Abstract
Longevity is a more complex process than is often thought. The adult life span can be naturally partitioned into two phases: the health span and the senescence span. The transition between them is characterized by the downward inflection of the survival curve. The evidence shows that there are three ways to increase longevity, only one of which involves an increase in the values of both mean and maximum life spans. In that case, the extra longevity is expressed as an extension of the health span, whereas the senescent span is little affected if at all. The delayed onset of senescence phenotype is the most desirable way of extending the life span. This multiphasic view of the life span is supported by a variety of literature data and springs from an evolutionary view of the aging process. Gene activity during the life span can best be viewed in terms of gene networks, their progressive increase in fidelity during development, their maintenance during much of the health span, their progressive loss of stringent feedback control as the force of natural selection wanes, and the stochastic destabilization of key cellular functions during the senescent phase. This systems biology overview should be of conceptual value in understanding the biology of specific long-lived mutants and selected strains.
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Abbreviations
- DOS:
-
Delayed onset of senescence
- MEMN:
-
Macrophage-enriched metabolic network
- PD:
-
Population doubling
- QTL:
-
Quantitative trait loci
- SNP:
-
Single nucleotide polymorphism
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Arking, R. (2009). The Genetic Architecture of Longevity. In: Sell, C., Lorenzini, A., Brown-Borg, H. (eds) Life-Span Extension. Aging Medicine. Humana Press. https://doi.org/10.1007/978-1-60327-507-1_4
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