Age-Related Genetic Decline describes the progressive accumulation of genomic and epigenomic alterations that compromise cellular function and regulatory fidelity as an organism ages. It encompasses phenomena like telomere shortening, increased somatic mutations, and dysregulation of gene expression profiles, collectively driving the physiological manifestations of senescence. In the context of hormonal health, this decline directly impacts the responsiveness and output of endocrine glands, contributing to conditions like andropause and menopause. The integrity of the genome is paramount for sustaining optimal physiological function.
Origin
The concept stems from foundational theories of aging, particularly the ‘wear and tear’ hypothesis, but is modernized by molecular biology, integrating genetics (genesis, origin) and the physiology of aging. The recognition of specific genetic instability mechanisms, such as DNA repair pathway inefficiencies, provides the precise molecular origin for this systemic functional erosion. This biological framework helps clinicians explain the observed decline in homeostatic control and hormonal resilience.
Mechanism
The core mechanism involves the reduced efficiency of DNA repair systems and the accumulation of epigenetic noise, which inappropriately silences beneficial genes and activates detrimental ones. This genomic instability leads to the production of dysfunctional proteins and impaired cellular stress response pathways. Ultimately, the compromised genetic code translates into a reduced capacity for tissue maintenance and regeneration, critically affecting the precise production and signaling of hormones across the hypothalamic-pituitary-gonadal (HPG) and adrenal axes.
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