- Ageing is a gradual and multifactorial biological process characterised by the progressive decline of cellular, tissue and organ function over time. It reflects the cumulative impact of molecular damage, reduced repair capacity and alterations in genetic and epigenetic regulation. Although ageing is universal, its rate and manifestation vary widely between individuals due to differences in genetics, environment, lifestyle and metabolic health. At the cellular level, ageing involves changes in DNA integrity, protein stability, mitochondrial efficiency and immune responsiveness, all of which contribute to reduced physiological resilience.
- One of the central features of ageing is the accumulation of molecular damage. DNA is continuously exposed to endogenous and environmental stressors, and although repair mechanisms remain active throughout life, their efficiency declines with age. This leads to genomic instability and mutations that impair cellular function. Telomeres, the protective structures at chromosome ends, shorten with each cell division, eventually limiting the capacity of cells to proliferate. When telomeres become critically short, cells enter senescence, a state of permanent growth arrest accompanied by the secretion of inflammatory mediators that contribute to tissue dysfunction.
- Ageing also involves a decline in proteostasis, the cellular system responsible for maintaining properly folded and functional proteins. Misfolded or damaged proteins accumulate when chaperone activity and degradation pathways such as autophagy and the proteasome become less efficient. Mitochondrial dysfunction is another hallmark of ageing; reduced ATP production and increased reactive oxygen species impair cellular metabolism and promote oxidative damage. These changes collectively weaken the ability of cells to maintain homeostasis under stress.
- The immune system undergoes significant changes during ageing, a phenomenon known as immunosenescence. Adaptive immunity becomes less effective, reducing the body’s ability to respond to infections and vaccinations. At the same time, chronic low‑grade inflammation — often referred to as inflammaging — develops due to persistent activation of innate immune pathways and the presence of senescent cells. This inflammatory environment contributes to the development of age‑related diseases, including cardiovascular disease, neurodegeneration and metabolic disorders.
- Ageing is also shaped by metabolic and environmental factors. Nutrient availability, physical activity, exposure to toxins and lifestyle choices influence the rate at which molecular damage accumulates. For example, chronic nutrient deprivation activates adaptive pathways such as autophagy, which can slow aspects of ageing by enhancing cellular recycling and repair. Conversely, nutrient excess, chronic inflammation and oxidative stress accelerate biological ageing and increase susceptibility to disease.
- In humans, ageing manifests as reduced muscle mass, diminished cognitive function, impaired wound healing, decreased metabolic flexibility and increased vulnerability to chronic illness. Although ageing cannot be halted, research continues to explore interventions that may slow its progression, including caloric restriction, exercise, pharmacological agents targeting senescence and strategies that enhance mitochondrial function or proteostasis. Understanding the biological mechanisms of ageing provides essential insight into healthspan, longevity and the prevention of age‑related diseases.
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