Chapter 13. Memory, Learning, and Development
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Kevin Pelphrey, In September, the Florida State University football team made a visit to a Tallahassee middle school that would become famous. At lunchtime, student-athlete Travis Rudolph noticed sixth grader Bo Paske eating alone, so he joined Bo for the meal. Bo, who has autism, often sat by himself in the lunchroom. The world took note of the athlete’s gesture after his mother’s Facebook post about it went viral. “This is one day I didn’t have to worry if my sweet boy ate lunch alone, because he sat across from someone who is a hero in many eyes,” she wrote. This story touched people because it calls to mind something universal: the sting of social exclusion. We have all known children who often eat, or play, alone. And all of us have felt left out at one time or another. But although this experience may be universal, a new generation of children is experiencing a wave of inclusiveness. Technology of various types, often thought of as an isolating influence, can actually abet people’s good intentions or help those with autism learn to fit in. One new app called Sit With Us, invented by 16-year-old Natalie Hampton, helps vulnerable children who have difficulty finding a welcoming group in the lunchroom. Its motto is inspiring: “The first step to a warmer, more inclusive community can begin with LUNCH.” Sit With Us allows students to designate themselves as ‘ambassadors’ and to signal to anyone seeking company that they’re invited to join the ambassador’s table. © 2017 Scientific American
Ian Sample Science editor Tempting as it may be, it would be wrong to claim that with each generation humans are becoming more stupid. As scientists are often so keen to point out, it is a bit more complicated than that. A study from Iceland is the latest to raise the prospect of a downwards spiral into imbecility. The research from deCODE, a genetics firm in Reykjavik, finds that groups of genes that predispose people to spend more years in education became a little rarer in the country from 1910 to 1975. The scientists used a database of more than 100,000 Icelanders to see how dozens of gene variants that affect educational attainment appeared in the population over time. They found a shallow decline over the 65 year period, implying a downturn in the natural inclination to rack up qualifications. But the genes involved in education affected fertility too. Those who carried more “education genes” tended to have fewer children than others. This led the scientists to propose that the genes had become rarer in the population because, for all their qualifications, better educated people had contributed less than others to the Icelandic gene pool. Spending longer in education and the career opportunities that provides is not the sole reason that better educated people tend to start families later and have fewer children, the study suggests. Many people who carried lots of genes for prolonged education left the system early and yet still had fewer children that the others. “It isn’t the case that education, or the career opportunities it provides, prevents you from having more children,” said Kari Stefansson, who led the study. “If you are genetically predisposed to have a lot of education, you are also predisposed to have fewer children.” © 2017 Guardian News and Media Limited
By JANE E. BRODY Insomnia is like a thief in the night, robbing millions — especially those older than 60 — of much-needed restorative sleep. As the king laments in Shakespeare’s “Henry IV, Part 2”: O sleep, O gentle sleep, Nature’s soft nurse, how have I frightened thee. That thou no more will weigh my eyelids down, And steep my senses in forgetfulness? The causes of insomnia are many, and they increase in number and severity as people age. Yet the problem is often overlooked during routine checkups, which not only diminishes the quality of an older person’s life but may also cause or aggravate physical and emotional disorders, including symptoms of cognitive loss. Most everyone experiences episodic insomnia, a night during which the body seems to have forgotten how to sleep a requisite number of hours, if at all. As distressing as that may seem at the time, it pales in comparison to the effects on people for whom insomnia — difficulty falling asleep, staying asleep or awakening much too early — is a nightly affair. A survey done in 1995 by researchers at the National Institute on Aging among more than 9,000 people aged 65 and older living in three communities revealed that 28 percent had problems falling asleep and 42 percent reported difficulty with both falling asleep and staying asleep. The numbers affected are likely to be much larger now that millions spend their pre-sleep hours looking at electronic screens that can disrupt the body’s biological rhythms. Insomnia, Dr. Alon Y. Avidan says, “is a symptom, not a diagnosis” that can be a clue to an underlying and often treatable health problem and, when it persists, should be taken seriously. Dr. Avidan is director of the sleep clinic at the University of California, Los Angeles, David Geffen School of Medicine. © 2017 The New York Times Company
Michelle Trudeau When Samantha Deffler was young, her mother would often call her by her siblings' names — even the dog's name. "Rebecca, Jesse, Molly, Tucker, Samantha," she says. A lot of people mix up children's names or friends' names, but Deffler is a cognitive scientist at Rollins College, in Winter Park, Fla., and she wanted to find out why it happens. So she did a survey of 1,700 men and women of different ages, and she found that naming mistakes are very common. Most everyone sometimes mixes up the names of family and friends. Her findings were published in the journal Memory & Cognition. "It's a normal cognitive glitch," Deffler says. It's not related to a bad memory or to aging, but rather to how the brain categorizes names. It's like having special folders for family names and friends names stored in the brain. When people used the wrong name, overwhelmingly the name that was used was in the same category, Deffler says. It was in the same folder. And there was one group who was especially prone to the naming mix-ups. "Moms, especially moms," Deffler says. "Any mom I talked to says, 'You know, I've definitely done this.'" It works something like this: Say you've got an armful of groceries and you need some quick help from one of your kids. Your brain tries to rapidly retrieve the name from the family folder, but it may end up retrieving a related name instead, says Neil Mulligan, a cognitive scientist at UNC Chapel Hill. © 2017 npr
Keyword: Learning & Memory
Link ID: 23106 - Posted: 01.16.2017
Alison Abbott Bats have brain cells that keep track of their angle and distance to a target, researchers have discovered. The neurons, called ‘vector cells’, are a key piece of the mammalian’s brain complex navigation system — and something that neuroscientists have been seeking for years. Our brain’s navigation system has many types of cells, but a lot of them seem designed to keep track of where we are. Researchers know of ‘place’ cells, for example, which fire when animals are in a particular location, and ‘head direction’ cells that fire in response to changes in the direction the head is facing. Bats also have a kind of neuronal compass that enables them to orient themselves as they fly. The vector cells, by contrast, keep spatial track of where we are going. They are in the brain’s hippocampus, which is also where ‘place’ and ‘head-direction’ cells were discovered. That’s a surprise, considering how well this area has been studied by researchers, says Nachum Ulanovsky, who led the team at the Weizmann Institute of Science in Rehovot, Israel, that discovered the new cells. His team published their findings in Science on 12 January1. Finding the cells "was one of those very rare discovery moments in a researcher’s life,” says Ulanovsky. “My heart raced, I started jumping around.” The trick to finding them was a simple matter of experimental design, he says. © 2017 Macmillan Publishers Limited
By Peter Godfrey-Smith Adapted from Other Minds: The Octopus, the Sea and the Deep Origins of Consciousness, by Peter Godfrey-Smith. Copyright © 2016 by Peter Godfrey-Smith. Someone is watching you, intently, but you can't see them. Then you notice, drawn somehow by their eyes. You're amid a sponge garden, the seafloor scattered with shrublike clumps of bright orange sponge. Tangled in one of these sponges and the gray-green seaweed around it is an animal about the size of a cat. Its body seems to be everywhere and nowhere. The only parts you can keep a fix on are a small head and the two eyes. As you make your way around the sponge, so, too, do those eyes, keeping their distance, keeping part of the sponge between the two of you. The creature's color perfectly matches the seaweed, except that some of its skin is folded into tiny, towerlike peaks with tips that match the orange of the sponge. Eventually it raises its head high, then rockets away under jet propulsion. A second meeting with an octopus: this one is in a den. Shells are strewn in front, arranged with some pieces of old glass. You stop in front of its house, and the two of you look at each other. This one is small, about the size of a tennis ball. You reach forward a hand and stretch out one finger, and one octopus arm slowly uncoils and comes out to touch you. The suckers grab your skin, and the hold is disconcertingly tight. It tugs your finger, tasting it as it pulls you gently in. The arm is packed with sensors, hundreds of them in each of the dozens of suckers. The arm itself is alive with neurons, a nest of nervous activity. Behind the arm, large round eyes watch you the whole time. © 2017 Scientific American
By Ashley P. Taylor Neurodegenerative diseases are often associated with aging. To learn what happens within the aging brain and potentially gain information relevant to human health, researchers examined gene-expression patterns in postmortem brain samples. Overall, the researchers found, gene expression of glial cells changed more with age than did that of neurons. These gene-expression changes were most significant in the hippocampus and substantia nigra, regions damaged in Alzheimer’s and Parkinson’s diseases, respectively, according to the study published today (January 10) in Cell Reports. “Typically we have concentrated on neurons for studies of dementia, as they are the cells involved in brain processing and memories. [This] study demonstrates that glia are likely to be equally important,” study coauthors Jernej Ule and Rickie Patani of the Francis Crick Institute and University College London wrote in an email to The Scientist. “The authors’ effort in this comprehensive work is a ‘genomic tour de force,’ showing that, overall, non-neuronal cells undergo gene expression changes at a larger scale than previously thought in aging,” Andras Lakatos, a neuroscientist at the University of Cambridge, U.K., who was not involved in the study, wrote in an email. “This finding puts glial cells again at the center stage of functional importance in neurodegenerative conditions in which aging carries a proven risk.” © 1986-2017 The Scientist
By Andy Coghlan Can tiny brains grown in a dish reveal the secrets of sociability? Balls of brain tissue generated from stem cells are enabling us to understand the underlying differences between people who struggle to be sociable and those who have difficulty reining themselves in. Alysson Muotri at the University of California, San Diego, and his team created the mini-brains by exposing stem cells taken from the pulp of children’s milk teeth to cocktails of growth factors that help them mature. Eventually, they can develop as many as six layers of cerebral cortex – the outer surface of the brain. This region is much more sophisticated in humans than in other animals, and houses important circuitry governing our most complex thoughts and behaviours, including socialising with others. Each mini-brain is approximately 5 millimetres across. “Though they’re not as well defined as they are in a real brain, they resemble what you find in an embryonic fetus,” says Muotri. To understand how brain development affects sociability, the team used donated cells from children with autism and Rett syndrome, both of which are associated with impaired communication skills. They also used cells from children with Williams syndrome, a condition characterised by a hyper-sociable nature. People with Williams syndrome can be unable to restrain themselves from talking to complete strangers. © Copyright Reed Business Information Ltd.
Dima Amso, The early years of parenthood involve so many rewarding firsts—when your infant cracks a toothless grin, when he crawls and later walks, and, of course, when he utters a real, nonbabble word. A mother once told me she found it sad that if she were to pass away suddenly, her toddler wouldn't remember her or these exciting years. It is true that most of us don't remember much, if anything, from our infancy. So at what point do children start making long-term memories? I must first explain the different types of memory we possess. As I type this, I am using procedural memory—a form of motor memory in which my fingers just know how to type. In contrast, declarative memories represent two types of long-term recall—semantic and episodic. Semantic memory allows us to remember general facts—for example, that Alfred Hitchcock directed the film Vertigo; episodic memory encompasses our ability to recall personal experiences or facts—that Vertigo is my favorite film. Episodic memories are most relevant for understanding our childhood recollections. Making an episodic memory requires binding together different details of an event—when it happened and where, how we felt and who was there—and retrieving that information later. The processes involve the medial temporal lobes, most notably the hippocampus, and portions of the parietal and prefrontal cortices, which are very important in memory retrieval. Imaging studies often show that the same regions that encode an episode—for example, the visual cortex for vivid visual experiences—are active when we recall that memory, allowing for a kind of “mental time travel” or replay of the event. © 2017 Scientific American
By Greg Miller Babies born prematurely are prone to problems later in life—they’re more likely to develop autism or attention deficit hyperactivity disorder, and more likely to struggle in school. A new study that’s among the first to investigate brain activity in human fetuses suggests that the underlying neurological issues may begin in the womb. The findings provide the first direct evidence of altered brain function in fetuses that go on to be born prematurely, and they might ultimately point to ways to remediate or even prevent such early injuries. In the new study, published 9 January in Scientific Reports, developmental neuroscientist Moriah Thomason of Wayne State University School of Medicine in Detroit, Michigan, and colleagues report a difference in how certain brain regions communicate with each other in fetuses that were later born prematurely compared with fetuses that were carried to term. Although the findings are preliminary because the study was small, Thomason and other researchers say the work illustrates the potential (and the challenges) of the emerging field of fetal neuroimaging. “Harnessing the power of these advanced tools is offering us for the very first time the opportunity to explore the onset of neurologic insults that are happening in utero,” says Catherine Limperopoulos, a pediatric neuroscientist at Children’s National Medical Center in Washington, D.C. Thomason and colleagues used functional magnetic resonance imaging (fMRI) to investigate brain activity in 32 fetuses. The pregnant mothers were participants in a larger, long-term study of brain development led by Thomason. “The majority have just normal pregnancies, but they’re drawn from a low-resource population that’s at greater risk of early delivery and developmental problems,” she says. In the end, 14 of the fetuses were born prematurely. © 2017 American Association for the Advancement of Science.
Riley Beggin Matt Herich uses a tDCS device that was made by another student he met on Reddit. Four 9-volt batteries and sticky self-adhesive electrodes are connected by a circuit board that sends a constant small current to the user's brain. Courtesy of Matt Herich Last October, Matt Herich was listening to the news while he drove door to door delivering pizzas. A story came on the radio about a technology that sends an electric current through your brain to possibly make you better at some things — moving, remembering, learning. He was fascinated. The neurotechnology is called transcranial direct current stimulation, or tDCS for short. At its simplest, the method involves a device that uses little more than a 9-volt battery and some electrodes to send a low-intensity electrical current to a targeted area of the brain, typically via a headset. More than a 1,000 studies have been published in peer-reviewed journals over the last decade suggesting benefits of the technique — maybe regulating mood, possibly improving language skills — but its effects, good or bad, are far from clear. Although researchers see possibilities for tDCS in treating diseases and boosting performance, it's still an exploratory technology, says Mark George, editor-in-chief of Brain Stimulation, a leading journal on neuromodulation. And leading experts have warned against at-home use of such devices. © 2017 npr
Keyword: Learning & Memory
Link ID: 23071 - Posted: 01.09.2017
By Meredith Wadman In athletes who suffered a concussion, a protein in their blood may be able to predict when they can return to action. A new study finds that those who took longer to return to play had higher levels of a protein known as tau in their blood in the 6 hours following the trauma than players who were cleared to return to the field sooner. Tau blood testing isn’t ready for prime time, but experts say that if it pans out it would become an invaluable tool for coaches and physicians alike. Trainers, sports physicians, and neurologists deal with some 3.8 million sports-related concussions in the United States each year. But they still lack an objective medical test to establish whether someone has sustained the injury, and at what point they have recovered enough from one to resume playing. Instead, they are forced to rely on often-nebulous physical signs, and on players’ self-reporting of symptoms. And it’s known that players, keen to get back on the field, often minimize these. “We don’t want a biomarker that just says somebody had a concussion,” says study leader Jessica Gill, a neuroscientist at the National Institute of Nursing Research in Bethesda, Maryland. “We want a biomarker that says who needs to be out of play to recover.” Gill, with concussion physician Jeffrey Bazarian of the University of Rochester School of Medicine and Dentistry in New York, and colleagues took preseason blood samples from more than 600 male and female University of Rochester athletes who participate in contact sports: football, basketball, hockey, and lacrosse. In it, they measured levels of tau, a protein linked to traumatic brain injury and Alzheimer’s disease, which has been found to be elevated in the blood of Olympic boxers and concussed ice hockey players. © 2017 American Association for the Advancement of Science.
By Joshua A. Krisch At the core of Alzheimer’s disease are amyloid-beta (Aβ) peptides, which self-assemble into protein fibrils that form telltale plaques in the brain. Now, the results of a study published today (January 4) in Nature suggest that certain fibril formations are more likely to appear in cases of rapidly progressive Alzheimer’s disease, as opposed to less-severe subtypes. The findings increase scientists’ understanding of the structure of these fibrils, and may eventually contribute to new tests and treatments for Alzheimer’s disease. “It is generally believed that some form of the aggregated Aβ peptide leads to Alzheimer’s disease, and it’s conceivable that different fibril structures could lead to neurodegeneration with different degrees of aggressiveness,” said coauthor Robert Tycko, a principal investigator at the National Institute of Diabetes and Digestive Kidney Disease. “But the mechanism by which this happens is uncertain. Some structures may be more inert and benign. Others may be more inherently toxic or prone to spread throughout the brain tissue.” Prior research has demonstrated that Aβ fibrils with various molecular structures exhibit different levels of toxicity in neuronal cell cultures, a finding confirmed in subsequent mouse trials. One study even demonstrated that Aβ fibrils cultured from patients with rapidly progressive Alzheimer’s disease are different in size and resistance to chemical denaturation than those isolated from patients with more slowly progressing disease. Building on these observations, Tycko and colleagues set out to better characterize the structures of these fibrils and get a better handle on the potential correlations between structure and disease subtype. © 1986-2017 The Scientist
Link ID: 23066 - Posted: 01.07.2017
By Michael Price As we age, we get progressively better at recognizing and remembering someone’s face, eventually reaching peak proficiency at about 30 years old. A new study suggests that’s because brain tissue in a region dedicated to facial recognition continues to grow and develop throughout childhood and into adulthood, a process known as proliferation. The discovery may help scientists better understand the social evolution of our species, as speedy recollection of faces let our ancestors know at a glance whether to run, woo, or fight. The results are surprising because most scientists have assumed that brain development throughout one’s life depends almost exclusively on “synaptic pruning,” or the weeding out of unnecessary connections between neurons, says Brad Duchaine, a psychologist at Dartmouth College who was not involved with the study. “I expect these findings will lead to much greater interest in the role of proliferation in neural development.” Ten years ago, Kalanit Grill-Spector, a psychologist at Stanford University in Palo Alto, California, first noticed that several parts of the brain’s visual cortex, including a segment known as the fusiform gyrus that’s known to be involved in facial recognition, appeared to develop at different rates after birth. To get more detailed information on how the size of certain brain regions changes over time, she turned to a recently developed brain imaging technology known as quantitative magnetic resonance imaging (qMRI). The technique tracks how long it takes for protons, excited by the imaging machine’s strong magnetic field, to calm down. Like a top spinning on a crowded table, these protons will slow down more quickly if they’re surrounded by a lot of molecules—a proxy for measuring volume. © 2017 American Association for the Advancement of Science
By Gary Stix The last six months have witnessed the failure of two drugs in late-stage clinical trials for which the research community had high hopes. In truth, these new reports should not have come as too much of a surprise. Drug after drug continues to show little or no effect in helping the more than 5 million patients in the U.S. diagnosed with Alzheimer’s. Scientists who study neurodegenerative diseases have started to call for new approaches that go beyond targeting the amyloid in plaques and the tau in tangles, proteins that have been thought to be culprits in killing brain cells. One organization—The Alzheimer’s Drug Discovery Foundation (ADDF)—has for years provided funding to move untried ideas into clinical trials. Howard Fillit, the organization’s executive director, recently gave Scientific American his surprisingly optimistic view of where research and drug development for Alzheimer’s is headed. There have been recent failures of late-stage clinical trials and a figure often cited is that more than 99 percent of Alzheimer's drugs fail. Given all that, what level of confidence do you have for the field moving forward? There's a lot of reason for hope. There are over 130 different clinical trials going on now. I remember the days when there were none. We have had many failures. But I think one of the big advances that is creating hope is that we know how to do clinical trials better now. In a study that is being conducted by Biogen, everyone who was recruited into that study actually had Alzheimer's disease, for the first time. © 2017 Scientific American
Link ID: 23062 - Posted: 01.06.2017
By Alice Klein A tumour containing a miniature brain has been found growing on the ovary of a 16-year-old girl in Japan. The 10-centimetre-wide tumour was discovered when the girl had surgery to remove her appendix. When doctors cut the tumour out, they found clumps of greasy, matted hair inside, and a 3-centimetre-wide brain-like structure covered by a thin plate of skull bone. Closer analysis revealed that it was a smaller version of a cerebellum – which usually sits underneath the brain’s two hemispheres. A mass on one side resembled a brain stem – the structure that normally joins to the spinal cord. About one-fifth of ovarian tumours contain foreign tissue, including hair, teeth, cartilage, fat and muscle. These tumours, which are normally benign, are named teratomas after the Greek word “teras”, meaning monster. Although the cause of ovarian teratomas is unknown, one theory is that they arise when immature egg cells turn rogue, producing different body parts. Brain cells are often found in ovarian teratomas, but it is extremely unusual for them to organise themselves into proper brain-like structures, says Masayuki Shintaku at the Shiga Medical Centre for Adults in Japan, who studied the tumour. Angelique Riepsamen at the University of New South Wales in Australia, agrees. “Neural elements similar to that of the central nervous system are frequently reported in ovarian teratomas, but structures resembling the adult brain are rare.” © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 23059 - Posted: 01.06.2017
Hannah Devlin Science correspondent People living near a busy road have an increased risk of dementia, according to research that adds to concerns about the impact of air pollution on human health. Roughly one in 10 cases of Alzheimer’s in urban areas could be associated with living amid heavy traffic, the study estimated – although the research stopped short of showing that exposure to exhaust fumes causes neurodegeneration. Hong Chen, the scientist who led the work at Public Health Ontario, said: “Increasing population growth and urbanisation has placed many people close to heavy traffic, and with widespread exposure to traffic and growing rates of dementia, even a modest effect from near-road exposure could pose a large public health burden.” Previously, scientists have linked air pollution and traffic noise to reduced density of white matter (the brain’s connective tissue) and lower cognition. A recent study suggested that magnetic nano-particles from air pollution can make their way into brain tissue. The latest study, published in The Lancet, found that those who live closest to major traffic arteries were up to 12% more likely to be diagnosed with dementia – a small but significant increase in risk. The study, which tracked roughly 6.6 million people for more than a decade, could not determine whether pollution is directly harmful to the brain. The increased dementia risk could also be a knock-on effect of respiratory and cardiac problems caused by traffic fumes or due to other unhealthy life-style factors associated with living in built-up urban environments. © 2017 Guardian News and Media Limited
Eating a Mediterranean diet has been linked to less brain shrinkage in older adults. Human brains naturally shrink with age. But a study that followed 401 people in their 70s found that the brains of those who adhered more closely to a Mediterranean-style diet shrank significantly less over a period of three years. A typical Mediterranean diet contains a high amount of vegetables, fruits, olive oil, beans and cereal grains, moderate amounts of fish, dairy products, and wine, and only a small amount of red meat and poultry. “As we age, the brain shrinks and we lose brain cells, which can affect learning and memory,” says Michelle Luciano, at the University of Edinburgh, UK, who led the study. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.” The differences in brain shrinkage were measured using brain scans. Statistical analysis of diet data found that simply eating more fish and less meat were not associated with reduced shrinking. “While the study points to diet having a small effect on changes in brain size, it didn’t look at the effect on risk of dementia,” says David Reynolds, at the charity Alzheimer’s Research UK. “We would need to see follow-up studies in order to investigate any potential protective effects against problems with memory and thinking.” Other studies have found that being overweight seems to accelerate shrinking of the brain’s white matter. © Copyright Reed Business Information Ltd.
By LISA FELDMAN BARRETT Think about the people in your life who are 65 or older. Some of them are experiencing the usual mental difficulties of old age, like forgetfulness or a dwindling attention span. Yet others somehow manage to remain mentally sharp. My father-in-law, a retired doctor, is 83 and he still edits books and runs several medical websites. Why do some older people remain mentally nimble while others decline? “Superagers” (a term coined by the neurologist Marsel Mesulam) are those whose memory and attention isn’t merely above average for their age, but is actually on par with healthy, active 25-year-olds. My colleagues and I at Massachusetts General Hospital recently studied superagers to understand what made them tick. Our lab used functional magnetic resonance imaging to scan and compare the brains of 17 superagers with those of other people of similar age. We succeeded in identifying a set of brain regions that distinguished the two groups. These regions were thinner for regular agers, a result of age-related atrophy, but in superagers they were indistinguishable from those of young adults, seemingly untouched by the ravages of time. What are these crucial brain regions? If you asked most scientists to guess, they might nominate regions that are thought of as “cognitive” or dedicated to thinking, such as the lateral prefrontal cortex. However, that’s not what we found. Nearly all the action was in “emotional” regions, such as the midcingulate cortex and the anterior insula. My lab was not surprised by this discovery, because we’ve seen modern neuroscience debunk the notion that there is a distinction between “cognitive” and “emotional” brain regions. © 2017 The New York Times Company
Bret Stetka With a president-elect who has publicly supported the debunked claim that vaccines cause autism, suggested that climate change is a hoax dreamed up by the Chinese, and appointed to his Cabinet a retired neurosurgeon who doesn't buy the theory of evolution, things might look grim for science. Yet watching Patti Smith sing "A Hard Rain's a-Gonna Fall" live streamed from the Nobel Prize ceremony in early December to a room full of physicists, chemists and physicians — watching her twice choke up, each time stopping the song altogether, only to push on through all seven wordy minutes of one of Bob Dylan's most beloved songs — left me optimistic. Taking nothing away from the very real anxieties about future funding and support for science, neuroscience in particular has had plenty of promising leads that could help fulfill Alfred Nobel's mission to better humanity. In the spirit of optimism, and with input from the Society for Neuroscience, here are a few of the noteworthy neuroscientific achievements of 2016. One of the more fascinating fields of neuroscience of late entails mapping the crosstalk between our biomes, brains and immune systems. In July, a group from the University of Virginia published a study in Nature showing that the immune system, in addition to protecting us from a daily barrage of potentially infectious microbes, can also influence social behavior. The researchers had previously shown that a type of white blood cells called T cells influence learning behavior in mice by communicating with the brain. Now they've shown that blocking T cell access to the brain influences rodent social preferences. © 2016 npr