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A mechanistic survey of Alzheimer's disease

期刊

BIOPHYSICAL CHEMISTRY
卷 281, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.bpc.2021.106735

关键词

Alzheimer's disease; Amyloid-beta; Protein misfolding; Protein aggregation

资金

  1. University of Akron
  2. NSF [CBET-2107619]

向作者/读者索取更多资源

This article primarily discusses and summarizes the mechanistic causes of Alzheimer's disease (AD). Different mechanisms of AD could potentially work together to initiate, trigger, and promote the onset and development of the disease. Some of these mechanisms are also applicable to other amyloid diseases, explaining the pathogenesis and pathology spreading among these diseases.
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.

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