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Issue 1019 coverStrategies for Engineered Negligible Senescence: Why Genuine Control of Aging May Be Foreseeable Volume 1019 published June 2004
Ann. N.Y. Acad. Sci. 1019: 406–411 (2004). doi: 10.1196/annals.1297.073
Copyright © 2004 by the New York Academy of Sciences
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Articles by AMES, B. N.
Delaying the Mitochondrial Decay of Aging

BRUCE N. AMES

University of California, Berkeley, California 94720, and Children's Hospital Oakland Research Institute, Oakland, California 94609, USA

Address for correspondence: Dr. Bruce N. Ames, Nutritional Genomics Center, Children's Hospital Oakland Research Institute, 5700 Martin Luther King, Jr. Way, Oakland, CA 94609. Voice: 510-450-7627; fax: 510-450-7910. bames{at}chori.org
Ann. N.Y. Acad. Sci. 1019: 406-411 (2004).

Mitochondrial dysfunction may be a principal underlying event in aging, including the degenerative diseases of aging such as brain degeneration. Mitochondria provide energy for basic metabolic processes, and their decay with age impairs cellular metabolism and leads to cellular decline. Progress over the last decade in delaying the mitochondrial decay of aging is reviewed.

Key Words: acetyl carnitine • lipoic acid • reversing genetic disease • high-dose B-vitamin • vitamin, minerals, and aging • heme deficiency • zinc deficiency • biotin deficiency • vitamin B6 • pantothenic acid • copper deficiency




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