Author(s): Sikora E
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Abstract During the last three centuries the expected lifespan in civilized countries has increased several times. The fastest growing groups are seniors (65+) and centenarians. Increased lifespan results in postponing of aging and age-related diseases. On the other hand, an increase in the number of people suffering from age-related diseases can be observed. Studies concerning longevity and aging help to elucidate the mechanisms responsible for these processes and give hope for finding the recipe for a healthy and long lifespan. Aging and longevity are modulated by genetic, epigenetic and stochastic factors. Already some variants of genes which correlate with longevity are known. Products of these genes are involved in lipid metabolism and in nutrient sensing signaling pathways such as: insulin/IGF-1 and TOR. Good indicators for human polymorphism study are results obtained using model organisms such as S. cerevisiae, C. elegans, D. melanogaster and laboratory mice. Aging and longevity are evolutionary conserved. Evolutionary theories concerning aging can be divided into two general categories: programmed and non-programmed ones. According to programmed theories aging is adaptive and can lead to altruistic death of kins. Non-programmed theories predict that organisms only have a limited amount of energy that has to be divided between reproductive activities and the maintenance of the non-reproductive aspects of the organism. Aging is the effect of natural degrading processes that result in the accumulation of damage. Accumulation of damaged DNA and proteins can lead to cellular senescence, inflammaging and age-related diseases. Strategies for postponing aging mainly rely on protecting and/or eliminating these lesions.
This article was published in Postepy Biochem
and referenced in Journal of Computer Science & Systems Biology