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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 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