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Human Aging and Longevity: Genetic Aspects

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Aging of Organisms

Part of the book series: Biology of Aging and its Modulation ((BIMO,volume 4))

Abstract

In the light of evolutionary theory, human aging can be viewed as “a late-onset genetic disease that affects us all,” and, like in lower organisms, there surely are both public and private mechanisms that contribute to human aging [1]. Because of the surprising similarity between major genes and metabolic pathways that control longevity in yeast, worms, drosophila, and even mice, public mechanisms of aging currently attract most of the attention of comparative aging research. The apparent degree of evolutionary conservation of key metabolic pathways related to longevity and aging is in fact impressive [2]. However, as will be pointed out with respect to some of the somatic maintenance systems that are fairly recent additions to the vertebrate genome, there undoubtedly are a number of mechanisms of aging and longevity that are private to vertebrates and mammals. Senescent human phenotypes have been properly described as “non-adaptive, non-determinative, subject to stochastic events as well as highly polygenic modulations” such that there is little justification for a simplificationist view of human aging [3]. Even though we have learned a great deal about public mechanisms of aging in lower organisms that may be partly conserved in mammals, a purely comparative and reductonist approach must surely be abandoned in view of the complexity of the extremely long-lived human organism. No other species has such a highly developed central nervous system which controls, via the hypothalamic-pituitary axis, much of our neuroendocrine homeostasis. Because of the remarkable longevity and medicalization of our species, at least in the industrialized countries, the natural history and pathogenesis of aging and longevity has been extensively documented in humans, and there is a comprehensive clinical record of age-related changes of the human phenotype [4-6]. What has not been completely resolved with respect to human aging is the question whether aging occurs, like development, via an ordered and genetically regulated, i.e., programmed process, or whether it results from (random) wear-and-tear type accumulation of damage to DNA, proteins, cells and higher order structures of the human body. Clearly, a programmed process would be much more difficult to modify or reverse than a wear-and-tear type process whose course might be slowed down or even halted by preventive interventions. Most likely, the truth lies somewhere between these two alternatives, and human aging encompasses features that are both programmed and stochastic [7].

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Hoehn, H., Renner, A. (2003). Human Aging and Longevity: Genetic Aspects. In: Osiewacz, H.D. (eds) Aging of Organisms. Biology of Aging and its Modulation, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-0671-1_10

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