New Support for Amyloid-β Antimicrobial as Brain’s First Defense Against Infection

New Support for Amyloid-β Antimicrobial as Brain’s First Defense Against Infection
Alzheimer’s disease research and drug development has for the last several decades focused feircly on the elimination of amyloid-β — the protein that aggregates forming plaques in brain neurons of patients. Now, a new study suggests that the protein is part of the immune system, having an evolutionary important antimicrobial role in fighting invading pathogens by entrapping them in the sticky protein clusters. "Neurodegeneration in Alzheimer's disease has been thought to be caused by the abnormal behavior of amyloid-β molecules, which are known to gather into tough fibril-like structures called amyloid plaques within patients' brains," said senior study author Robert Moir of the Genetics and Aging Research Unit at Massachusetts General Hospital's Institute for Neurodegenerative Disease (MGH-MIND), said in a news release. "This widely held view has guided therapeutic strategies and drug development for more than 30 years, but our findings suggest that this view is incomplete." The presence and behavior of the amyloid-β protein has baffled researchers for ages, and the protein deposits associated to Alzheimer’s disease have been considered an accidental process caused by abnormal breakdown processes. The researchers behind the recent findings published in Science Translational Medicine, had already flagged the possibility that the explanation was not good enough six years ago when they published a study demonstrating the ability of amyloid-β to function as a
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