Telomeres are protective structures present at the ends of linear chromosomes that are important in preventing genome instability. Telomeres shorten as a result of cellular replication, leading to a permanent cell cycle arrest, also known as
replicative senescence. Senescent cells have been shown to accumulate in mammalian tissue with age and in a number of age-related diseases, suggesting that they might contribute to the loss of tissue function observed with age.
This is built into the system and, so far, has NO way of being altered much less stopped.
Aging in cellular lines has a lot to do with complexity. The most stable complex cells(neuruons), are least prone to dysplastic changes (cancers) but are the most prone to senescence.
Conversely rapidly turning over cells like blood cells, epitelial cells, skin cells are the least complex not as likely to age, but carry the greatest chance of dysplastic change.
Mammailan tissued have an upper limit to the amount of cell replications (those necessary for regeneration due to age)...That's IT
https://en.wikipedia.org/wiki/Cellular_senescence
quote: Transplantation of only a few (1 per 10,000) senescent cells into lean middle-aged mice was shown to be sufficient to induce frailty, early onset of aging-associated diseases, and premature death.
Biomarkers of cellular senescence have been shown to accumulate in tissues of older individuals.
The accumulation of senescent cells in tissues of vertebrates with age is thought to contribute to the development of ageing-related diseases, including Alzheimer's disease, Amyotrophic lateral sclerosis, type 2 diabetes, and various cancers
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