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- W4320724694 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." @default.
- W4320724694 created "2023-02-15" @default.
- W4320724694 creator A5050249978 @default.
- W4320724694 date "2023-04-04" @default.
- W4320724694 modified "2023-10-17" @default.
- W4320724694 title "The Alzheimer’s Disease Mitochondrial Cascade Hypothesis: A Current Overview" @default.
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