Programmed Aging is a biological theory asserting that the process of senescence is not purely a random accumulation of damage but is, at least in part, actively regulated by specific genetic and molecular pathways that have evolved to control lifespan and govern the timing of developmental decline. This perspective suggests that aging is a quasi-program, a continuation of developmental processes, that can potentially be modulated or reset through targeted intervention in these regulatory pathways. It contrasts with the “damage accumulation” theories of aging.
Origin
This theory has its roots in evolutionary biology and molecular genetics, particularly observations in model organisms where single gene mutations can dramatically extend or shorten lifespan. The identification of conserved signaling pathways, such as the Insulin/IGF-1 signaling pathway, that directly regulate the rate of aging across species provided strong evidence for this programmatic control. This framework forms the basis for much of modern longevity research.
Mechanism
The mechanism centers on the activation or suppression of specific longevity assurance pathways and their interplay with endocrine signals. For example, nutrient-sensing pathways like mTOR and AMPK act as key regulators, integrating metabolic status with the cellular stress response and the rate of cellular senescence. By pharmacologically or nutritionally modulating these evolutionarily conserved pathways, the aim is to slow the execution of the aging program, thereby extending healthspan and functional capacity.
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