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Sylvain E. Lesné (born 1974) is a French neuroscientist and associate professor at the Department of Neuroscience at the University of Minnesota (UMN) Medical School, known for his research into Alzheimer's disease. He is the primary author of a controversial 2006 Nature paper, "A specific amyloid-β protein assembly in the brain impairs ...
In 2006, three of her research papers made a list of the eighteen papers that had contributed the most to Alzheimer's research. [20] Ashe is a co-author on a 2006 paper published in Nature (retracted in 2024 [10]), entitled "A specific amyloid-β protein assembly in the brain impairs memory".
Amyloid beta (Aβ, Abeta or beta-amyloid) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. [2] The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol ...
In 2015, Hardy became the UK’s first recipient of the Breakthrough Prize in Life Sciences for "discovering mutations in the amyloid precursor protein (APP) gene that cause early-onset Alzheimer’s disease, linking the accumulation of APP-derived beta-amyloid peptide to Alzheimer’s pathogenesis, and inspiring new strategies for disease ...
The beta-amyloid fragment is crucial in the formation of amyloid plaques in Alzheimer's disease. Alzheimer's disease has been identified as a protein misfolding disease , a proteopathy , caused by the accumulation of abnormally folded amyloid beta protein into amyloid plaques, and tau protein into neurofibrillary tangles in the brain. [ 77 ]
Aducanumab, sold under the brand name Aduhelm, is a monoclonal antibody designed to treat Alzheimer's disease. [2] [3] It is a monoclonal antibody [3] [2] that targets aggregated forms (plaque) [4] [5] of amyloid beta (Aβ) found in the brains of people with Alzheimer's disease to reduce its buildup.
The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. [1]
Two amyloid plaques from the brain of a patient with Alzheimer's disease. In this photomicrograph, neurites are darkly stained with the Naoumenko-Feigin silver method, and the pink elements (including the plaque cores) are stained with the periodic acid-Schiff (PAS) counterstain. The bar is 20 microns (0.02 mm) in length.