Article ; Online: The Alzheimer's Disease Mitochondrial Cascade Hypothesis: A Current Overview.
Journal of Alzheimer's disease : JAD
2023 Volume 92, Issue 3, Page(s) 751–768
Abstract: Viable Alzheimer's disease (AD) hypotheses must account for its age-dependence; commonality; association with amyloid precursor protein, tau, and apolipoprotein E biology; connection with vascular, inflammation, and insulin signaling changes; and ... ...
Abstract | Viable Alzheimer's disease (AD) hypotheses must account for its age-dependence; commonality; association with amyloid precursor protein, tau, and apolipoprotein E biology; connection with vascular, inflammation, and insulin signaling changes; and systemic features. Mitochondria and parameters influenced by mitochondria could link these diverse characteristics. Mitochondrial biology can initiate changes in pathways tied to AD and mediate the dysfunction that produces the clinical phenotype. For these reasons, conceptualizing a mitochondrial cascade hypothesis is a straightforward process and data accumulating over decades argue the validity of its principles. Alternative AD hypotheses may yet account for its mitochondria-related phenomena, but absent this happening a primary mitochondrial cascade hypothesis will continue to evolve and attract interest. |
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MeSH term(s) | Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Mitochondria/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Signal Transduction |
Chemical Substances | Amyloid beta-Peptides ; Amyloid beta-Protein Precursor |
Language | English |
Publishing date | 2023-02-20 |
Publishing country | Netherlands |
Document type | Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't |
ZDB-ID | 1440127-7 |
ISSN | 1875-8908 ; 1387-2877 |
ISSN (online) | 1875-8908 |
ISSN | 1387-2877 |
DOI | 10.3233/JAD-221286 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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