Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By Emily Underwood In the 1930s, neurosurgeon Wilder Penfield pioneered a daring new kind of cartography. As a stenographer took notes, he delicately touched an electrode to the exposed brains of his awake, consenting patients and asked what they felt as electrical current hit different areas. Penfield wanted to better predict which brain functions would be threatened when surgeons had to remove tumors or chunks of tissue that were triggering epileptic seizures. Stimulating adjacent brain regions, he found, produced sensations in corresponding body parts: hand, forearm, elbow. The result of his mapping was the iconic “homunculus”: a map on the brain’s wrinkled outer layer representing the surface of the body. Penfield then ventured into more mysterious territory. When he probed the insula, a deep fold of cortex, some patients felt nauseated or gassy; others belched or vomited. “My stomach is upset and I smell something like medicine,” one said. Penfield found those visceral signals harder to decipher than the brain’s map of the body’s surface. Brain regions responsible for different internal sensations seemed to overlap. Sensory regions were hard to distinguish from those that sent motor instructions such as telling the intestines to contract. Penfield once asked participants to swallow an electrode to detect changes in gut contractions while he stimulated their brains. But his map of the inner organs was blurry and ambiguous—and stayed that way for most of the next century. Decades later, scientists are starting to unravel how our wet, spongy, slippery organs talk to the brain and how the brain talks back. That two-way communication, known as interoception, encompasses a complex, bodywide system of nerves and hormones. Much recent exploration has focused on the vagus nerve: a massive, meandering network of more than 100,000 fibers that travel from nearly every internal organ to the base of the brain and back again. © 2021 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 27850 - Posted: 06.11.2021

By Mitch Leslie For the past 3 years, about 6000 middle-aged and elderly Australians have pumped iron, loaded up on greens and whole grains, strived to quell stress, and challenged their wits with computer exercises, all in an effort to preserve their cognition. They’re part of a clinical trial called Maintain Your Brain, one of about 30 current or planned studies that eschew pharmaceutical interventions and test whether altering multiple aspects of participants’ lives improves brain health. Such multidomain studies may finally reveal whether modifying diet, exercise, and other factors can slow cognitive decline as people age—or even prevent dementia. “There’s a lot of hope for multidomain trials,” says psychologist Kaarin Anstey of the University of New South Wales, Sydney, one of the principal investigators of the Maintain Your Brain trial, which will finish by the end of this year. Although people can’t escape some mental decline as they get older, lifestyle exerts a powerful influence over the risk of developing dementia—the type of severe cognitive impairment seen in conditions such as Alzheimer’s disease. Last year, an international committee of scientists and psychiatrists known as the Lancet Commission on dementia prevention, intervention, and care estimated that so-called modifiable factors account for 40% of dementia risk. Their report highlighted a dozen factors, including many familiar villains—diabetes, high blood pressure, smoking, obesity, and lack of exercise. Researchers are still probing exactly how these risk factors steal people’s faculties, but they’ve identified some likely mechanisms. Lack of physical activity may impair cognition, for instance, because exercise stimulates formation of new neurons and soothes brain inflammation. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers; Obesity
Link ID: 27834 - Posted: 05.29.2021

By Gina Kolata Obesity has stalked Marleen Greenleaf, 58, all of her life. Like most people with obesity, she tried diet after diet. But the weight always came back. With that, she has suffered a lifetime of scorn and stigma. Jeering comments from strangers when she walked down the street. Family members who told her, when she trained for a half-marathon, “I don’t think it’s good for you.” Then, in 2018, Ms. Greenleaf, an administrator at a charter school in Washington, D.C., participated in a clinical trial for semaglutide, which is a new type of obesity drug, known as incretins. Over the course of the 68-week study, Ms. Greenleaf slowly lost 40 pounds. Until then, she had always believed that she could control her weight if she really tried. “I thought I just needed more motivation,” she said. But when she took semaglutide, she said that “immediately, the urge to eat just dissipated.” Incretins appear to elicit significant weight loss in most patients, enough to make a real medical and aesthetic difference. But experts hope that the drugs also do something else: change how society feels about people with obesity, and how people with obesity feel about themselves. If these new drugs allow obesity to be treated like a chronic disease — with medications that must be taken for a lifetime — the thought is that doctors, patients and the public might understand that obesity is truly a medical condition. © 2021 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 27821 - Posted: 05.15.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27803 - Posted: 05.05.2021

by Peter Hess Deleting the autism-related gene CHD8 from the intestines induces significant gastrointestinal and behavioral changes in mice, according to a new unpublished study. The results suggest that changes to the gut are involved in some of the behavioral traits seen in people with CHD8 mutations, says lead researcher Evan Elliott, assistant professor of molecular and behavioral neuroscience at Bar-Ilan University in Ramat Gan, Israel. Elliott’s team presented the findings virtually this week at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Up to 90 percent of people with CHD8 mutations report gastrointestinal issues such as constipation, Elliott says. Most also have autism. Mice missing one copy of CHD8 have unusually thin and permeable small intestines, Elliott and his colleagues found. The reason seems to be that these mice have fewer mucus-producing goblet cells than controls, resulting in thinner organ walls and less mucus lining the digestive tract. CHD8 regulates the expression of other genes, so Elliott’s team looked at gene expression levels in the CHD8 mice’s intestinal epithelial cells via RNA sequencing. The mice expressed 920 genes differently than control mice did. These include an increase in the expression of genes involved in inflammatory responses and in antimicrobial activity. The latter set may be the body’s way of compensating for increased microbial populations, Elliott says. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27801 - Posted: 05.05.2021

by Angie Voyles Askham Mice that lack CNTNAP2, a gene linked to autism, have an atypical collection of microbes in their intestines, according to a new study. Treating the mice with a strain of gut bacteria commonly found in wildtype mice, people and other mammals improves their social behavior. The CNTNAP2 mice are hyperactive, and those raised in isolation prefer to spend time alone or with a familiar cagemate rather than with a stranger mouse. But when they grow up alongside wildtype littermates, their social deficits — but not their hyperactivity — disappear, the study shows. Because mice that live together eat one another’s feces, which can alter the microbial content of their guts, the researchers wondered if a change in the microbiome might be driving the change in the isolated animals’ social behaviors. “It was sort of a serendipitous discovery,” says lead investigator Mauro Costa-Mattioli, professor of neuroscience at Baylor College of Medicine in Houston, Texas. The findings highlight how some autism traits associated with genetic mutations may be shaped, and potentially eased, via changes to the gut microbiome. Figuring out which behaviors can be attributed to the environment is particularly helpful for thinking about treatments because the environment can be changed, whereas “genetics is still hard to correct,” says Sarkis Mazmanian, professor of microbiology at the California Institute of Technology in Pasadena, who was not involved in the work. © 2021 Simons Foundation

Keyword: Autism
Link ID: 27746 - Posted: 03.27.2021

Kayla Hounsell · CBC News · Sarah White has always been a 'picky eater' but says the pandemic exacerbated her difficult relationship with food. It ultimately led to a diagnosis of avoidant restrictive food intake disorder. (Eric Woolliscroft/CBC) Sarah White sets a timer to remind herself to eat. She sets it six times a day so that she eats three meals and three snacks. White says she's always been a "picky eater." But when she started working from home, her routine was interrupted and her already difficult relationship with food became dangerous. It ultimately led to an eating disorder diagnosis during the pandemic. "I had all of the time in the world to eat, but I was finding I wasn't eating nearly as much as I should have been," White, 33, said during a physically distanced interview at her Halifax apartment. "It started to feel a lot more serious than it had in the past." There's been an alarming spike in the number of people seeking help for eating disorders. The National Eating Disorder Information Centre says the volume of inquiries to its help line and online chat service has been up 100 per cent during the pandemic. "There's been literature coming out across the world really suggesting that the numbers are skyrocketing and we're trying to understand why that is," said Dr. Jennifer Couturier, principal investigator for the Canadian Consensus Panel for In May, the panel, which consists of clinicians, policymakers, parents and youth, received a $50,000 federal grant to determine how best to treat eating disorders during a pandemic, particularly in children and young adults under 25. Couturier says she feels this age group hasn't received a lot of attention when it comes to research generally. ©2021 CBC/Radio-Canada.

Keyword: Anorexia & Bulimia
Link ID: 27729 - Posted: 03.13.2021

By Andreas von Bubnoff The world is getting fatter. More than 40 percent of U.S. adults are obese — almost three times more than in 1980. One reason for this weight gain is Americans are consuming more: National figures suggest an increase of about 200 daily calories between the early 1970s and 2010. Another is more snacking. In 2010, U.S. adults ate about 20 percent more of their daily calories as snacks than they did 50 years ago. But there is more to rising obesity rates than endless grazing. What also matters is timing, some experts believe. We eat when we shouldn’t, and don’t give our bodies a long enough break in between. We didn’t evolve to eat day and night, says neuroscientist Dominic D’Agostino of the University of South Florida. Until the dawn of agriculture about 12,000 years ago, we subsisted on hunting and gathering and often had to perform those activities with empty bellies. “We are hard-wired,” D’Agostino says, “to undergo periodic intermittent fasting.” What’s more, people are now eating at times of the day when historically they would have been asleep, says Satchin Panda, a circadian biologist at the Salk Institute for Biological Studies in La Jolla, Calif., who co-wrote an overview on the timing of eating in the 2019 Annual Review of Nutrition. For thousands of years, he says, our nightly fast probably started much earlier than in these times of late-night television. Although the research is still mixed, the timing of eating seems to matter for body weight and health. Studies suggest significant potential benefits from fasting every other day or so — or, on a daily basis, eating only when we would normally be awake, within a window of 12 hours or fewer — a practice known as time-restricted eating. © 1996-2021 The Washington Post

Keyword: Obesity
Link ID: 27710 - Posted: 02.28.2021

By Anahad O’Connor Five years ago, a group of nutrition scientists studied what Americans eat and reached a striking conclusion: More than half of all the calories that the average American consumes comes from ultra-processed foods, which they defined as “industrial formulations” that combine large amounts of sugar, salt, oils, fats and other additives. Highly processed foods continue to dominate the American diet, despite being linked to obesity, heart disease, Type 2 diabetes and other health problems. They are cheap and convenient, and engineered to taste good. They are aggressively marketed by the food industry. But a growing number of scientists say another reason these foods are so heavily consumed is that for many people they are not just tempting but addictive, a notion that has sparked controversy among researchers. Recently, the American Journal of Clinical Nutrition explored the science behind food addiction and whether ultra-processed foods might be contributing to overeating and obesity. It featured a debate between two of the leading experts on the subject, Ashley Gearhardt, associate professor in the psychology department at the University of Michigan, and Dr. Johannes Hebebrand, head of the department of child and adolescent psychiatry, psychosomatics and psychotherapy at the University of Duisburg-Essen in Germany. Dr. Gearhardt, a clinical psychologist, helped develop the Yale Food Addiction Scale, a survey that is used to determine whether a person shows signs of addictive behavior toward food. In one study involving more than 500 people, she and her colleagues found that certain foods were especially likely to elicit “addictive-like” eating behaviors, such as intense cravings, a loss of control, and an inability to cut back despite experiencing harmful consequences and a strong desire to stop eating them. At the top of the list were pizza, chocolate, potato chips, cookies, ice cream, French fries and cheeseburgers. © 2021 The New York Times Company

Keyword: Obesity; Drug Abuse
Link ID: 27706 - Posted: 02.23.2021

By Gina Kolata For the first time, a drug has been shown so effective against obesity that patients may dodge many of its worst consequences, including diabetes, researchers reported on Wednesday. The drug, semaglutide, made by Novo Nordisk, already is marketed as a treatment for Type 2 diabetes. In a clinical trial published in the New England Journal of Medicine, researchers at Northwestern University in Chicago tested semaglutide at a much higher dose as an anti-obesity medication. Nearly 2,000 participants, at 129 centers in 16 countries, injected themselves weekly with semaglutide or a placebo for 68 weeks. Those who got the drug lost close to 15 percent of their body weight, on average, compared with 2.4 percent among those receiving the placebo. More than a third of the participants receiving the drug lost more than 20 percent of their weight. Symptoms of diabetes and pre-diabetes improved in many patients. Those results far exceed the amount of weight loss observed in clinical trials of other obesity medications, experts said. The drug is a “game-changer,” said Dr. Robert F. Kushner, an obesity researcher at Northwestern University Feinberg School of Medicine, who led the study. “This is the start of a new era of effective treatments for obesity.” Dr. Clifford Rosen of Maine Medical Center Research Institute, who was not involved in the trial, said, “I think it has a huge potential for weight loss.” Gastrointestinal symptoms among the participants were “really marginal — nothing like with weight loss drugs in the past,” added Dr. Rosen, an editor at the New England Journal of Medicine and a co-author of an editorial accompanying the study. For decades, scientists have searched for ways to help growing numbers of people struggling with obesity. Five currently available anti-obesity drugs have side effects that limit their use. The most effective, phentermine, brings about a 7.5 percent weight loss, on average, and can be taken only for a short time. After it is stopped, even that amount of weight is regained. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27688 - Posted: 02.13.2021

Cassandra Willyard In 2006, soon after she launched her own laboratory, neuroscientist Jane Foster discovered something she felt sure would set her field abuzz. She and her team were working with two groups of mice: one with a healthy selection of microorganisms in their guts, and one that lacked a microbiome. They noticed that the mice without gut bacteria seemed less anxious than their healthy equivalents. When placed in a maze with some open paths and some walled-in ones, they preferred the exposed paths. The bacteria in the gut seemed to be influencing their brain and behaviour. Foster, at McMaster University in Toronto, Canada, wrote up the study and submitted it for publication. It was rejected. She rewrote it and sent it out again. Rejected. “People didn’t buy it. They thought it was an artefact,” she says. Finally, after three years and seven submissions, she got an acceptance letter1. John Cryan, a neuroscientist at University College Cork in Ireland, joined the field about the same time as Foster did, and knows exactly how she felt. When he began talking about the connections between bacteria living in the gut and the brain, “I felt very evangelical”, he says. He recalls one Alzheimer’s disease conference at which he presented in 2014. “I’ve never given a talk in a room where there was less interest.” Today, however, the gut–brain axis is a feature at major neuroscience meetings, and Cryan says he is no longer “this crazy guy from Ireland”. Thousands of publications over the past decade have revealed that the trillions of bacteria in the gut could have profound effects on the brain, and might be tied to a whole host of disorders. Funders such as the US National Institutes of Health are investing millions of dollars in exploring the connection. © 2021 Springer Nature Limited

Keyword: Obesity; Alzheimers
Link ID: 27678 - Posted: 02.03.2021

by Sarah DeWeerdt Children with autism may have a subtly different set of bacteria in their gut than their non-autistic siblings, according to unpublished data presented virtually on Tuesday at the 2021 Society for Neuroscience Global Connectome. The prospect that manipulating the microbiome could ease gastrointestinal problems and other autism traits has tantalized many families of autistic children. But studies of the gut microbiome in people with autism are scarce and have shown conflicting results, and mouse studies can be difficult to interpret. For the new work, researchers recruited 111 families that each have two children — one with autism and one without — born within two years of each other and aged 2 to 7 years old. “We tried to be as careful as possible by using a control cohort that were siblings,” says study leader Maude David, assistant professor of microbiology at Oregon State University in Corvallis. This study design helped control for variables such as household environment, pets and other factors that can shape the microbiome, she says. The researchers collected stool samples from the children at three time points, two weeks apart. The repeated sampling reduced the likelihood that short-term shifts in the children’s gut microbiome — due to transient environmental influences, such as day-to-day dietary changes — would skew the results. © 2021 Simons Foundation

Keyword: Autism
Link ID: 27644 - Posted: 01.15.2021

Sophie Balisky, 26, says she struggled with anorexia and bulimia through most of her teens but got help three years ago and was doing great — until COVID hit and she lost her job as a flight attendant. She found herself reverting to old coping patterns in dealing with stressful and uncertain situations. "I was actually quite shocked, I was a bit taken aback, because I consider myself to be quite strong in my coping against my eating tendencies," said Balisky. Advocates for those who struggle with eating disorders say the pandemic is exacerbating the problem — prompting a greater need for community supports. Experts believe the problem is related to the stress, uncertainty and isolation that stems from the pandemic and related-restrictions and say it's not only a problem in the province but around the world. Some eating disorder support groups in Alberta who connect with people of all ages say they have seen a steady rise in demand since the pandemic hit. The Eating Disorder Support Network of Alberta is reporting a 5½ times increase in participants year-over-year between the period from March to the end of August. "So a huge surge through this," said Lauren Berlinguette, executive director of the support network. Another community-based agency that offers support to those who are struggling as well as their families, the Calgary Silver Linings Foundation, says it's experiencing a substantial increase in demand, too. The number of participants in all of its adult programs went from 37 to 64 participants, year-over-year. ©2020 CBC/Radio-Canada.

Keyword: Anorexia & Bulimia
Link ID: 27627 - Posted: 12.15.2020

By Gretchen Reynolds Can exercise help us shed pounds? An interesting new study involving overweight men and women found that working out can help us lose weight, in part by remodeling appetite hormones. But to benefit, the study suggests, we most likely have to exercise a lot — burning at least 3,000 calories a week. In the study, that meant working out six days a week for up to an hour, or around 300 minutes a week. The relationship between working out and our waistlines is famously snarled. The process seems as if it should straightforward: We exercise, expend calories and, if life and metabolisms were just, develop an energy deficit. At that point, we would start to use stored fat to fuel our bodies’ continuing operations, leaving us leaner. But our bodies are not always cooperative. Primed by evolution to maintain energy stores in case of famine, our bodies tend to undermine our attempts to drop pounds. Start working out and your appetite rises, so you consume more calories, compensating for those lost. The upshot, according to many past studies of exercise and weight loss, is that most people who start a new exercise program without also strictly monitoring what they eat do not lose as much weight as they expect — and some pack on pounds. But Kyle Flack, an assistant professor of nutrition at the University of Kentucky, began to wonder a few years ago if this outcome was inevitable. Maybe, he speculated, there was a ceiling to people’s caloric compensations after exercise, meaning that if they upped their exercise hours, they would compensate for fewer of the lost calories and lose weight. © 2020 The New York Times Company

Keyword: Obesity
Link ID: 27617 - Posted: 12.09.2020

by Laura Dattaro In 1983, psychologist Christopher Gillberg posed a provocative question to the readers of the British Journal of Psychiatry: Could autism and anorexia nervosa share underlying causes? Gillberg’s curiosity came in part from his observations of three autistic boys whose female cousins all had the eating disorder, which is characterized by food restrictions, low body weight, an intense fear of gaining weight and a distorted body image. Gillberg, professor of child and adolescent psychiatry at the University of Gothenburg in Sweden, initially suggested that anorexia is the ‘female form of autism.’ Although that idea wasn’t entirely accurate, his suspicions that eating disorders and autism are linked have borne out: People with anorexia are more likely to be autistic than those without it, studies show. There are fewer data demonstrating that autistic people are at particularly high risk for eating disorders, but experts say it’s likely. How often do anorexia and autism overlap? Estimates vary, though most researchers agree that roughly 20 percent of people with anorexia are autistic. Both conditions are rare — about 1 percent of people are autistic and 0.3 percent have anorexia — and most research so far has examined the prevalence of autism in people with anorexia, not the reverse. Among 60 women receiving treatment for an eating disorder at a clinic in the United Kingdom, for example, 14 of them, or 23 percent, scored above the diagnostic cutoff on a test called the Autism Diagnostic Observation Schedule (ADOS). Similarly, about one-third of people with anorexia have been diagnosed with autism, according to a long-running study that has followed 51 people with anorexia and 51 controls in Sweden since the 1980s. © 2020 Simons Foundation

Keyword: Autism; Anorexia & Bulimia
Link ID: 27616 - Posted: 12.09.2020

By Katherine J. Wu For a rodent that resembles the love child of a skunk and a steel wool brush, the African crested rat carries itself with a surprising amount of swagger. The rats “very much have the personality of something that knows it’s poisonous,” says Sara Weinstein, a biologist at the University of Utah and the Smithsonian Conservation Biology Institute who studies them. In sharp contrast to most of their skittish rodent kin, Lophiomys imhausi lumber about with the languidness of porcupines. When cornered, they fluff up the fur along their backs into a tip-frosted mohawk, revealing rows of black-and-white bands that run like racing stripes down their flanks — and, at their center, a thicket of specialized brown hairs with a honeycomb-like texture. Those spongy hairs contain a poison powerful enough to bring an elephant to its knees, and are central to Dr. Weinstein’s recent research, which confirmed ideas about how this rat makes itself so deadly. Give them a chance and African crested rats will take nibbles from the branch of a poison arrow tree. It’s not for nutrition. Instead, they will chew chunks of the plants and spit them back out into their fur, anointing themselves with a form of chemical armor that most likely protects them from predators like hyenas and wild dogs. The ritual transforms the rats into the world’s only known toxic rodents, and ranks them among the few mammals that borrow poisons from plants. Dr. Weinstein’s research, which was published last week in the Journal of Mammalogy, is not the first to document the crested rats’ bizarre behavior. But the new paper adds weight to an idea described nearly a decade ago, and offers an early glimpse into the animals’ social lives. First documented in the scientific literature in 1867, the rarely-glimpsed African crested rat “has captured so much interest for so long,” said Kwasi Wrensford, a behavioral ecologist at the University of California, Berkeley who wasn’t involved in the study. “We’re now just starting to unpack what makes this animal tick.” © 2020 The New York Times Company

Keyword: Neurotoxins; Learning & Memory
Link ID: 27592 - Posted: 11.27.2020

by Peter Hess / Mutations in a top autism gene called SYNGAP1 slow the rate at which zebrafish digest food and pass waste. The findings may explain why some people with SYNGAP1 mutations have gastrointestinal (GI) problems. Researchers presented the unpublished work on Tuesday and Wednesday at the 2020 International SYNGAP1 Scientific Conference, which took place virtually because of the coronavirus pandemic. They also began recruiting people with SYNGAP1 mutations at the meeting for an ongoing study of gut function. “It’s been in the literature, this link between GI symptoms and [autism], for a long time, with not a lot of progress on the mechanisms,” says lead researcher Julia Dallman, associate professor of biology at the University of Miami in Florida, who presented the findings on Wednesday. In the brain, SYNGAP1 functions mainly at synapses, or the junctions between neurons, and helps the cells exchange chemical messages. Mutations in the gene are strongly linked to autism, seizures, intellectual disability and sleep problems. Prompted by families’ anecdotal reports of constipation, reflux and overeating in people with SYNGAP1 mutations, Dallman and her colleagues decided to explore the gene’s role in the gut. The young zebrafish’s transparent skin allowed the researchers to trace the movement of microscopic fluorescent beads — mixed into the fish’s food — through the gut. In this way, they measured how quickly and how strongly the digestive tract moves food and waste. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27590 - Posted: 11.21.2020

The membranes surrounding our brains are in a never-ending battle against deadly infections, as germs constantly try to elude watchful immune cells and sneak past a special protective barrier called the meninges. In a study involving mice and human autopsy tissue, researchers at the National Institutes of Health and Cambridge University have shown that some of these immune cells are trained to fight these infections by first spending time in the gut. “This finding opens a new area of neuroimmunology, showing that gut-educated antibody-producing cells inhabit and defend regions that surround the central nervous system,” said Dorian McGavern, Ph.D., senior investigator at NINDS and co-senior author of the study, which was published in Nature. The central nervous system (CNS) is protected from pathogens both by a three-membrane barrier called the meninges and by immune cells within those membranes. The CNS is also walled off from the rest of the body by specialized blood vessels that are tightly sealed by the blood brain barrier. This is not the case, however, in the dura mater, the outermost layer of the meninges. Blood vessels in this compartment are not sealed, and large venous structures, referred to as the sinuses, carry slow moving blood back to the heart. The combination of slow blood flow and proximity to the brain requires strong immune protection to stop potential infections in their tracks. “The immune system has invested heavily in the dura mater,” said Dr. McGavern. “The venous sinuses within the dura act like drainage bins, and, consequently, are a place where pathogens can accumulate and potentially enter the brain. It makes sense that the immune system would set up camp in this vulnerable area.”

Keyword: Neuroimmunology
Link ID: 27569 - Posted: 11.07.2020

Shawna Williams In Greek mythology, Orpheus descends to the underworld and persuades Hades to allow him to take his dead wife, Eurydice, back to the realm of the living. Hades agrees, but tells Orpheus that he must not look back until he has exited the underworld. Despite the warning, Orpheus glances behind him on his way out to check whether Eurydice is indeed following him—and loses her forever. The story hints at a dark side to curiosity, a drive to seek certain kinds of knowledge even when doing so is risky—and even if the information serves no practical purpose at the time. In fact, the way people pursue information they’re curious about can resemble the drive to attain more tangible rewards such as food—a parallel that hasn’t been lost on scientists. To investigate the apparent similarity between curiosity and hunger, researchers led by Kou Murayama of the University of Reading in the UK recently devised an experiment to compare how the brain processes desires for food and knowledge, and the risks people are willing to take to satisfy those desires. Beginning in 2016, the team recruited 32 volunteers and instructed them not to eat for at least two hours before coming into the lab. After they arrived, the volunteers’ fingers were hooked up to electrodes that could deliver a weak current, and researchers calibrated the level of electricity to what each participant reported was uncomfortable, but not painful. Then, still hooked up to the electrodes, the volunteers were asked to gamble: they viewed either a photo of a food item or a video of a magician performing a trick, followed by a visual depiction of their odds of “winning” that round (which ranged from 1:6 to 5:6). © 1986–2020 The Scientist.

Keyword: Attention; Obesity
Link ID: 27535 - Posted: 10.21.2020

Jon Hamilton Researchers appear to have shown how the brain creates two different kinds of thirst. The process involves two types of brain cells, one that responds to a decline in fluid in our bodies, while the other monitors levels of salt and other minerals, a team reports in the journal Nature. Together, these specialized thirst cells seem to determine whether animals and people crave pure water or something like a sports drink, which contains salt and other minerals. "Our brain can detect these two distinct stimuli with different cell types," says Yuki Oka, a professor of biology at Caltech and the study's lead author. The finding appears to help answer "this question that we've been trying to ask for decades and decades and decades," says Sean Stocker, a professor at the University of Pittsburgh who studies water and salt balance in the body. Stocker was not involved in the study. Oka's research is part of an effort to understand the brain biology underlying behavior that's seen in people and many animals. Article continues after sponsor message For example, people who've just finished a long, sweaty workout often experience a special kind of thirst. "Pure water doesn't do it, right? It's not enough," Oka says. "You need water and salt to recover. And we can easily imagine that under such condition, we crave [a] sport drink." Sports drinks like Gatorade generally include a mix of salt and sugar, as well as water. To understand what triggers this type of thirst, Oka's team studied cells in two regions of mouse brains. Both regions are known to contain neurons involved in the sensation of thirst. © 2020 npr

Keyword: Miscellaneous
Link ID: 27527 - Posted: 10.16.2020