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Updated: Jun 27, 2026

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
Published on: May 22, 2018
Preventing beta-amyloid fibrillization and deposition: beta-sheet breakers and pathological chaperone inhibitors
Thomas Wisniewski1, Martin Sadowski
1Department of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. Thomas.wisniewski@nyumc.org
Abstract:
Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble beta-amyloid (sAbeta) to oligomeric, fibrillar Abeta. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the disease-associated state; these proteins have been termed 'pathological chaperones'. In a number of AD models, intervention that block soluble Abeta aggregation, including beta-sheet breakers, and compounds that block interactions with pathological chaperones, have been shown to be highly effective. When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology.
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