Affiliations: [a] University of California, Berkeley, CA, USA | [b] Correspondence: Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA, USA. Tel.: +1 510 450 7625; Fax: +1 510 597 7128; E-mail: bames@chori.org | Institut für Biochemie und Molekularbiologie I, Heinrich-Heine-Universität Düsseldorf, Universitätsstr. 1, D-40225 Düsseldorf, Germany Tel.: +49 211 811 5358; Fax: +49 211 811 3029; E-mail: polidori@uni-duesseldorf.de
Abstract: Mitochondrial decay due to oxidant byproducts is a principal underlying contributor to aging, including the degenerative diseases of aging such as brain degeneration [15,23,32]. The energy for basic metabolic processes comes from mitochondria, and their decay with age impairs cellular metabolism and leads to cellular decline. Our progress over the last decade in delaying the mitochondrial decay of aging is briefly reviewed.
