Science of Aging Knowledge Environment 

About: Science of Aging Knowledge Environment is an academic journal published by American Association for the Advancement of Science. The journal publishes majorly in the area(s): Longevity & Cancer. It has an ISSN identifier of 1539-6150. Over the lifetime, 328 publications have been published receiving 17165 citations. The journal is also known as: SAGE KE & Science's SAGE KE.

Pleiotropy, Natural Selection, and the Evolution of Senescence

Abstract: A new individual entering a population may be said to have a reproductive probability distribution. The reproductive probability is zero from zygote to reproductive maturity. Later, perhaps shortly...

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

Abstract: Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stre...

Mutation selection and the natural history of cancer

Abstract: Survival of the rapidly renewing tissues of long-lived animals like man requires that they be protected against the natural selection of fitter variant cells (that is, the spontaneous appearance of...

Life-Span Study of SPF Fischer 344 Male Rats Fed Ad Libitum or Restricted Diets: Longevity, Growth, Lean Body Mass and Disease

Abstract: A life-span study was carried out on longevity, pathologic lesions, growth, lean body mass, and selected aspects of muscle of barrier-maintained SPF Fischer 344 rats fed either ad libitum (Group A)...

Selection for Delayed Senescence in Drosophila melanogaster

Abstract: Understanding the mechanism whereby the aging process is controlled has proven to be a uniquely difficult biological problem. Many theories have been put forth offering explanations for the phenomenon of senescence on a variety of different levels ranging from cellular, biochemical, and physiological to genetic and evolutionary. Many of these explanations are nonexclusive, which adds redundancy to confusion in considering the whole body of theory. Many of the cellular and/or biochemical mechanisms proposed amount to little more than detailed discussions of various possible gene end-products, which are themselves the subject of genetic and evolutionary theories. And even among these, no single theory predominates. J. B. S. Haldane (1941) and P. B. Medawar (1952) advanced the first theory of senescence incorporating a modem genetic and evolutionary perspective on the aging process. Their theory postulates the existence of specialized age-of-onset modifier genes which repress the action of other genes that are deleterious until an advanced age has been reached. Little harm results from the expression of the mutations then, however, and senescence gradually ensues with their derepression. In this theory, selection modifies life span by simply increasing or decreasing the period over which such modifiers are effective. Williams (19 57) later expanded on this, introducing the notion that the genes influencing senescence might themselves act pleiotropically with reciprocal effects at early and late ages. In this theory, the beneficial effects of genes early in life are weighed in evolution against their late life effects; youthful vigor must be accompanied by an early senescence and short life, while a delayed senescence and long life occur at the cost of youthful vitality. Apart from further extension of these ideas by Hamilton (1966) and Emlen (1 970), no new major theories of the evolution of senescence have arisen since Williams (1957). One reason for this may be that until recently, the few experimental tests performed contributed comparatively little substantiating information toward these theories. Early attempts at modifying life span through artificial selection include that of Glass (1960), who withheld mating in Drosophila to enforce an early versus late age-specific pattern of reproduction. This produced a slight increase in the longevity of late-reproducing lines. Wattiaux (1968) also found an increase in longevity in Drosophila under selection for an agespecific pattern of reproduction. This was followed by Sokal's (1970) study showing that continuous reproduction at an early age reduced median life span in Tribolium. Mertz (1975) found similar trends in an even later study. Taylor and Condra (1980) and Barclay and Gregory (1982) report changes in the longevity of Drosophila populations under rand K-selection or when exposed to predation. Concurrently with these, Lints and Hoste (1974, 1977) published the results of a well designed and extensive experiment that also selected for increased longevity in D. melanogaster through an early or late age-specific schedule of reproduction. But life span fluctuated wildly throughout the 13 generations of selection here, declining by 70% in the first few generations and then recovering. Further experiments (Lints et al., 1979)