A "mitochondrial cascade hypothesis" for sporadic Alzheimer's disease.

By R. Swerdlow, Shaharyar M. Khan. Medical Hypotheses, 2004

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Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “Notably, in 2004 Swerdlow and Khan proposed a “mitochondrial cascade hypothesis”, which stated that each individual’s genetically determined and environmentally influenced mitochondrial function are primary factors influencing late-onset AD pathology [8].”
The Alzheimer's Disease Mitochondrial Cascade Hypothesis: Progress and Perspectives (2013, methodology): “We first proposed the AD mitochondrial cascade hypothesis in 2004 [24].”
Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. (2010, background): “Swerdlow and Khan [16,17] proposed the mitochondrial cascade hypothesis to explain late-onset, sporadic AD.”
Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. (2006, background): “In late-onset, sporadic AD, an age-dependent increase of reactive oxygen species has been identified as a key factor in the development and progression of AD ( 12 ,20,24).”