Aging

Disease / Phenomenon

Aging is not a single condition but the cumulative, lifelong drift of biological systems away from their youthful operating range. Across every tissue, damage accrues faster than repair can clear it: DNA lesions escape correction, proteins misfold and aggregate, mitochondria lose efficiency, and the extracellular matrix stiffens. The visible consequences — reduced muscle mass and bone density, slower wound healing, declining immune competence, changes in skin, vision, and cognition — are downstream expressions of these molecular shifts. Aging is also the dominant risk multiplier for most chronic disease; cardiovascular disease, cancer, neurodegeneration, and metabolic dysfunction all become far more probable as biological age advances, which is why aging biology is increasingly studied as a modifiable process rather than a fixed schedule.

Researchers commonly group the underlying mechanisms into recognized hallmarks: genomic instability, telomere attrition, epigenetic drift, loss of proteostasis, deregulated nutrient sensing through pathways such as mTOR, AMPK, insulin/IGF-1, and sirtuins, mitochondrial dysfunction, cellular senescence with its inflammatory secretory phenotype, stem cell exhaustion, and altered intercellular communication. Chronic low-grade inflammation, often called inflammaging, links many of them together. This page organizes aging into those biological processes, traces the molecular pathways within each, and identifies the biomarkers used to quantify them.