Chapter 13. Memory, Learning, and Development

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Maanvi Singh Teenagers aren't exactly known for their responsible decision making. But some young people are especially prone to making rash, risky decisions about sex, drugs and alcohol. Individual differences in the brain's working memory — which allows people to draw on and use information to make decisions — could help explain why some adolescents are especially impulsive when it comes to sex, according to a study published Wednesday in Child Development. "Working memory is the ability to keep different things in mind when you're making decisions or problem solving," explains Atika Khurana, an assistant professor of counseling psychology at the University of Oregon who led the study. Khurana and her colleagues rounded up 360 adolescents, ages 12 to 15, and assessed their working memory using a series of tests. For example, the researchers told the participants a string of random numbers and asked them to repeat what they heard in reverse order. "We basically tested their ability to keep information in mind while making decisions," Khurana says. The researchers then tracked all the participants for two years, and asked about the teens' sexual activity. And through another series of tests and surveys, the researcher tried to gauge how likely each teen was to act without thinking, to make rash decisions and take risks. There was a correlation between weaker working memory and the likelihood that a teen would have sex — including unprotected sex — at a younger age. And they were more likely to act without much deliberation. That trend held true even after the researchers accounted for the teenagers' age, socioeconomic status and gender. © 2015 NPR

Keyword: Development of the Brain; Learning & Memory
Link ID: 21070 - Posted: 06.18.2015

By Nicholas Bakalar A new study has found a simple way to significantly reduce teenage smoking: raise the tobacco sales age to 21. In 2005, Needham, Mass., did just that, while surrounding communities kept their age limit at 18. Researchers surveyed 16,000 high school students in Needham and 16 surrounding communities four times between 2006 and 2012, gathering data on their smoking habits. The study is in Tobacco Control. Over the seven years, the number of children under 18 buying cigarettes in Needham decreased to 11.6 percent from 18.4 percent, while in the surrounding communities it hardly changed — down to 19 percent from 19.4. In 2006, 12.9 percent of students in Needham and 14.8 percent of students in surrounding communities reported having smoked in the past 30 days. By 2010, 6.7 percent of Needham students reported smoking, compared with 12 percent in other towns. At the end of the study in 2012, smoking had declined to 5.5 percent in Needham and 8.5 percent outside. “More than 80 percent of smokers begin before 18,” said the lead author, Shari Kessel Schneider, project director at the Education Development Center in Waltham, Mass. “Our findings provide strong support for initiatives going on all across the country to increase the sales age as a means for decreasing youth access to cigarettes, initiation of smoking, and ultimately addiction.” © 2015 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 21069 - Posted: 06.18.2015

By James Gallagher Health editor, BBC News website Scientists have discovered a chemical in blood that indicates whether people will have declining brain function. Looking for the earliest signs of Alzheimer's disease, they analysed levels of 1,129 proteins circulating in the blood of more than 200 twins. These were compared with data from cognitive-function tests over the next decade, in Translational Psychiatry. And levels of one protein, MAPKAPK5, tended to be lower in those people whose brains declined. MAPKAPK5 is involved in relaying chemical messages within the body, although its connection with cognitive decline is unclear. Dementia cases are expected to treble globally by 2050, but there is no cure or treatment. It can take more than a decade from the first changes in the brain to culminate in symptoms such as memory loss, confusion and personality change. And drug companies believe they need to treat patients years before symptoms appear in order to protect the brain. Dr Steven Kiddle, a Medical Research Council scientist at King's College London, told the BBC News website: "People think it may be hard to reverse 20 years of potential damage to your brain. "But if you could start much earlier in that process, then you might be able to find something that works." He said a blood test could help identify people for clinical trials. But he added: "A test you could go in to your doctor to say, 'Do I have Alzheimer's disease or not?' I think that's a long way off." © 2015 BBC

Keyword: Alzheimers
Link ID: 21064 - Posted: 06.17.2015

You remember your first kiss. You remember your childhood phone number, where you parked your car, and the last time you got really drunk. You probably remember the digits of pi, or at least the first three of them (slacker). Each day you accumulate fresh memories—kissing new people, acquiring different phone numbers and (possibly) competing in pi-memorizing championships (we would root for you). With all those new adventures stacking up, you might start worrying that your brain is growing full. But, wait—is that how it works? Can your brain run out of space, like a hard drive? It depends on what kind of memory you’re talking about. “It’s not like each memory takes a cell and then that cell is used up,” says Nelson Cowan, cognitive psychologist at the University of Missouri. Over the long term, memories are encoded in neural patterns—circuits of connected neurons. And your brain’s ability to knit together new patterns is limitless, so theoretically the number of memories stored in those patterns is limitless as well. Memories don’t always keep to themselves, though. They can crossbreed, like similar but distinct species, creating the recollection equivalent of a mule. If you can’t remember it, a memory is pretty much worthless—and similar memories can interfere with each other, getting in the way of surfacing the right one. Though memory interference is well documented, researchers like Cowan are still guessing at the phenomenon’s neural mechanics.

Keyword: Learning & Memory
Link ID: 21061 - Posted: 06.17.2015

by Meghan Rosen When we brought Baby S home from the hospital six months ago, his big sister, B, was instantly smitten. She leaned her curly head over his car seat, tickled his toes and cooed like a pro — in a voice squeakier than Mickey Mouse’s. B’s voice — already a happy toddler squeal — sounded as if she'd sucked in some helium. My husband and I wondered about her higher pitch. Are humans hardwired to chitchat squeakily to babies, or did B pick up vocal cues from us? (I don’t sound like that, do I?) If I’m like other mothers, I probably do. American English-speaking moms dial up their pitch drastically when talking to their children. But dads’ voices tend to stay steady, researchers reported May 19 in Pittsburgh at the 169th Meeting of the Acoustical Society of America. “Dads talk to kids like they talk to adults,” says study coauthor Mark VanDam, a speech scientist at Washington State University. But that doesn’t mean fathers are doing anything wrong, he says. Rather, they may be doing something right: offering their kids a kind of conversational bridge to the outside world. Scientists have studied infant- or child-directed speech (often called “motherese” or “parentese”) for decades. In American English, this type of babytalk typically uses high pitch, short utterances, repetition, loud volume and slowed-down speech. Mothers who speak German Japanese, French, and other languages also tweak their pitch and pace when talking to children. But no one had really studied dads, VanDam says. © Society for Science & the Public 2000 - 2015.

Keyword: Language; Development of the Brain
Link ID: 21050 - Posted: 06.15.2015

By Nicholas Bakalar Statins, the widely used cholesterol-lowering drugs, have been blamed for memory loss, but a new study suggests that the association is an illusion. The report, in JAMA Internal Medicine, found that the apparent association was likely a result of detection bias — visiting the doctor and starting a new medicine makes people more acutely aware of health issues they might otherwise not notice. Researchers compared 482,543 statin users with the same number of people using no lipid-lowering drugs and with 26,484 people using non-statin lipid lowering drugs. Use of statin drugs was associated with an increase in memory loss during the first 30 days of starting the drugs compared with people who did not take cholesterol-lowering drugs. But so was use of non-statin lipid-lowering drugs. After accounting for many health and behavioral variables, the scientists concluded that either all lipid lowering drugs, statins or not, cause memory loss or, more likely, that previous findings were based on the expectations of the patients rather than any physiological effect of the medicine. “As you think about whether you should be taking statins, there are questions about uncommon side effects worth raising,” said the lead author, Dr. Brian L. Strom, chancellor of Rutgers Biomedical and Health Sciences. “But the question of impairing memory is a nonissue.” © 2015 The New York Times Company

Keyword: Learning & Memory
Link ID: 21047 - Posted: 06.15.2015

By Jessica Schmerler Approximately one in 68 children is identified with some form of autism, from extremely mild to severe, according to the U.S. Centers for Disease Control. On average, diagnosis does not occur until after age four, yet all evidence indicates that early intervention is the best way to maximize the treatment impact. Various tests that look for signs of autism in infants have not been conclusive but a new exercise could improve early diagnosis, and also help reduce worry among parents that they did not intervene as soon as possible. The two most widely used tests to measure symptoms, the Autism Observation Scale for Infants (AOSI) and the Autism Diagnostic Observation Schedule (ADOS), cannot be used before the ages of 12 or 16 months respectively. The AOSI measures precursors to symptoms, such as a baby’s response to name, eye contact, social reciprocity, and imitation. The ADOS measures the characteristics and severity of autism symptoms such as social affectation and repetitive and restrictive behaviors. Now a group of scientists at the Babylab at Birkbeck, University of London think they have identified a marker that can predict symptom development more accurately and at an earlier age: enhanced visual attention. Experts have long recognized that certain individuals with autism have superior visual skills, such as increased visual memory or artistic talent. Perhaps the most well known example is Temple Grandin, a high-functioning woman with autism who wrote, “I used to become very frustrated when a verbal thinker could not understand something I was trying to express because he or she couldn’t see the picture that was crystal clear to me.” © 2015 Scientific American

Keyword: Autism; Attention
Link ID: 21045 - Posted: 06.13.2015

Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.

Keyword: Schizophrenia; Neurotoxins
Link ID: 21038 - Posted: 06.10.2015

James Gorman When researchers found a group of brain cells in the fruit fly that function like a compass, they were very satisfied. They had found what they were looking for. But, said Vivek Jayaraman, when he and Johannes D. Seelig realized that the cells were actually arranged in a physical circle in the brain, so they looked just like a compass, they were taken aback. “It’s kind of like a cosmic joke that they are arranged like that,” he said. Dr. Jayaraman was investigating a kind of navigation called dead reckoning, or, in technical terms, angular path integration. It is the most basic way a moving creature knows where it is and where it is going. In dead reckoning, animals use visual cues, like landmarks, and also a sense of where their bodies are pointed. It is very different from other ways animals navigate, such as the use of polarized light from the sun or sensitivity to the earth’s magnetic field. The researchers published their findings in Nature last month. Dr. Jayaraman had narrowed down the likely location of directional tracking based on other research. So he expected to find activity in the ellipsoid body, a very small region of a very small brain. Dr. Jayaraman and Mr. Seelig, at the Janelia Research Campus of the Howard Hughes Medical Institute in Virginia, engineered neurons there to light up when they were active, and they recorded the activity with a microscopic technique called two-photon calcium imaging that gives a real-time visual picture of the brain in action in a living animal. © 2015 The New York Times Company

Keyword: Learning & Memory
Link ID: 21027 - Posted: 06.08.2015

By Sue Bailey, The Canadian Press Scientific studies increasingly suggest marijuana may not be the risk-free high that teens — and sometimes their parents — think it is, researchers say. Yet pot is still widely perceived by young smokers as relatively harmless, said Dr. Romina Mizrahi, director of the Focus on Youth Psychosis Prevention clinic and research program at the Centre for Addiction and Mental Health. She cites a growing body of research that warns of significantly higher incidence of hallucinations, paranoia and the triggering of psychotic illness in adolescent users who are most predisposed. "When you look at the studies in general, you can safely say that in those that are vulnerable, it doubles the risk." Such fallout is increasingly evident in the 19-bed crisis monitoring unit at the Children's Hospital of Eastern Ontario in Ottawa. "I see more and more cases of substance-induced psychosis," said Dr. Sinthu Suntharalingam, a child and adolescent psychiatrist. "The most common substance that's abused is cannabis." One or two cases a week are now arriving on average. "They will present with active hallucinations," Suntharalingam said. "Parents will be very scared. They don't know what's going on. "They'll be seeing things, hearing things, sometimes they will try to self-harm or go after other people." Potential effects need to be better understood She and Mizrahi, an associate professor in psychiatry at University of Toronto, are among other front-line professionals who say more must be done to help kids understand potential effects. "They know the hard drugs, what they can do," Suntharalingam said. "Acid, they'll tell us it can cause all these things so they stay away from it. But marijuana? They'll be: 'Oh, everybody does it."' Mizrahi said the message isn't getting through. ©2015 CBC/Radio-Canada.

Keyword: Drug Abuse; Development of the Brain
Link ID: 21025 - Posted: 06.08.2015

by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.

Keyword: Epigenetics; Schizophrenia
Link ID: 21022 - Posted: 06.06.2015

By Fiona Kumfor, Sicong Tu and The Conversation The brain is truly a marvel. A seemingly endless library, whose shelves house our most precious memories as well as our lifetime’s knowledge. But is there a point where it reaches capacity? In other words, can the brain be “full”? The answer is a resounding no, because, well, brains are more sophisticated than that. A study published in Nature Neuroscience earlier this year shows that instead of just crowding in, old information is sometimes pushed out of the brain for new memories to form. Previous behavioural studies have shown that learning new information can lead to forgetting. But in this study, researchers used new neuroimaging techniques to demonstrate for the first time how this effect occurs in the brain. The experiment The paper’s authors set out to investigate what happens in the brain when we try to remember information that’s very similar to what we already know. This is important because similar information is more likely to interfere with existing knowledge, and it’s the stuff that crowds without being useful. To do this, they examined how brain activity changes when we try to remember a “target” memory, that is, when we try to recall something very specific, at the same time as trying to remember something similar (a “competing” memory). Participants were taught to associate a single word (say, the word sand) with two different images—such as one of Marilyn Monroe and the other of a hat. © 2015 Scientific American

Keyword: Learning & Memory
Link ID: 21013 - Posted: 06.03.2015

Rebecca Hersher Greg O'Brien sees things that he knows aren't there, and these visual disturbances are becoming more frequent. That's not uncommon; up to 50 percent of people who have Alzheimer's disease experience hallucinations, delusions or psychotic symptoms, recent research suggests. At first, he just saw spider-like forms floating in his peripheral vision, O'Brien says. "They move in platoons." But in the last year or so, the hallucinations have been more varied, and often more disturbing. A lion. A bird. Sprays of blood among the spiders. Over the past five months, O'Brien has turned on an audio recorder when the hallucinations start, in hopes of giving NPR listeners insight into what Alzheimer's feels like. For now, he says, "I'm able to function. But I fear the day, which I know will come, when I can't." Interview Highlights [It's] St. Patrick's Day, about 9 o'clock in the morning in my office, and they're coming again. Those hallucinations. Those things that just come into the mind when the mind plays games. And then I see the bird flying in tighter and tighter and tighter circles. And all of a sudden, the bird — beak first — it darted almost in a suicide mission, exploding into my heart. Today I'm just seeing this thing in front of me. It looks like a lion, almost looks like something you'd see in The Lion King, and there are birds above it. It's floating, and it disintegrates ... it disintegrates ... it disintegrates.

Keyword: Alzheimers; Vision
Link ID: 21003 - Posted: 06.01.2015

by Jessica Hamzelou Memories that seem to be lost forever may be lurking in the brain after all, ready to be reawakened. The finding, based on experiments in mice, could eventually give us a way to revive memories in people with Alzheimer's or amnesia. When we learn something, sets of neurons in the brain strengthen their mutual connections to lay down lasting memories. Or at least that's the theory. Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology decided to put it to the test. The team first developed a clever technique to selectively label the neurons representing what is known as a memory engram – in other words, the brain cells involved in forming a specific memory. They did this by genetically engineering mice so they had extra genes in all their neurons. As a result, when neurons fire as a memory is formed, they produce red proteins visible under a microscope, allowing the researchers to tell which cells were part of the engram. They also inserted a gene that made the neurons fire when illuminated by blue light. To mimic memory loss, some of the mice were given a drug that blocks the strengthening of connections between neurons. This made the animals forget their fear of the cage. But the telltale red proteins allowed Tonegawa's team to work out which neurons had been involved in storing the fear memory. They then attempted to reactivate just these neurons using blue light. Sure enough, after the engram had been reactivated, the mice again acted as if they were afraid of the cage. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory
Link ID: 21001 - Posted: 05.30.2015

Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,

Keyword: Alzheimers; Prions
Link ID: 21000 - Posted: 05.30.2015

A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but... An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains. Sergiu Pasca, M.D. External Web Site Policy, of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods. Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.

Keyword: Development of the Brain
Link ID: 20998 - Posted: 05.30.2015

by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd

Keyword: Parkinsons; Stem Cells
Link ID: 20989 - Posted: 05.27.2015

Children developed better fine-motor skills when the clamping of their umbilical cord at birth was delayed several minutes compared with just seconds, according to a new randomized trial. Delaying clamping allows fetal blood circulating in the placenta to be transfused to the infant, which has been shown to reduce iron deficiency at four to six months of age. Now the longer term benefits of a delay are becoming clearer. Researchers in Sweden randomly assigned 382 full-term infants born after low-risk pregnancies to be clamped at least three minutes after delivery or within 10 seconds of birth. When the children were four, a psychologist assessed them on standard tests of IQ, motor skills and behaviour. The parents also filled in questionnaires about their child's communication and social skills. "Delayed cord clamping compared with early cord clamping improved scores and reduced the number of children having low scores in fine-motor skills and social domains," the study's lead author, Dr. Ola Andersson of Uppsala University in Sweden, and his co-authors said in Tuesday's issue of JAMA Pediatrics. The fine-motor skill tests showed those in the delayed clamping group had a more mature pencil grip. There was also a difference in boys, who researchers said are generally more prone to iron deficiency than girls. Boys showed more improvements in fine-motor skills with delayed clamping. Andersson said delayed cord clamping can have quite an effect on the amount of iron in the blood, which is important for brain development just after birth. ©2015 CBC/Radio-Canada.

Keyword: Development of the Brain
Link ID: 20988 - Posted: 05.27.2015

By Tina Hesman Saey Combatants in the age-old battle of nature versus nurture may finally be able to lay down their arms. On average, both nature and nurture contribute roughly equally to determining human traits. Researchers compiled data from half a century’s worth of studies on more than 14 million pairs of twins. The researchers measured heritability — the amount of variation in a characteristic that can be attributed to genes — for a wide variety of human traits including blood pressure, the structure of the eyeball and mental or behavioral disorders. All traits are heritable to some degree, the researchers report May 18 in Nature Genetics. Traits overall had an average heritability of 49 percent, meaning it’s a draw between genes and environment. Individual traits can be more strongly influenced by one or the other. 100% Fraction of human traits with a genetic component 49% Fraction of variability in human traits determined by genes T.J.C. Polderman et al. Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature Genetics. Published online May 18, 2015. doi:10.1038/ng.3285. © Society for Science & the Public 2000 - 2015.

Keyword: Genes & Behavior; Development of the Brain
Link ID: 20985 - Posted: 05.27.2015

By Esther Hsieh Imagine you are enjoying your golden years, driving to your daily appointment for some painless brain zapping that is helping to stave off memory loss. That's the hope of a new study, in which people who learned associations (such as a random word and an image) after transcranial magnetic stimulation (TMS) were better able to learn more pairings days and weeks later—with no further stimulation needed. TMS uses a magnetic coil placed on the head to increase electrical signaling a few centimeters into the brain. Past studies have found that TMS can boost cognition and memory during stimulation, but this is the first to show that such gains can last even after the TMS regimen is completed. In the new study, which was published in Science, neuroscientists first used brain imaging to identify the associative memory network of 16 young, healthy participants. This network, based around the hippocampus, glues together things such as sights, places, sounds and time to form a memory, explains neuroscientist Joel Voss of Northwestern University, a senior author of the paper. Next, the researchers applied TMS behind the left ear of each participant for 20 minutes for five consecutive days to stimulate this memory network. To see if participants' associative memory improved, one day after the stimulation regimen finished they were tested for their ability to learn random words paired with faces. Subjects who had had TMS performed 33 percent better, compared with those who received placebo treatments, such as sham stimulation. © 2015 Scientific American

Keyword: Learning & Memory; Brain imaging
Link ID: 20977 - Posted: 05.25.2015