A mechanistic survey of Alzheimer's disease

Abstract

Alzheimer's disease (AD) is the most common, age-dependent neurodegenerative disorder. While AD has been intensively studied from different aspects, there is no effective cure for AD, largely due to a lack of a clear mechanistic understanding of AD. In this mini-review, we mainly focus on the discussion and summary of mechanistic causes of Alzheimer's disease (AD). While different AD mechanisms illustrate different molecular and cellular pathways in AD pathogenesis, they do not necessarily exclude each other. Instead, some of them could work together to initiate, trigger, and promote the onset and development of AD. In a broader viewpoint, some AD mechanisms (e.g., amyloid aggregation mechanism, microbial infection/neuroinflammation mechanism, and amyloid cross-seeding mechanism) could also be applicable to other amyloid diseases including type II diabetes, Parkinson's disease, and prion disease. Such common mechanisms for AD and other amyloid diseases explain not only the pathogenesis of individual amyloid diseases, but also the spreading of pathologies between these diseases, which will inspire new strategies for therapeutic intervention and prevention for AD.

Keywords: Alzheimer's disease; Amyloid-beta; Protein aggregation; Protein misfolding.