning forms, often have trouble establishing this sort of a social connection with other people. Researchers are delving into what’s going on behind the eyes when these magical moments occur, and the hormones and neural substrates involved may offer hope of helping people with autism. University of Cambridge neuroscientist Bonnie Auyeung and colleagues gave oxytocin—a compound commonly referred to as the “love hormone,” as it’s been found to play roles in maternal and romantic bonding—to both normal men and those with a high-functioning form of autism also called Asperger’s syndrome. The scientists then tracked the eye movements of the study subjects and found that, compared with controls, those who received oxytocin via nasal spray showed increases in the number of fixations—pauses of about 300 milliseconds—on the eye region of an interviewer’s face and in the fraction of time spent looking at this region during a brief interview (Translational Psychiatry, doi:10.1038/tp.2014.146, 2015). Oxytocin, a neuropeptide hormone secreted by the pituitary gland, has long been known to activate receptors in the uterus and mammary glands, facilitating labor and milk letdown. But research on the neural effects of oxytocin has been accelerated by the availability of a nasal spray formulation of the hormone, which can deliver it more directly to the brain, also rich with oxytocin receptors. Auyeung adds that her study used a unique experimental setup. “Other studies have shown that [oxytocin] increases looking at the eye region when presented with a picture of a face,” Auyeung says. “The new part is that we are using a live interaction.”
By Virginia Morell Fourteen years ago, a bird named Betty stunned scientists with her humanlike ability to invent and use tools. Captured from the wild and shown a tiny basket of meat trapped in a plastic tube, the New Caledonian crow bent a straight piece of wire into a hook and retrieved the food. Researchers hailed the observation as evidence that these crows could invent new tools on the fly—a sign of complex, abstract thought that became regarded as one of the best demonstrations of this ability in an animal other than a human. But a new study casts doubt on at least some of Betty’s supposed intuition. Scientists have long agreed that New Caledonian crows (Corvus moneduloides), which are found only on the South Pacific island of the same name, are accomplished toolmakers. At the time of Betty’s feat, researchers knew that in the wild these crows could shape either stiff or flexible twigs into tools with a tiny, barblike hook at one end, which they used to lever grubs from rotting logs. They also make rakelike tools from the leaves of the screw pine (Pandanus) tree. But Betty appeared to take things to the next level. Not only did she fashion a hook from a material she’d never previously encountered—a behavior not observed in the wild—she seemed to know she needed this specific shape to solve her particular puzzle. © 2016 American Association for the Advancement of Science. A
Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.