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Novel Drug Prevents Amyloid Plaques, a Hallmark of Alzheimer s Disease

Novel Drug Prevents Amyloid Plaques, a Hallmark of Alzheimer’s Disease In animal models, the new compound modulated a key enzyme, reducing or eliminating production of problematic protein fragments; human clinical trials needed March 02, 2021  |  Scott LaFee News release Amyloid plaques are pathological hallmarks of Alzheimer’s disease (AD) clumps of misfolded proteins that accumulate in the brain, disrupting and killing neurons and resulting in the progressive cognitive impairment that is characteristic of the widespread neurological disorder. In a new study, published March 2, 2021 in the Journal of Experimental Medicine (JEM), researchers at University of California San Diego School of Medicine, Massachusetts General Hospital and elsewhere have identified a new drug that could prevent AD by modulating, rather than inhibiting, a key enzyme involved in forming amyloid plaques.

How does your brain process emotions? Answer could help address loneliness epidemic

 E-Mail IMAGE: Jyoti Mishra, PhD, is the senior author of the study, director of the NEATLabs and assistant professor in the Department of Psychiatry at UC San Diego School of Medicine. view more  Credit: UC San Diego Health Sciences Research over the last decade has shown that loneliness is an important determinant of health. It is associated with considerable physical and mental health risks and increased mortality. Previous studies have also shown that wisdom could serve as a protective factor against loneliness. This inverse relationship between loneliness and wisdom may be based in different brain processes. In a study published in the March 5, 2021 online edition of

Novel Drug Prevents Amyloid Plaques, a Hallmark of Alzheimer s Disease

Novel Drug Prevents Amyloid Plaques, a Hallmark of Alzheimer s Disease
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Novel drug prevents amyloid plaques, a hallmark of Alzheimer s disease

Researchers at UC San Diego School of Medicine and elsewhere have identified a new drug that could prevent AD by modulating, rather than inhibiting, a key enzyme involved in forming amyloid plaques.

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