A new Yale study has revealed that neurons — the energy-hungry cells that connect and direct activity in the brain — are equipped with “backup batteries” that kick in to keep the brain running during periods of metabolic stress.
Writing in Proceedings of the National Academy of Sciences, researchers describe how neurons store their own glycogen, a form of sugar that helps neurons stay resilient when their main energy sources falter.
LONDON, Ont. – Dementia poses a major health challenge with no safe, affordable treatments to slow its progression.
Researchers at Lawson Research Institute (Lawson), the research arm of St. Joseph’s Health Care London, are investigating whether Ambroxol — a cough medicine used safely for decades in Europe — can slow dementia in people with Parkinson’s disease.
Published today in the prestigious JAMA Neurology, this 12-month clinical trial involving 55 participants with Parkinson’s disease dementia (PDD) monitored memory, psychiatric symptoms and GFAP, a blood marker linked to brain damage.
Parkinson’s disease dementia causes memory loss, confusion, hallucinations and mood changes. About half of those diagnosed with Parkinson’s develop dementia within 10 years, profoundly affecting patients, families and the health care system.
When was the last time you sat down and tried to learn something? How did you approach it? Did you make flashcards for hard-to-remember terms and concepts, ask a friend to quiz you on the subject or simply jump into the deep end with a new project?
New research from Northeastern University psychology professor Aaron Seitz published in Current Opinion in Neurobiology suggests that whenever we learn something new—if we’re successful—what we’ve actually done is tricked our brains into a learnable state. He calls this “incidental learning.”
“‘Incidental learning’ typically refers to what we learn without explicit intention,” Seitz says. A good example of this comes from “statistical regularity” in one’s surroundings, he says.
From the very beginning, MIT Professor Mark Bear’s philosophy for the textbook “Neuroscience: Exploring the Brain” was to provide an accessible and exciting introduction to the field while still giving undergraduates a rigorous scientific foundation. In the 30 years since its first print printing in 1995, the treasured 975-page tome has gone on to become the leading introductory neuroscience textbook, reaching hundreds of thousands of students at hundreds of universities around the world.
“We strive to present the hard science without making the science hard,” says Bear, the Picower Professor in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences at MIT. The fifth edition of the textbook is out today from the publisher Jones & Bartlett Learning.
Bear says the book is conceived, written, and illustrated to instill students with the state of knowledge in the field without assuming prior sophistication in science. When he first started writing it in the late 1980s — in an effort soon joined by his co-authors and former Brown University colleagues Barry Connors and Michael Paradiso — there simply were no undergraduate neuroscience textbooks. Up until then, first as a graduate teaching assistant and then as a young professor, Bear taught Brown’s pioneering introductory neuroscience class with a spiral-bound stack of photocopied studies and other scrounged readings.
A specially engineered antibody that can accurately deliver RNA treatments into hard-to-reach and hard-to-treat tumors significantly improved survival and reduced tumor sizes in animal models, according to a study reported in Science Translational Medicine.
The study provides evidence that, once injected into the bloodstream, the antibody TMAB3, combined with a type of RNA that stimulates an innate immune reaction, can localize to tumors and penetrate and destroy stubborn diseased cells in pancreatic, brain, and skin cancers.
“Delivery of RNA-based therapies to tumors has been a challenge. Our finding that TMAB3 can form antibody/RNA complexes capable of delivering RNA payloads to tumors provides a new approach to overcome this challenge,” says Peter Glazer, senior author and Robert E. Hunter Professor of Therapeutic Radiology and Genetics at Yale School of Medicine (YSM).
Stroke kills millions, but Osaka researchers have unveiled GAI-17, a drug that halts toxic GAPDH clumping, slashes brain damage and paralysis in mice—even when given six hours post-stroke—and shows no major side effects, hinting at a single therapy that could also tackle Alzheimer’s and other tough neurological disorders.
In the last decade, the incidence of restrictive eating disorders in children, like anorexia-nervosa and avoidant/restrictive food intake disorders (ARFID), has doubled. These disorders have severe consequences for growing children, resulting in nutritional deficiencies and problems with bone development, statural growth and puberty. Most studies have focused on the effects of these disorders in older individuals, and little is currently known about how restrictive eating disorders affect the brain in children or what mechanisms in the brain might be responsible for this restrictive eating behavior.
To get a better understanding of how these early-onset eating disorders work in the brain, researcher Clara Moreau and her team conducted MRI brain scans on 290 children, of which 124 had been hospitalized for early-onset anorexia-nervosa (EO-AN), 50 had been hospitalized for ARFID, and 116 were children with no eating disorders. All participants were under 13 years old, and those who were hospitalized had very low body mass index (BMI) due to restrictive eating. The results were published in Nature Mental Health.
Although EO-AN and AFRID both result in low BMI and malnutrition due to restrictive eating, they are distinct disorders. EO-AN—as well as later onset anorexia-nervosa—is characterized by restrictive eating arising from a distorted body image, while restrictive eating in AFRID arises from sensory issues, such as a dislike of certain food textures, a lack of interest in food or fear of negative health consequences from food. These differences indicate that the disorders probably arise from different mechanisms in the brain.