Ageing is an inevitable biological process characterised by a gradual decline in physical and functional abilities. Understanding why humans age involves exploring various theories and mechanisms at the cellular and molecular levels.
At the core of ageing lies the gradual accumulation of cellular damage over time. One prominent theory is the free radical theory, which posits that ageing results from the accumulation of damage caused by free radicals—unstable molecules generated during normal metabolic processes. These free radicals can damage DNA, proteins, and other cellular components, leading to the progressive deterioration of cells and tissues.
Another significant factor is telomere shortening. Telomeres are protective caps at the ends of chromosomes that prevent them from deteriorating or fusing with neighbouring chromosomes. Each time a cell divides, telomeres shorten, and when they become too short, the cell can no longer divide and becomes senescent or dies. This process contributes to ageing by reducing the regenerative capacity of tissues.
The mitochondrial theory of ageing emphasises the role of mitochondria, the powerhouses of the cell. Mitochondrial DNA is particularly susceptible to damage from free radicals. As damage accumulates, mitochondrial function declines, leading to reduced energy production and increased cellular dysfunction.
Recent scientific advancements are paving the way for interventions aimed at slowing down the ageing process and extending healthy lifespan.
Senolytics are a promising class of drugs designed to target and eliminate senescent cells—cells that have stopped dividing and accumulate with age, contributing to inflammation and tissue dysfunction. By removing these cells, senolytics can potentially delay age-related diseases and improve overall health.
Telomerase activation is another area of research. Telomerase is an enzyme that can extend telomeres, thereby potentially rejuvenating cells and enhancing their longevity. Although currently limited to laboratory studies, telomerase activation holds promise for future therapies.
Caloric restriction mimetics aim to replicate the beneficial effects of caloric restriction—known to extend lifespan in various organisms—without the need to reduce calorie intake. Compounds like resveratrol and rapamycin have shown potential in mimicking these effects, promoting cellular health and longevity.
Moreover, advancements in gene editing technologies, such as CRISPR, are being explored to repair genetic mutations associated with ageing and age-related diseases. This could revolutionise the way we approach ageing by addressing its root causes at the genetic level.
While ageing is a complex and multifaceted process, scientific understanding has significantly advanced. Innovations in targeting cellular mechanisms, removing senescent cells, and genetic interventions offer promising avenues to slow down ageing and enhance the quality of life. As research progresses, the prospect of extending healthy human lifespan moves closer to reality, offering hope for a future where ageing is not just a decline, but a period of sustained vitality.
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