The mitochondrial-lysosomal axis theory of aging: accumulation of damaged mitochondria as a result of imperfect autophagocytosis.

By U. Brunk, A. Terman. European Journal of Biochemistry, 2002

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Aldehyde Sources, Metabolism, Molecular Toxicity Mechanisms, and Possible Effects on Human Health (2005, background): “This theory originated because during aging mitochondria progressively undergo structural alterations associated with decreased energy production, whereas lysosomes accumulate lipofuscin particularly in postmitotic cells such as neurons and cardiac myocytes (Brunk and Terman, 2002).”
The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span (2004, methodology): “Use of GFP as a reporter was described by Chalfie et al. (Chalfie et al., 1994). daf-16 RNAi treatment was performed by feeding according to Kamath et al. (Kamath et al., 2000) to examine whether the expression of daf-15::gfp is regulated by DAF-16.”
Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease (2005, background): “, 2005), probably by eliminating damaged mitochondria (Brunk and Terman, 2002), and is reCorrespondence to Ralph A.”
Differential aging of the brain: patterns, cognitive correlates and modifiers. (2006, neutral): “, 1997), cumulative mitochondrial damage (Brunk and Terman, 2002), reduction in DNA repair ability, and failure to remove neurons with damaged nuclear DNA (Rutten et al.”