Sandra G. Boodman First she toppled off a ladder. Then Carol Hardy-Fanta tripped on a step outside her western Massachusetts home while gazing at her cellphone. Next she fell three times during a five-mile hike after catching her left foot on a rock or tree root. At first, Hardy-Fanta thought her repeated stumbles had a simple cause: She was distracted. But when she racked up more than 30 falls in a three-year period — some for no apparent reason — she repeatedly asked her doctors whether an undiagnosed medical problem might be causing her to “drop like a log.” The 10 doctors she consulted between 2016 and 2019 — four orthopedists, three neurologists, a rheumatologist, a podiatrist and her internist — reached disparate conclusions. One suggested she was clumsy. Others suspected her problem was primarily orthopedic or could find no clear explanation. It wasn't until September 2019 that a scan revealed what Hardy-Fanta had come to suspect — a diagnosis she said several of her doctors had brushed off. “These are the smartest people,” said Hardy-Fanta, now 71, whose husband is a Boston physician. “They really wanted to help” but appeared to be misled by her symptoms. “If someone’s falling that much, they should really pay attention.” The falls started in 2016, shortly after Hardy-Fanta and her husband sold their house in a Boston suburb and began splitting their time between a condo in the city and what she described as their “dream home” in the Berkshires. Hardy-Fanta had retired as director of a university think tank. Her fourth book on women and politics had just been published. She was in excellent health, which she regarded as a legacy from her mother, who remained mentally sharp and physically able until shortly before her death at age 100. Hardy-Fanta said she was looking forward to traveling with her husband and taking long bike rides along the scenic rural roads that snake through the Berkshires.

Keyword: Parkinsons
Link ID: 27216 - Posted: 04.27.2020

by Peter Hess The mood-stabilizing drug lithium eases repetitive behaviors seen in mice missing SHANK3, an autism gene, according to a new study1. The findings suggest lithium merits further study as a treatment for some people with autism, even though the drug has troublesome side effects, including tremors and impaired memory. “Lithium is, of course, a rather difficult, non-ideal treatment,” says lead investigator Gina Turrigiano, professor of vision science at Brandeis University in Waltham, Massachusetts. “It’s really hard to get people on a lithium regimen that they can tolerate well.” But understanding why lithium works may set the stage for better treatments, she says. About 1 percent of people with autism have mutations in SHANK3. Deletion or mutation of the gene can also lead to Phelan-McDermid syndrome, which is characterized by intellectual disability, delayed speech and, often, autism. Case studies of people with Phelan-McDermid syndrome also suggest that lithium eases behavior problems associated with the condition2. Previous work has shown that SHANK3 helps stabilize neuronal circuits by adjusting excitatory and inhibitory signaling like a thermostat. This process, called homeostatic plasticity, allows neurons to respond to changes in sensory input. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27215 - Posted: 04.27.2020

By Sam Roberts Donald Kennedy, a neurobiologist who headed the Food and Drug Administration before becoming president of Stanford University, where he oversaw major expansions of its campus and curriculum and weathered a crisis over research spending, died on April 21 in Redwood City, Calif. He was 88. His death, at a residential care facility, was caused by complications of the new coronavirus, his wife, Robin Kennedy, said. He had suffered a severe stroke in 2015. Stanford had been Dr. Kennedy’s life since 1960, when, not yet 30, he joined its faculty as an assistant professor of biology. And except for a stint in the late 1970s as head of the F.D.A. under President Jimmy Carter, he remained wedded to the university, becoming provost and then president in 1980, beginning an 11-year tenure. It was a productive one. During his presidency the university opened the Stanford Humanities Center and campuses in Oxford, England; Kyoto, Japan; and Washington; diversified the Western culture curriculum; and raised $1.2 billion in a five-year centennial campaign, although by the end of the decade the university was facing deficits. His tenure also coincided with fiery debates over antiwar protests and academic freedom by both professors and students, divestiture of the university’s holdings in companys doing business in South Africa, and $160 million in damage inflicted by the Loma Prieta Earthquake in 1989. A would-be writer who had become a neurobiologist in college adventitiously, Dr. Kennedy found his leadership under the microscope in the early 1990s, when the university was accused — and later cleared — of improperly billing the Navy for research expenses. The accusations were aired by federal auditors and Representative John D. Dingell Jr., a tenacious Michigan Democrat, who said that Stanford may have billed the government for as much as $200 million in improper expenses on research contracts for over a decade. © 2020 The New York Times Company

Keyword: Miscellaneous
Link ID: 27214 - Posted: 04.27.2020

By E. Ray Dorsey, Todd Sherer, Michael S. Okun, Bastiaan R. Bloem The number of people with Parkinson’s disease more than doubled from 1990 to 2015 and could double again by 2040. An aging population alone does not account for this rise. Air pollution, metal production, certain industrial chemicals, and some synthetic pesticides are linked to Parkinson’s. Yet we are doing little to manage known risk factors. Neither our increased awareness of the disease nor our lengthening life spans can fully account for the upsurge in diagnoses that we now face. Our knowledge of another neurological disorder, multiple sclerosis, has increased too, and we have improved diagnostic tools for it. Rates for multiple sclerosis have indeed gone up, but that increase is nothing like the exponential rise of Parkinson’s (see figure below). As for aging, more people are, of course, living longer. For example, from 1900 to 2014, the number of individuals over age 65 in the United Kingdom increased about sixfold. However, over that same period, the number of deaths due to Parkinson’s disease increased almost three times faster. Parkinson’s disease is characterized by tremors, slowness in movement, stiffness, and difficulties with balance and walking. It can also cause a wide range of symptoms that are not visible—loss of smell, constipation, sleep disorders, and depression. Most people with Parkinson’s are diagnosed in their fifties or later. But it is not just a disease of the elderly. Up to 10 percent of those with the condition develop the disease in their forties or younger. © 2020 Sigma Xi, The Scientific Research Honor Society

Keyword: Parkinsons; Neurotoxins
Link ID: 27213 - Posted: 04.24.2020

by Lauren Schenkman Mice with mutations in a gene called DLG2 are anxious and asocial; they also sleep poorly and overgroom themselves, according to a new study1. These characteristics resemble those seen in some people with autism. The results offer the first evidence that mutations in DLG2 may account for some of the condition’s behavioral traits. “This study is a baby step indicating DLG2’s implication in [autism’s] core behavioral symptoms,” says lead investigator Soo Young Kim, assistant professor of pharmacy at Yeungnam University in Gyeongsan, South Korea. A 2013 study reported that mice and people with DLG2 mutations have differences in learning, attention and other cognitive processes2. Last year, a study of nearly 500 families with two or more autistic children identified DLG2 as a candidate gene for autism3. The new work offers “a more full picture” of DLG2’s effect on behavior, says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland. Grant led the 2013 work but was not involved in the new study. “It’s a useful contribution.” Kim and her colleagues bred male mice that have two mutant copies of DLG2. The animals lack the corresponding protein, which forms part of a neuron’s scaffolding. DLG4, another gene implicated in autism, has a similar role. © 2020 Simons Foundation

Keyword: Autism; Schizophrenia
Link ID: 27212 - Posted: 04.24.2020

By Ann Gibbons If you think you got your freckles, red hair, or even narcolepsy from a Neanderthal in your family tree, think again. People around the world do carry traces of Neanderthals in their genomes. But a study of tens of thousands of Icelanders finds their Neanderthal legacy had little or no impact on most of their physical traits or disease risk. Paleogeneticists realized about 10 years ago that most Europeans and Asians inherited 1% to 2% of their genomes from Neanderthals. And Melanesians and Australian Aboriginals get another 3% to 6% of their DNA from Denisovans, Neanderthal cousins who ranged across Asia 50,000 to 200,000 years ago or so. A steady stream of studies suggested gene variants from these archaic peoples might raise the risk of depression, blood clotting, diabetes, and other disorders in living people. The archaic DNA may also be altering the shape of our skulls; boosting our immune systems; and influencing our eye color, hair color, and sensitivity to the Sun, according to scans of genomic and health data in biobanks and medical databases. But the new study, which looked for archaic DNA in living Icelanders, challenges many of those claims. Researchers from Aarhus University in Denmark scanned the full genomes of 27,566 Icelanders in a database at deCODE Genetics in Iceland, seeking unusual archaic gene variants. The researchers ended up with a large catalog of 56,000 to 112,000 potentially archaic variants—and a few surprises. They found, for example, that Icelanders had inherited 3.3% of their archaic DNA from Denisovans and 12.2% from unknown sources. (84.5% came from close relatives of the reference Neanderthals.) © 2020 American Association for the Advancement of Science.

Keyword: Evolution; Genes & Behavior
Link ID: 27211 - Posted: 04.24.2020

Christie Wilcox Sex might be biology’s most difficult enigma. The downsides of relying on sex to reproduce are undeniable: It takes two individuals, each of whom gets to pass on only part of their genome. Because these individuals generally have to get fairly intimate, they make themselves vulnerable to physical harm or infections from their partner. Asexual reproduction, or self-cloning, has none of these disadvantages. Clones can be made anywhere and anytime, and they receive the full complement of an individual’s genes. Yet despite all its benefits, asexual reproduction is the exception, not the norm, among organisms that have compartmentalized cells (eukaryotes). In plants, for example — which are somewhat known for their genetic flexibility — less than 1% of species are thought to reproduce asexually often. Among animals, only one out of every thousand known species is exclusively asexual. For centuries, biologists have pondered this apparent paradox. In 1932, the geneticist Hermann Muller, whose work on radiation-induced mutations would eventually garner a Nobel Prize, believed he had the answer. “Genetics has finally solved the age-old problem of the reason for the existence (i.e., the function) of sexuality and sex,” he boasted in The American Naturalist. He went on to explain, “Sexuality, through recombination, is a means for making the fullest use of the possibilities of gene mutations.” All Rights Reserved © 2020

Keyword: Sexual Behavior; Evolution
Link ID: 27210 - Posted: 04.24.2020

By Benjamin Powers On the 10th floor of a nondescript building at Columbia University, test subjects with electrodes attached to their heads watch a driver’s view of a car going down a street through a virtual reality headset. All the while, images of pianos and sailboats pop up to the left and right of each test subject’s field of vision, drawing their attention. The experiment, headed by Paul Sajda, a biomedical engineer and the director of Columbia’s Laboratory for Intelligent Imaging and Neural Computing, monitors the subjects’ brain activity through electroencephalography technology (EEG), while the VR headset tracks their eye movement to see where they’re looking — a setup in which a computer interacts directly with brain waves, called a brain computer interface (BCI). In the Columbia experiment, the goal is to use the information from the brain to train artificial intelligence in self-driving cars, so they can monitor when, or if, drivers are paying attention. BCIs are popping up in a range of fields, from soldiers piloting a swarm of drones at the Defense Advanced Research Projects Agency (DARPA) to a Chinese school monitoring students’ attention. The devices are also used in medicine, including versions that let people who have been paralyzed operate a tablet with their mind or that give epileptic patients advance warning of a seizure. And in July 2019, Elon Musk, the CEO and founder of Tesla and other technology companies, showed off the work of his venture Neuralink, which could implant BCIs in people’s brains to achieve “a symbiosis with artificial intelligence.”

Keyword: Robotics; Brain imaging
Link ID: 27209 - Posted: 04.22.2020

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