Genetics of aging

Science

Volumn 278, Issue 5337, 1997, Pages 407-411

  Finch, Caleb E ^a   Tanzi, Rudolph E ^b  

^a UNIVERSITY OF SOUTHERN CALIFORNIA   (United States)

^b MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AGING; ALZHEIMER DISEASE; APOPTOSIS; ARTICLE; CELL DEATH; ENVIRONMENTAL FACTOR; GENE EXPRESSION; GENETIC RISK; GENETIC VARIABILITY; GENETICS; HERITABILITY; LIFESPAN; LONGEVITY; NUTRITION; PENETRANCE; PRIORITY JOURNAL; SENESCENCE; SURVIVAL;

AGING; ALZHEIMER DISEASE; ANIMALS; APOPTOSIS; GENE EXPRESSION; HUMANS; LONGEVITY; MUTATION; RISK FACTORS; VARIATION (GENETICS);

INVERTEBRATA; MAMMALIA;

EID: 0030713963     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.278.5337.407     Document Type: Article

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89. Variations in life-spans must also depend on local conditions. For example, total life-spans of C. elegans can be more than threefold as long if a lack of nutrients during development triggers the dauer larval stage; the dauer may last 70 days without altering the adult phase, once food becomes sufficient (2, 20-23). Social and reproductive interactions can also increase mortality risk in flies and mice. The present sampling of populations under protected conditions nonetheless has similar variations in lifespan that give a sense of baseline variations [see also (10, 25)].
90. These projects were supported by grants from the National Institute on Aging (C.E.F. and R.E.T.), the National Institute of Neurological Disorders and Stroke (R.E.T.), and the Metropolitan Life Foundation (R.E.T.). T. Johnson, G. McClearn, R. Miller, M. Tater, and J. Tower gave helpful comments.