* To whom correspondence should be addressed.
Received May 17, 2018; Revision received June 4, 2018
Drug development for the treatment of Alzheimer’s disease (AD) has been for a long time focused on agents that were expected to support endogenous β-amyloid (Aβ) in a monomeric state and destroy soluble Aβ oligomers and insoluble Aβ aggregates. However, this strategy has failed over the last 20 years and was eventually abandoned. In this review, we propose a new approach to the anti-amyloid AD therapy based on the latest achievements in understanding molecular causes of cerebral amyloidosis in AD animal models.
KEY WORDS: Alzheimer’s disease, amyloid-β, isoaspartate, zinc, protein–protein complexes, cerebral β-amyloidosis