by Peter Hess Early sleep problems predict repetitive behaviors later in childhood1. And toddlers who overreact or underreact to sensory stimuli have more repetitive behaviors and other autism traits later on2. Together, the findings from two independent studies suggest that early behavioral differences may set the stage for restricted and repetitive behaviors, a core characteristic of autism also associated with other conditions of brain development. The studies also highlight areas for early intervention, particularly if further research identifies causal links between these traits. “Addressing sleep problems might be able to improve trajectories,” says Annette Estes, director of the University of Washington Autism Center in Seattle, who led the sleep study. Autistic children are twice as likely to have trouble sleeping as typical children. Their poor sleep has been linked to severe traits including severe repetitive and restricted behaviors. The new study is unusual in that it links sleep problems with a subset of ‘higher-order’ restrictive and repetitive behaviors that include restricted interests, rituals or routines and an insistence on sameness. The study involved 38 autistic children aged 2 to 6 years and 19 children with developmental delay aged 2 to 4. Parents completed a standardized questionnaire about their children’s sleep problems at age 4 — including difficulty falling asleep, short sleep duration and parasomnias such as sleepwalking and night terrors. Clinicians assessed autism traits, including repetitive behaviors, around age 2 and at two or three later points in time. © 2020 Simons Foundation

Keyword: Autism; Sleep
Link ID: 27208 - Posted: 04.22.2020

Abby Olena Instead of a traditional lymphatic system, the brain harbors a so-called glymphatic system, a network of tunnels surrounding arteries and veins through which fluid enters and waste products drain from the brain. In a study published March 25 in Science Translational Medicine, researchers show that the rodent eye also has a glymphatic system that takes out the trash through spaces surrounding the veins within the optic nerve. They also found that this system may be compromised in glaucoma and is capable of clearing amyloid-β, the build up of which has been implicated in the development of Alzheimer’s disease, glaucoma, and age-related macular degeneration. The work began in the group of Maiken Nedergaard, a neuroscientist with labs at both the University of Rochester Medical School and the University of Copenhagen, who described the glymphatic system of the brain in 2012. Xiaowei Wang, then a graduate student in Nedergaard’s group and now a postdoc at the University of California, San Francisco, was interested in the eye and spearheaded the search for an ocular glymphatic system. At that point, nobody had speculated that the optic nerve—in addition to transmitting electrical signals—is also a fluid transport highway, Nedergaard says. As Wang’s project was getting underway, Nedergaard met Lu Chen, a neuroscientist at the University of California, Berkeley, at a meeting. Chen’s group had done previous research on ocular lymphatics that focused on the front of the eye. There, the majority of the aqueous humor—the fluid that fills the chamber between the cornea and the lens—drains from the eye to the surrounding vasculature through a circular lymph-like vessel called Schlemm’s canal. This helps regulate intraocular pressure. Chen tells The Scientist that she and Nedergaard decided to collaborate to connect the knowledge about the front of the eye with their questions about the back of the eye. © 1986–2020 The Scientist

Keyword: Brain imaging; Vision
Link ID: 27207 - Posted: 04.22.2020

By Laura Sanders Neuroscientists love a good metaphor. Through the years, plumbing, telegraph wires and computers have all been enlisted to help explain how the brain operates, neurobiologist and historian Matthew Cobb writes in The Idea of the Brain. And like any metaphor, those approximations all fall short. Cobb leads a fascinating tour of how concepts of the brain have morphed over time. His writing is clear, thoughtful and, when called for, funny. He describes experiments by neurosurgeon Wilder Penfield, who zapped awake patients’ brains with electricity to provoke reactions. Zapping certain places consistently dredged up memories, which Cobb calls “oneiric experiences.” His footnote on the term: “Look it up. It’s exactly the right word.” I did, and it was. Cobb runs though the history of certain concepts used to explain how the brain works, including electricity, evolution and neurons. Next comes a section on the present, which includes discussions of memory, circuits and consciousness. Cobb offers tastes of the latest research, and a heavy dose of realism. Memory studies have made progress, but “we are still far from understanding what is happening when we remember,” Cobb writes. Despite big efforts, “we still only dimly understand what is going on when we see.” Our understanding of how antidepressants work? “Virtually non-existent.” This real talk is refreshing, and Cobb uses it to great effect to argue that neuroscience is stymied. “There have been many similar moments in the past, when brain researchers became uncertain about how to proceed,” he writes. Scientists have amassed an impressive stockpile of brain facts, but a true understanding of how the brain works eludes us. © Society for Science & the Public 2000–2020

Keyword: Miscellaneous
Link ID: 27206 - Posted: 04.22.2020

By Roni Caryn Rabin Obesity may be one of the most important predictors of severe coronavirus illness, new studies say. It’s an alarming finding for the United States, which has one of the highest obesity rates in the world. Though people with obesity frequently have other medical problems, the new studies point to the condition in and of itself as the most significant risk factor, after only older age, for being hospitalized with Covid-19, the illness caused by the coronavirus. Young adults with obesity appear to be at particular risk, studies show. The research is preliminary, and not peer reviewed, but it buttresses anecdotal reports from doctors who say they have been struck by how many seriously ill younger patients of theirs with obesity are otherwise healthy. No one knows why obesity makes Covid-19 worse, but hypotheses abound. Some coronavirus patients with obesity may already have compromised respiratory function that preceded the infection. Abdominal obesity, more prominent in men, can cause compression of the diaphragm, lungs and chest capacity. Obesity is known to cause chronic, low-grade inflammation and an increase in circulating, pro-inflammatory cytokines, which may play a role in the worst Covid-19 outcomes. Some 42 percent of American adults — nearly 80 million people — live with obesity. That is a prevalence rate far exceeding those of other countries hit hard by the coronavirus, like China and Italy. The new findings about obesity risks are bad news for all Americans, but particularly for African-Americans and other people of color, who have higher rates of obesity and are already bearing a disproportionate burden of Covid-19 deaths. High rates of obesity are also prevalent among low-income white Americans, who may also be adversely affected, experts say. More than half of Covid-19 deaths in the United States so far have been in New York and New Jersey, but the new findings mean the coronavirus could exact a steep toll in regions like the South and the Midwest, where obesity is more prevalent than in the Northeast. © 2020 The New York Times Company

Keyword: Obesity; Neuroimmunology
Link ID: 27205 - Posted: 04.17.2020

by Laura Dattaro Children with autistic older siblings have bigger neural responses than controls do in the brain networks that process faces, according to a new study1. The researchers followed these children from infancy to age 7, looking for relationships between neural signals and the children’s face-processing abilities that remained consistent during this period of development. The work is the first to track face processing in so-called ‘baby sibs’ — children who have autistic older siblings. Baby sibs are 20 times as likely to be diagnosed with autism as typical children are, and they often show autism traits early in life. For this reason, researchers frequently study them to get new clues about autism’s underlying biology. The new study shows the importance of monitoring neural activity and behavior over time to better understand autism, says lead investigator Tony Charman, chair of clinical child psychology at King’s College London in the United Kingdom. “If you measure both the neurocognitive abilities and the behaviors at multiple time points, maybe you get a better handle on the causal mechanisms,” Charman says. “If you understand the mechanisms, you’ve got at least a basis for talking about mechanistic-based interventions” — targeted therapies that might help ease autism traits. The team used electroencephalography (EEG) to measure the brain’s responses to faces and objects. One distinctive response, called the P1, occurs about 100 milliseconds after seeing any visual stimulus and is usually larger and faster when looking at a face. The N170 follows about 70 milliseconds later, mostly in the brain’s right hemisphere. This response is thought to mark the moment when the brain distinguishes a face from an object, or one face from another. In autistic children, the N170 is slower than in typical children2. © 2020 Simons Foundation

Keyword: Autism; Attention
Link ID: 27204 - Posted: 04.17.2020

By Elizabeth Pennisi Ring-tailed lemurs have a peculiar habit of shaking their tails at potential rivals. New research shows that during the breeding season, a male’s trembling tail may instead be whisking sexy odors toward potential mates. The work is still preliminary, but chemical analyses have revealed the odor is a mixture of three chemicals that seem to pique a female’s interest. The new work “calls attention to the often underappreciated fact” that odors play an important role in primate societies, says Peter Kappeler, a primatologist at the University of Göttingen. Insects often use behavior-altering odors called pheromones to attract mates. So do mice. But biochemist Kazushige Touhara at the University of Tokyo wanted to know whether primates—including humans—use them as well. Some researchers say yes, but the existence of such “sex attractants” remains controversial. Ring-tailed lemurs (Lemur catta), named for their fluffy gray and black tails, are unusual among their fellow primates. Males have glands on their wrists that produce chemicals that quickly vaporize when exposed to air—similar to pheromones. They rub their wrists on their tails to transfer the odors before they vaporize, then shake their tails to broadcast the scent. For most of the year, these lemurs make bitter, leathery smelling chemicals used to keep other males at bay. But during the breeding season, they instead emit a sweet scent, Touhara says. He and his colleagues collected these secretions from the wrist glands with a tiny pipette and analyzed the chemical components. © 2020 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Chemical Senses (Smell & Taste)
Link ID: 27203 - Posted: 04.17.2020

By John Pickrell Joseph Schubert spends hours at a time lying in the dirt of the Australian outback watching for tiny flickers in the sparse, ground-hugging foliage. The 22-year-old arachnologist is searching for flea-sized peacock spiders, and he admits, he’s a little obsessed. But it wasn’t always so. Schubert grew up fearing spiders, with parents who were “absolutely terrified” of the eight-legged crawlers. “I was taught that every single spider in the house was going to kill me, and we should squish it and get rid of it,” he says. Then Schubert stumbled across some photographs of Australia’s endemic peacock spiders, a group named for the adult males’ vivid coloring and flamboyant dance moves aimed at wooing a mate (SN: 9/9/16; SN: 12/8/15). And he was hooked. “They raise their third pair of legs and dance around and show off like they are the most amazing animals on the planet, which in my eyes they are.” He decided to pursue a career in arachnology. And despite not quite having completed his undergraduate degree in biology, he’s begun working part time at Museums Victoria in Melbourne, and has already made a mark. Of the 86 known peacock spider species — each just 2.5 to 6 millimeters in length — 12 have been described by Schubert, including seven named in the March 27 Zootaxa. Those seven were found at a range of sites across Australia, including the barren dunes and shrublands of Victoria state’s Little Desert and the red rocks and arid outback gorges of Kalbarri National Park, north of Perth. © Society for Science & the Public 2000–2020

Keyword: Sexual Behavior; Evolution
Link ID: 27202 - Posted: 04.17.2020

Brenda Patoine Can the key to consciousness be found in the folds of the cerebrum? Can the simple unfettered state of “being conscious” be localized in the brain, its properties deconstructed to precisely timed patterns of neural firing? Finding the answers is the goal of a $20 million international research program to search for the neural footprints of consciousness. The broad, multi-year initiative—termed Accelerating Research in Consciousness (ARC)—is being funded by the Templeton World Charity Foundation. In the first phase, representing $5 million, two leading brain theories of consciousness with diametrically opposed assumptions will face off to test their hypotheses. ARC pits the Integrated Information Theory (IIT) and the Global Neuronal Workplace (GNW) theory directly against one another, in what Templeton calls “adversarial collaboration,” to settle some fundamental questions about how, when, and where the brain processes subjective awareness of ourselves and the world around us. The two theoretical models are in stark contrast to one another: their definitions and assumptions of what constitutes consciousness differ and their whole approach to the subject is fundamentally different. What they have in common is that they both study the neural correlates of consciousness. IIT is the brainchild of Giulio Tononi, a professor and director of the Wisconsin Institute for Sleep and Consciousness at the University of Wisconsin. GNW has been elaborated by Stanislas Dehaene of INSERM/Unicog, in concert with Lionel Naccache of Sorbonne/INSERM, Jean-Pierre Changeux of Institut Pasteur, and others. These two theories were selected by Christof Koch, a leading consciousness researcher who is serving as an advisor to the Templeton project, because each has an established following among scientists and a “preponderance of evidence” backing them, says Koch, who now heads the Allen Institute for Brain Science. © 2020 The Dana Foundation.

Keyword: Consciousness
Link ID: 27201 - Posted: 04.16.2020

By Kelly Servick For the first time in decades, researchers may have a new way to tweak brain signals to treat psychosis and other symptoms of schizophrenia. Results from a 245-person clinical trial hint that a compound called SEP-363856, which seems to act on neural receptors involved in dopamine signaling, might address a broader range of schizophrenia symptoms than currently available drugs do—and with fewer side effects. “If these results are confirmed, this will be big, big news,” says Jeffrey Lieberman, a psychiatrist at Columbia University. The drug’s developer, Sunovion Pharmaceuticals Inc., identified it through an unusual screening process not guided by the brain circuits and receptors already implicated in the disease, Lieberman says. “It was a big gamble on their part. This study suggests that it may pay off.” The biological basis of schizophrenia remains a puzzle, but researchers have linked patients’ hallucinations and delusions to an excess of the chemical messenger dopamine. To inhibit dopamine signaling, existing antipsychotic drugs bind to a type of dopamine receptor on neurons called D2. These drugs help control abnormal perceptions and thoughts—the “positive” symptoms of schizophrenia. But they don’t do much to address either cognitive impairments or the “negative” symptoms, including lack of motivation, dulled emotion, and social withdrawal. “Those negative symptoms are often the most devastating,” says Diana Perkins, a psychiatrist at the University of North Carolina, Chapel Hill. “A person can become, at the most extreme, robotlike.” © 2020 American Association for the Advancement of Science.

Keyword: Schizophrenia
Link ID: 27200 - Posted: 04.16.2020

By Joel Shurkin I have learned that when someone you love has Alzheimer's, he or she is not the only one facing memory issues. Do we remember the bright, sunny person full of life and creativity, or do we remember the person who no longer recognizes us, who lies in a bed in a nursing home, gasping for air? Do we remember the lover with whom we could share our body, our thoughts and our adventures or the person who cannot finish a sentence or find the bathroom? How do we live with the fact that the individual actually died years before his or her body stopped? The ghastliness of Alzheimer's seems to push out everything else. I am finding it hard to remember ordinary life with Carol before Alzheimer's. My wife, Carol Howard, was diagnosed with early-onset Alzheimer's in her early 60s. I slowly watched her disintegrate, watched her beautiful mind be deconstructed part by part, watched sentience slowly fade until she was, well, not here. When she learned the diagnosis, she was determined to fight the disease. She enlisted in two clinical trials of potential drugs, both of which failed. When we realized what was inevitable, she told me that she wanted me to scream for her when she was gone. She was angry that several decades' worth of Alzheimer's research had produced no hope. There is no cure; there is no good treatment. I will tell you who she was and what she became. She was a woman of great beauty, with eyes of summer-sky blue. She was peaceful and brilliant, gentle and kind. I met her when she took a science communication course I taught at the University of California, Santa Cruz. She always put the right word in precisely the right place. Carol studied marine biology and wrote a popular book about her doctoral work with two Atlantic bottlenose dolphins. For 15 idyllic years we lived in the redwood forest of the Santa Cruz Mountains, writing. She eventually moved with me to Baltimore and worked at the Center for Alternatives to Animal Testing at the Johns Hopkins Bloomberg School of Public Health, an excellent job that she loved. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 27199 - Posted: 04.16.2020

By Tanya Lewis In March 2019 biotechnology giant Biogen stopped two big trials of its experimental Alzheimer's disease drug aducanumab because it did not appear to improve memory in declining patients. Then, in a surprise reversal several months later, the company and its partner, Japanese drugmaker Eisai, said they would ask the U.S. Food and Drug Administration to approve the treatment. A new analysis, Biogen said, showed that a subset of people on the highest doses in one trial did benefit from the compound, which dissolves clumps of a protein called beta-amyloid within the brain. The back-and-forth decisions, along with the failure of a slew of other amyloid-clearing compounds, have left experts divided about whether treating amyloid buildup—long thought to be the best target for an Alzheimer's therapy—is still a promising approach. Some of the scientists rethinking the so-called amyloid hypothesis helped to generate it in the first place. “I would say it has legs, but it's limping,” says geneticist John Hardy, who co-authored the genetic studies that pioneered the idea more than two decades ago. According to Hardy, who runs a molecular neuroscience program at University College London's Institute of Neurology, “the [concept] we drew in 1998 is cartoonishly oversimplistic. There were lots of question marks. We thought those questions would be filled in within a couple of years. And yet 20 years later they are not filled in.” Other experts, though, still contend that the amyloid hypothesis is a strong explanation and that treatments targeting the protein are the right way to go. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 27198 - Posted: 04.16.2020

Carl Sherman The world of neuroscience and psychiatry sat up and took notice last March when the Food and Drug Administration (FDA) approved brexanolone (Zulresso) for postpartum depression. It was the first drug specifically approved for the condition, which afflicts some 15 percent of women just before or shortly after childbirth. The event was a pivotal chapter in a neuroscience story that began three-quarters of a century ago with the 1941 discovery by Hans Selye (best known for his pioneering research into the nature of stress) that hormones including progesterone could affect the brain to induce deep anesthesia. Fast-forward 40 years to the discovery that a number of hormones—termed “neurosteroids” by the neuroscientist/endocrinologist Étienne-Émile Baulieu, a key figure in this work—are synthesized within the nervous system itself. In their National Institutes of Mental Health (NIMH) lab, Steven Paul and colleagues showed that several of these compounds work by binding to receptors on brain cells that are activated by GABA, the most plentiful inhibitory neurotransmitter in the brain. The GABA-A receptor is the site of action of several sedating central nervous system (CNS) drugs, including benzodiazepines (Valium, Librium), barbiturates, and many anesthetics. Neurosteroids can also bind to receptors for glutamate, the brain’s principal excitatory neurotransmitter. Paul and Robert Purdy proposed that, with its effect on both GABAergic and glutaminergic systems, neuroactive steroids (a term they coined to include synthetic analogues as well as the naturally-occurring hormones themselves) help regulate excitation throughout the brain. Excitation is a major factor in conditions such as epilepsy. Although there are many neuroactive steroids, the lion’s share of research has focused on allopregnanolone, a progesterone derivative. © 2020 The Dana Foundation.

Keyword: Depression; Stress
Link ID: 27197 - Posted: 04.16.2020

Researchers have discovered a technique for directly reprogramming skin cells into light-sensing rod photoreceptors used for vision. The lab-made rods enabled blind mice to detect light after the cells were transplanted into the animals’ eyes. The work, funded by the National Eye Institute (NEI), published April 15 in Nature. The NEI is part of the National Institutes of Health. Up until now, researchers have replaced dying photoreceptors in animal models by creating stem cells from skin or blood cells, programming those stem cells to become photoreceptors, which are then transplanted into the back of the eye. In the new study, scientists show that it is possible to skip the stem-cell intermediary step and directly reprogram skins cells into photoreceptors for transplantation into the retina. “This is the first study to show that direct, chemical reprogramming can produce retinal-like cells, which gives us a new and faster strategy for developing therapies for age-related macular degeneration and other retinal disorders caused by the loss of photoreceptors,” said Anand Swaroop, Ph.D., senior investigator in the NEI Neurobiology, Neurodegeneration, and Repair Laboratory, which characterized the reprogrammed rod photoreceptor cells by gene expression analysis. “Of immediate benefit will be the ability to quickly develop disease models so we can study mechanisms of disease. The new strategy will also help us design better cell replacement approaches,” he said. Scientists have studied induced pluripotent stem (iPS) cells with intense interest over the past decade. IPSCs are developed in a lab from adult cells —rather than fetal tissue— and can be used to make nearly any type of replacement cell or tissue. But iPS cell reprogramming protocols can take six months before cells or tissues are ready for transplantation. By contrast, the direct reprogramming described in the current study coaxed skin cells into functional photoreceptors ready for transplantation in only 10 days. The researchers demonstrated their technique in mouse eyes, using both mouse- and human-derived skin cells.

Keyword: Vision; Stem Cells
Link ID: 27196 - Posted: 04.16.2020

Gregory Berns, M.D., Ph.D. There is no official census for dogs and cats, but in 2016, the American Veterinary Medical Association estimated that 59 percent of households in the United States had a pet. Although the numbers of dogs and cats remains debatable, dogs continue to gain in popularity with 38 percent of households having at least one. Families with children are even more likely to have a dog (55 percent). With all due respect to cats, dogs have insinuated themselves into human society, forming deep emotional bonds with us and compelling us to feed and shelter them. Worldwide, the dog population is approaching one billion, the majority free-ranging. Even though many people are convinced they know what their dog is thinking, little is actually known about what is going on in dogs’ heads. This may be surprising because the field of experimental psychology had its birth with Pavlov and his salivating dogs. But as dogs gained traction as household pets, in many cases achieving the status of family members, their use as research subjects fell out of favor. In large part, this was a result of the Animal Welfare Act of 1966, which set standards for the treatment of animals in research and put an end to the practice of stealing pets for experimentation. How strange it is then that these creatures, whose nearest relatives are wolves, live with us and even share our beds, yet we know almost nothing about what they’re thinking. In the last decade or so, however, the situation has begun to change, and we are in the midst of a renaissance of canine cognitive science. Research labs have sprung up around the world, and dogs participate not as involuntary subjects, but as partners in scientific discovery. This new research is beginning to shed light on what it’s like to be a dog and the nature of the dog-human bond. © 2020 The Dana Foundation.

Keyword: Brain imaging; Evolution
Link ID: 27195 - Posted: 04.16.2020

Abby Olena Base editors, which convert one nucleotide to another without a double-strand DNA break, have the potential to treat diseases caused by mutant genes. One drawback, though, is that the DNA that encodes CRISPR base editors is long—too long to fit in the adeno-associated viruses (AAVs) most commonly used for gene therapy. In a study published in Molecular Therapy on January 13, researchers split the DNA encoding a base editor into two AAV vectors and injected them into a mouse model of inherited amyotrophic lateral sclerosis (ALS). The strategy disabled the disease-causing gene, improving the animals’ symptoms and prolonging their lives. “We’d like to be able to make gene editing tools that can fit inside an AAV vector. Unfortunately, some of the tools are so big that they can’t fit inside, so in this study, they were able to come up with a solution to that by using a split protein,” says David Segal, a biochemist at the University of California, Davis, who was not involved in the work. “It’s not the first time that that system has been used, but it’s the first time it’s been applied to this kind of base editor.” Pablo Perez-Pinera, a bioengineer at University of Illinois at Urbana-Champaign, and colleagues developed a strategy to split the base editor into two chunks. In a study published in 2019, they generated two different AAV vectors, each containing a portion of coding DNA for an adenine-to-thymine base editor. They also included sequences encoding so-called inteins—short peptides that when they are expressed within proteins stick together and cleave themselves out, a bit like introns in RNA. The researchers built the inteins into the vectors such that when the inteins produced by the two vectors dimerized, bringing the two base editor parts together, and then excised themselves, they left behind a full-length, functional base editor. © 1986–2020 The Scientist

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 27194 - Posted: 04.15.2020

By Kenneth S. Kosik No fundamental obstacle prevents us from developing an effective treatment for Alzheimer's disease. Other troubles of human nature, such as violence, greed and intolerance, have a bewildering variety of daunting causes and uncertainties. But Alzheimer's, at its core, is a problem of cell biology whose solution should be well within our reach. There is a fairly good chance that the scientific community might already have an unrecognized treatment stored away in a laboratory freezer among numerous vials of chemicals. And major insights may now reside, waiting to be noticed, in big databases or registries of clinical records, neuropsychological profiles, brain-imaging studies, biological markers in blood and spinal fluid, genomes, protein analyses, neuron recordings, or animal and cell culture models. But we have missed those clues because for decades we have spent too much time chasing every glossy new finding in Alzheimer's research and too little time thinking deeply about the underlying biology of this ailment. Instead our work has been driven by a number of assumptions. Among those assumptions has been the central and dominant role of the protein fragment called beta-amyloid. A large amount of data supports the idea that beta-amyloid plays an important part in the disease. We have developed drugs that can reduce concentrations of the protein fragments in people with Alzheimer's, yet by and large they have not stopped patients' cognitive decline in any meaningful way. It now seems simplistic to conclude that eliminating or inhibiting beta-amyloid will cure or treat those suffering from the disease, especially without far deeper and more comprehensive knowledge of how it develops and progresses [see “The Amyloid Drug Struggle”]. We have not been barking up a completely wrong research tree, but our zeal has led us to ignore other trees and even the roots of this particular one. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 27193 - Posted: 04.15.2020

According to a recent analysis of data from two major eye disease studies, adherence to the Mediterranean diet – high in vegetables, whole grains, fish, and olive oil – correlates with higher cognitive function. Dietary factors also seem to play a role in slowing cognitive decline. Researchers at the National Eye Institute (NEI), part of the National Institutes of Health, led the analysis of data from the Age-Related Eye Disease Study (AREDS) and AREDS2. They published their results today in Alzheimer’s and Dementia: the Journal of the Alzheimer’s Association. “We do not always pay attention to our diets. We need to explore how nutrition affects the brain and the eye” said Emily Chew, M.D., director of the NEI Division of Epidemiology and Clinical Applications and lead author of the studies. The researchers examined the effects of nine components of the Mediterranean diet on cognition. The diet emphasizes consumption of whole fruits, vegetables, whole grains, nuts, legumes, fish, and olive oil, as well as reduced consumption of red meat and alcohol. AREDS and AREDS2 assessed over years the effect of vitamins on age-related macular degeneration (AMD), which damages the light-sensitive retina. AREDS included about 4,000 participants with and without AMD, and AREDS2 included about 4,000 participants with AMD. The researchers assessed AREDS and AREDS2 participants for diet at the start of the studies. The AREDS study tested participants’ cognitive function at five years, while AREDS2 tested cognitive function in participants at baseline and again two, four, and 10 years later. The researchers used standardized tests based on the Modified Mini-Mental State Examination to evaluate cognitive function as well as other tests. They assessed diet with a questionnaire that asked participants their average consumption of each Mediterranean diet component over the previous year.

Keyword: Alzheimers; Obesity
Link ID: 27192 - Posted: 04.15.2020

By Gary Stix Consumer genetic tests can sometimes result in a terrible surprise appearing in the same report that divulges whether one has a cilantro aversion or wet or dry earwax. Test takers may receive the devastating news that they have a version of a gene—apolipoprotein E epsilon 4 (APOE e4)—that greatly increases their chances of getting Alzheimer’s disease. The shock can be so great that some will seek solace in a support group to help them adjust to the possibility that they could run into cognitive problems beginning in their 50s or 60s. One thing that makes the information so difficult to absorb is that there is no certainty about it. A person with one copy of the APOE e4 gene is more than three times as likely to wind up with Alzheimer’s (one copy can be inherited from each parent). A hit of two copies increases the risk by 10 times or more. APOE e4 may also reduce the age of the disease’s onset by up to a decade. Still, not everyone who is an APOE e4 carrier will ultimately receive a diagnosis for Alzheimer’s, the most common form of dementia. Given the ambiguities, scientists have long wondered whether other genes might counterbalance APOE e4's effects. A new paper may have found a candidate for just such a gene. Advertisement An analysis across multiple studies—with results from more than 20,000 individuals—found that APOE e4 carriers between the ages of 60 and 80 who also had a particular variant of a gene called klotho (named for Clotho, one of the Greek Fates, who spins the thread of life) were 30 percent less likely to receive an Alzheimer's diagnosis than carriers without it. People in their late 70s with a single copy of the klotho variant were also less apt to experience the initial cognitive losses (mild cognitive impairments) that often precede an Alzheimer’s diagnosis. Study participants with the relevant variant also had reduced signs of the hallmark clumps of beta-amyloid protein that turn up in the brain before symptoms arise. © 2020 Scientific American,

Keyword: Alzheimers; Genes & Behavior
Link ID: 27191 - Posted: 04.15.2020

Peter Rhys-Evans For the past 150 years, scientists and laypeople alike have accepted a “savanna” scenario of human evolution. The theory, primarily based on fossil evidence, suggests that because our ancestral ape family members were living in the trees of East African forests, and because we humans live on terra firma, our primate ancestors simply came down from the trees onto the grasslands and stood upright to see farther over the vegetation, increasing their efficiency as hunter-gatherers. In the late 19th century, anthropologists only had a few Neanderthal fossils to study, and science had very little knowledge of genetics and evolutionary changes. So this savanna theory of human evolution became ingrained in anthropological dogma and has remained the established explanation of early hominin evolution following the genetic split from our primate cousins 6 million to 7 million years ago. But in 1960, a different twist on human evolution emerged. That year, marine biologist Sir Alister Hardy wrote an article in New Scientist suggesting a possible aquatic phase in our evolution, noting Homo sapiens’s differences from other primates and similarities to other aquatic and semi-aquatic mammals. In 1967, zoologist Desmond Morris published The Naked Ape, which explored different theories about why modern humans lost their fur. Morris mentioned Hardy’s “aquatic ape” hypothesis as an “ingenious” theory that sufficiently explained “why we are so nimble in the water today and why our closest living relatives, the chimpanzees, are so helpless and quickly drown.” © 1986–2020 The Scientist

Keyword: Evolution
Link ID: 27190 - Posted: 04.15.2020

Our ability to study networks within the nervous system has been limited by the tools available to observe large volumes of cells at once. An ultra-fast, 3D imaging technique called SCAPE microscopy, developed through the National Institutes of Health (NIH)’s Brain Research through Advancing Innovative Technologies (BRAIN) Initiative, allows a greater volume of tissue to be viewed in a way that is much less damaging to delicate networks of living cells. In a study published in Science, researchers used SCAPE to watch for the first time how the mouse olfactory epithelium — the part of the nervous system that directly perceives smells — reacted in real time to complex odors. They found that those nerve cells may play a larger and more complex role in interpreting smells than was previously understood. “This is an elegant demonstration of the power of BRAIN Initiative technologies to provide new insights into how the brain decodes information to produce sensations, thoughts, and actions,” said Edmund Talley, Ph.D., program director, National Institute of Neurological Disorders and Stroke (NINDS), a part of NIH. The SCAPE microscope was developed in the laboratory of Elizabeth M.C. Hillman, Ph.D., professor of biomedical engineering and radiology and principal investigator at Columbia’s Zuckerman Institute in New York City. “SCAPE microscopy has been incredibly enabling for studies where large volumes need to be observed at once and in real time,” said Dr. Hillman. “Because the cells and tissues can be left intact and visualized at high speeds in three dimensions, we are able to explore many new questions that could not be studied previously.”

Keyword: Brain imaging; Chemical Senses (Smell & Taste)
Link ID: 27189 - Posted: 04.14.2020