Chapter 13. Memory, Learning, and Development
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Rae Ellen Bichell Initially, Clint Perry wanted to make a vending machine for bumblebees. He wanted to understand how they solve problems. Perry, a cognitive biologist at Queen Mary University of London, is interested in testing the limits of animal intelligence. "I want to know: How does the brain do stuff? How does it make decisions? How does it keep memory?" says Perry. And how big does a brain need to be in order to do all of those things? He decided to test this on bumblebees by presenting the insects with a puzzle that they'd likely never encounter in the wild. He didn't end up building that vending machine, but he did put bees through a similar scenario. Perry and his colleagues wrote Thursday in the journal Science that, despite bees' miniature brains, they can solve new problems quickly just by observing a demonstration. This suggests that bees, which are important crop pollinators, could in time adapt to new food sources if their environment changed. As we have reported on The Salt before, bee populations around the world have declined in recent years. Scientists think a changing environment is at least partly responsible. Perry and colleagues built a platform with a porous ball sitting at the center of it. If a bee went up to the ball, it would find that it could access a reward, sugar water. One by one, bumblebees walked onto the platform, explored a bit, and then slurped up the sugar water in the middle. "Essentially, the first experiment was: Can bees learn to roll a ball?" says Perry. © 2017 npr
By Claudia Wallis Dinosaurs, Star Wars, train schedules, Disney princesses, maps, LEGO—subjects such as these can become all-consuming passions for children on the autism spectrum. What therapists and educators often call “circumscribed” or “restricted” interests (or, more generously, “special” interests) make up a characteristic symptom of autism spectrum disorder (ASD). The current edition of psychiatry’s Diagnostic and Statistical Manual of Mental Disorders describes them as “highly restricted, fixated interests that are abnormal in intensity or focus.” Roughly 90 percent of high-functioning kids with ASD display at least one such interest during their elementary school years, according to a 2007 survey conducted at the Yale University Child Study Center, one of the few studies to have examined the topic. For a family with an affected child, this kind of narrow preoccupation can be tedious and exhausting. Imagine a kid who will talk about nothing but the exits on the New Jersey Turnpike or the Captain Underpants book series. (Both actual examples.) Therapists and educators have traditionally tried to suppress or modulate a child’s special interest, or use it as a tool for behavior modification: Keep your hands still and stop flapping, and you will get to watch a Star Wars clip; complete your homework or no Harry Potter. But what if these obsessions themselves can be turned into pathways to growth? What if these intellectual cul-de-sacs can open up worlds? That is the idea explored in the film Life, Animated, a contender for the Academy Award for Best Documentary this Sunday night. © 2017 Scientific American
Link ID: 23277 - Posted: 02.24.2017
Jon Brock What if I told you that we can now identify babies who are going to develop autism based on a simple brain scan? This, in essence, is the seductive pitch for a study published last week in the journal Nature, and making headlines around the world. Early identification and diagnosis is one of the major goals of autism research. By definition, people with autism have difficulties with social interaction and communication. But these skills take many years to develop, even in typically developing (i.e., non-autistic) children. Potential early signs of autism are extremely difficult to pick out amidst the natural variation in behaviour and temperament that exists between all babies. A brain scan for autism would be a major step forward. But is the hype justified? Are we really on the brink of a new era in autism diagnostics? Without wishing to detract from the efforts of everyone involved in the study, it’s important to look at the results critically, both in terms of the scientific findings and their potential implications for clinical practice. The study, led by Heather Cody Hazlett at the University of North Carolina, was part of a larger research program investigating the development of babies who have an older sibling with autism. Because autism runs in families, these babies are much more likely to develop autism than babies from the general population.
Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.
Link ID: 23274 - Posted: 02.24.2017
By RONI CARYN RABIN Older adults who started sleeping more than nine hours a night — but had not previously slept so much — were at more than double the risk of developing dementia a decade later than those who slept nine hours or less, researchers report. The increased risk was not seen in people who had always slept more than nine hours. “We’re not suggesting you go wake up Grandpa. We think this might be a marker for the risk of dementia, not a cause” of the illness, said Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine and the senior author of the study, in Neurology. Using data from 2,457 people, average age 72, who were part of a study in Framingham, Mass., the researchers found that those with a new habit of excessive slumber were at a greater risk of all forms of dementia, including Alzheimer’s, which is characterized by a buildup of beta amyloid, a toxic protein fragment that forms plaques in the brain. “My suspicion is that this is a compensatory mechanism: that at a time when amyloid is building up in the brain, people may be sleeping longer as the body is reacting and trying to remove it from the brain,” Dr. Seshadri added. © 2017 The New York Times Company
Link ID: 23270 - Posted: 02.24.2017
Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.
By WINNIE HU Ruth Brunn finally said yes to marijuana. She is 98. She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb. “I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.” Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own. From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects. For some people, it is a last resort when nothing else helps. Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease. © 2017 The New York Times Company
By JANE E. BRODY “Feeling My Way Into Blindness,” an essay published in The New York Times in November by Edward Hoagland, an 84-year-old nature and travel writer and novelist, expressed common fears about the effects of vision loss on quality of life. Mr. Hoagland, who became blind about four years ago, projected deep-seated sadness in describing the challenges he faces of pouring coffee, not missing the toilet, locating a phone number, finding the food on his plate, and knowing to whom he is speaking, not to mention shopping and traveling, when he often must depend on the kindness of strangers. And, of course, he sorely misses nature’s inspiring vistas and inhabitants that fueled his writing, though he can still hear birds chatter in the trees, leaves rustle in the wind and waves crash on the shore. Mr. Hoagland is hardly alone in his distress. According to Action for Blind People, a British support organization, those who have lost some or all sight “struggle with a range of emotions — from shock, anger, sadness and frustration to depression and grief.” When eyesight fails, some people become socially disengaged, leading to isolation and loneliness. Anxiety about a host of issues — falls, medication errors, loss of employment, social blunders — is common. A recent study from researchers at the Wilmer Eye Institute at Johns Hopkins University School of Medicine found that most Americans regard loss of eyesight as the worst ailment that could happen to them, surpassing such conditions as loss of limb, memory, hearing or speech, or having H.I.V./AIDS. Indeed, low vision ranks behind arthritis and heart disease as the third most common chronic cause of impaired functioning in people over 70, Dr. Eric A. Rosenberg of Weill Cornell Medical College and Laura C. Sperazza, a New York optometrist, wrote in American Family Physician. © 2017 The New York Times Company
Bret Stetka In a series of recent interviews, President Donald Trump's longtime personal physician Dr. Harold N. Bornstein told The New York Times that our new commander in chief has what amounts to a pretty unremarkable medical chart. Like about a quarter of American adults, Trump is on a statin for high cholesterol. He also takes a daily baby aspirin for heart health, an occasional antibiotic for rosacea, a skin condition, and Propecia, a pill to promote hair growth. Bornstein also told the Times that should he be appointed White House doctor, he probably wouldn't test the president for baseline dementia risk, something many doctors have argued should be mandatory. At 70, Trump is the oldest American president to ever take office. Couple his age with a family history of dementia — his father Fred developed Alzheimer's disease in his 80s — and one could argue that the question of baseline cognitive testing for the U.S. head of state has taken on new relevance. An assortment of fairly simple tests exist that can establish a reference point for cognitive capacity and detect early symptoms of mental decline. One of the most common such screens is the Mini-Mental Status Examination, a series of questions that gauges attention, orientation and short-term memory. It takes about five to 10 minutes to complete. Yet admitting vulnerability of any kind isn't something politicians have been keen to do. The true health of politicians has likely been cloaked in secrecy since the days of Mesopotamian kings, but definitely since the Wilson administration. © 2017 npr
Link ID: 23243 - Posted: 02.17.2017
Ewen Callaway Researchers have no way to tell whether young babies may later be diagnosed with autism. But brain scans could help, a small study suggests. By scanning the brains of babies whose siblings have autism, researchers say they have been able to make reasonably accurate forecasts about which of these high-risk infants will later develop autism themselves. The findings raise the prospect of diagnosing autism spectrum disorder (ASD) months before children develop symptoms, a goal that has proved elusive. Nature looks at the new study and its implications. Why has it been so tough to diagnose autism in infants? Children typically show symptoms of ASD, such as difficulty making eye contact, after the age of 2. Researchers believe that the brain changes underlying ASD begin much earlier — possibly even in the womb. But behavioural assessments haven't been helpful in predicting who will get autism, says Joseph Piven, a psychiatrist at the University of North Carolina (UNC) in Chapel Hill, who co-led the study, published online in Nature1. “Children who end up with autism at 2 or 3, they don’t look like they have autism in the first year," he says. Certain rare mutations are linked to ASD, but the vast majority of cases cannot be pinned to a single or even a handful of genetic risk factors. Beginning in the 1990s, Piven and other researchers noticed that children with autism tended to have larger brains than developmentally normal children, suggesting that brain growth could be a biomarker for ASD. But Piven and colleague Heather Cody Hazlett, a psychologist at UNC-Chapel Hill, say it had not been clear when overgrowth occurred. What did their latest study look at? © 2017 Macmillan Publishers Limited,
By Amy Ellis Nutt For the first time, scientists can point to substantial empirical evidence that people with attention-deficit/hyperactivity disorder have brain structures that differ from those of people without ADHD. The common disorder, they conclude, should be considered a problem of delayed brain maturation and not, as it is often portrayed, a problem of motivation or parenting. In conducting the largest brain imaging study of its kind, an international team of researchers found that ADHD involves decreased volume in key brain regions, in particular the amygdala, which is responsible for regulating the emotions. Although the study, published Wednesday in the Lancet Psychiatry, included children, adolescents and adults, the scientists said the greatest differences in brain volume appeared in the brains of children. Of seven subcortical brain regions targeted in the study, five, including the amygdala, were found to be smaller in those with ADHD, compared with those in a control group. The other regions that showed reductions in volume were: the caudate nucleus (which has been linked to goal-directed action), the putamen (involved in learning and responding to stimuli), the nucleus accumbens (which processes rewards and motivation) and the hippocampus (where memories are formed). © 1996-2017 The Washington Post
By John Carroll, Scratch yet another Phase III Alzheimer’s drug hopeful. Merck announced late Tuesday that it is shuttering its EPOCH trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues. This is one of Merck’s top late-stage drugs, and news of the failure drove down the pharma giant’s shares in after-market trading by 2.45%. BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab — which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down. Merck’s effort was the most advanced in the pipeline, but Eli Lilly and others are still in hot pursuit with their own persistent BACE efforts. Teams from Biogen/Eisai and Novartis/Amgen are also beavering away on BACE. “Alzheimer’s disease is one of the most pressing and daunting medical issues of our time, with inherent, substantial challenges to developing an effective disease-modifying therapy for people with mild-to-moderate disease. Studies such as EPOCH are critical, and we are indebted to the patients in this study and their caregivers,” said Dr. Roger M. Perlmutter, president, Merck Research Laboratories. © 2017 American Association for the Advancement of Science.
Link ID: 23238 - Posted: 02.16.2017
By Jesse Singal Those who advocate for sound, evidence-based research about autism are extremely alarmed about Donald Trump, and for good reason: In addition to Trump’s ties to Andrew Wakefield, the disgraced British doctor whose debunked research helped fuel the false idea of links between childhood vaccines and autism, Robert F. Kennedy Jr., a notorious anti-vaxxer himself, told reporters back in January that Trump planned to tap him as chair of a commission on “vaccine safety.” There is no question at this point that Trump has significant connections to a pseudoscientific medical movement that spreads dangerous, disproven ideas. Today, Trump gave nervous observers yet more reason to worry. It occurred at a White House event in which Trump and Secretary of Education Betsy DeVos met with a bunch of educators. Trump seemed to fixate, for a moment, on one educator named Jane (her last name is hard to make out) after she explained that she is the principal of a special education center in Virginia. The sequence starts at about 5:38 in this video: After Jane noted that many of her students have autism, Trump asked, “Have you seen a big increase in the autism, with the children?” Jane replied in the affirmative, but seemed to couch her response as being more about an increase in demand for services — she didn’t explicitly agree there’s been a big increase in the overall rate. Trump continued: “So what’s going on with autism? When you look at the tremendous increase, it’s really — it’s such an incredible — it’s really a horrible thing to watch, the tremendous amount of increase. Do you have any idea? And you’re seeing it in the school?” Jane replied — again, in a way that seems a bit noncommittal vis-à-vis Trump’s claim — that the rate of autism is something like 1-in-66 or 1-in-68 children. To which Trump responds: “Well now, it’s gotta be even lower [presumably meaning higher, rate-wise] than that, which is just amazing — well, maybe we can do something.” (Jane had the rate right, and Trump is incorrect that it has crept higher.) © 2017, New York Media LLC.
Link ID: 23233 - Posted: 02.15.2017
Jon Hamilton Researchers have created mice that appear impervious to the lure of cocaine. Even after the genetically engineered animals were given the drug repeatedly, they did not appear to crave it the way typical mice do, a team reports in Nature Neuroscience. "They didn't keep going into the room where they received the cocaine and they seemed to be just as happy exploring all around the cage," says Shernaz Bamji, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia in Vancouver. "Addiction is a form of learning," Bamji says. And somehow, these mice never learned to associate the pleasurable feelings produced by cocaine with the place where they received the drug. The result was startling because the scientists thought these mice would be especially susceptible to addiction. "We repeated the experiment several times to see if we had made a mistake," Bamji says. The reason for the team's surprise had to do with proteins that affect learning. The animals had been genetically engineered to produce high levels of proteins called cadherins in the brain's "reward circuit," which plays an important role in addiction. And genetic studies have suggested that people with high levels of cadherins are more susceptible to drug addiction. Cadherins act a bit like glue, binding cells together. Usually this glue enhances learning by strengthening the connections, or synapses, between brain cells. © 2017 npr
Ian Sample Science editor Children who are born very prematurely are at greater risk of developing mental health and social problems that can persist well into adulthood, according to one of the largest reviews of evidence. Those with an extremely low birth weight, at less than a kilogram, are more likely to have attention disorders and social difficulties as children, and feel more shyness, anxiety and depression as adults, than those born a healthy weight. The review draws on findings from 41 published studies over the past 26 years and highlights the need for doctors to follow closely how children born very prematurely fare as they become teenagers and adults. “It is important that families and doctors be aware of the potential for these early-emerging mental health problems in children born at extremely low birth weight, since at least some of them endure into adulthood,” said Karen Mathewson, a psychologist at McMaster University in Ontario. Improvements in neonatal care in the past two decades mean that more children who are born very prematurely now survive. In a healthy pregnancy, a baby can reach 1kg (a little more than 2lbs) within 27 weeks, or the end of the second trimester. The study, which involves data from 13,000 children in 12 different countries, follows previous research that found a greater tendency for very low birth weight children to have lower IQs and autism and more trouble with relationships and careers as they reach adulthood and venture into the world. © 2017 Guardian News and Media Limited
After A Stroke At 33, A Writer Relies On Journals To Piece Together Her Own Story On New Year's Eve, 2006, Christine Hyung-Oak Lee developed a splitting headache. She was 33, and her world turned upside down — as in, she literally saw the world upside down. Suddenly, she could hold things in her mind for only 15 minutes at a time. She was a writer who now couldn't recall words or craft sentences. She remembers looking at the phone and thinking to herself: What is the phone number for 911? Days later, she learned she'd had a stroke. "I had a 15-minute short-term memory, like Dory the fish in Finding Nemo," Lee wrote in a Buzzfeed essay chronicling her experience. "My doctors instructed me to log happenings with timestamps in my Moleskine journal. That, they said, would be my working short-term memory. My memento to my mori." Lee used those journals to reconstruct her experience in a new memoir called Tell Me Everything You Don't Remember. She talks with NPR's Scott Simon about the silver linings of memory loss and the unexpected grief that came with her recovery. Interview Highlights On what it's like to have a 15-minute memory You don't even fathom the magnitude of your loss — or at least I didn't. I couldn't plan for the future. I couldn't think of the past. I had no regrets. So it's literally living in the moment. I was experiencing something that people go to yoga and Zen retreats to achieve. So it was quite pleasant. It was not pleasant for the people around me. But in that period of my recovery, where I couldn't remember everything, I think I was incredibly at peace and happy. On having an "invisible" disability It was frustrating. On the one hand, you want people to know: Hey, slow down for me. Hey, I'm going through a crisis. On the other hand, I was also privileged to be disabled in a way that wasn't visible. So people also didn't treat me any differently. So it was very isolating. ... When I told people that I was sick and I needed them to slow down, along with that came this need to explain my position and I ... felt a lot of resentment for having to do with that. © 2017 npr
Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,
“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.
In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.
Link ID: 23205 - Posted: 02.09.2017
By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist