BiotechNews1

Originally published by Tokyo University of Science, on February 13, 2024 Researchers discovered that activating a specific group of oxytocin neurons in the mouse brain improves performance in novel object recognition tasks. Credit: Akiyoshi Saitoh, Tokyo University of Science Oxytocin ( OXT) is a hormone that is known for its effects on psychological well-being and emotional bonding in animals . Interestingly, research has shown that this natural chemical in the brain plays a c rucial role in other cognitive processes as well, including learning and memory . Now, scientists may have discovered exactly how OXT influences memory in animals by studying "OXT neurons" that contain OXT receptors and function differently based on the availability of the chemical in the brain . In a recent study published in PLOS One , a group of researchers, headed by Professor Akiyoshi Saitoh, along with Junpei Takahashi from the Tokyo University of Science , delved into the complex

Originally published by Massachusetts Institute of Technology, on September 28, 2023 Credit: Wikimedia Commons Alzheimer's disease affects more than 6 million people in the United States, and there are very few FDA-approved treatments that can slow the progression of the disease. In hopes of discovering new targets for potential Alzheimer's treatments , MIT researchers have performed the broadest analysis yet of the genomic, epigenomic, and transcriptomic changes that occur in every cell type in the brains of Alzheimer's patients. Using more than 2 million cells from more than 400 postmortem brain samples , the researchers analyzed how gene expression is disrupted as Alzheimer's progresses . They also tracked changes in cells' epigenomic modifications , which help to determine which genes are turned on or off in a particular cell. Together, these approaches offer the most detailed picture yet of the genetic and molecular underpinnings of Alzheimer'

Originally published by Delthia Ricks , Medical Xpress, on August 30, 2023 Credit: Pixabay/CC0 Public Domain Losing the activity of a key ion channel in the brain may contribute to the buildup of a devastating and toxic protein responsible for the clumps of plaque that accumulate in Alzheimer's disease , a team of neurobiologists in China has found. Stunningly, this team has also shown—at least in animal-model studies—that this protein, a key hallmark of Alzheimer's, can be diminished in the living brain by manipulating the ion channel . The suspect protein is amyloid-beta , which becomes pervasive in the brain tissue of patients with Alzheimer's disease. Toxic, gooey amyloid-β accumulates in wads between neurons and disrupts the function of these vital brain cells . The ion channel is known simply as TRPM7 , and it may contribute to the buildup of toxic amyloid-β when the channel itself ceases to function properly, according to scientists at State Key Laborator

  Originally published by University of Sydney on August 24, 2023 Nanoscale scan image showing protein condensate interaction. Credit: The University of Sydney Many diseases affecting the brain and nervous system are linked to the formation of protein aggregates , or solid condensates , in cells from their liquid form condensate, but little is known about this process . This liquid-to-solid transition can trigger the formation of what are called amyloid fibrils . These can further form plaques in neurons causing neurodegenerative diseases such as Alzheimer's . Biomedical engineers at the University of Sydney , in collaboration with scientists at the University of Cambridge and Harvard University , have now developed sophisticated optical techniques to monitor at close range the process by which these protein aggregates form. By testing a protein associated with amyotrophic lateral sclerosis—ALS disease, which affected astrophysicist Professor Stephen Hawking—

  Originally p ublished b By Heather McKenzie on May 24, 2023   Pictured: Illustration of amyloid-beta oligomers accumulating into plaques on neurons/iStock, selvanegra In January, the FDA approved Eisai  and Biogen ’s Leqembi (lecanemab) to treat Alzheimer’s disease based on the antibody’s ability to reduce the accumulation of amyloid-beta plaques in the brain. Now, a recently published study has further clarified the drug’s mechanism of action, with potential implications for the future of Alzheimer’s drug development. Antibodies such as Leqembi work by binding to and neutralizing amyloid-beta protein oligomers, free-floating clumps of the amyloid-beta (Aβ) protein. These oligomers further aggregate into the notorious amyloid plaques that are characteristic of Alzheimer’s disease (AD). Original article  

  Originally published by Stephanie Pappas on May 15, 2023 The discovery of a gene variant that protects against an early, insidious form of Alzheimer's could lead to new treatments for the disease.   A man carried a genetic mutation that set him up to develop early-onset Alzheimer's disease, but another gene kept him healthy for many years. (Image credit: byakkaya via Getty Images) A newly discovered genetic variant protects against a particularly devastating form of early Alzheimer's disease , raising scientists' hopes of finding treatments that can prevent or slow the progression of this and other forms of the disease.  Read more