Telomere Theory of Aging

The telomere theory of aging was formulated in the 1990s after scientists discovered that telomeres shorten during the aging of human fibroblasts [11]. Telomeres represent the terminal region of the DNA helix, made up of repetitive DNA sequences that aid in preventing incomplete replication and instability [13]. They are essentially "caps" on the ends of linear chromosomes, composed of 10-20 kb of hexa-meric repeats, TTAGGG [14] ; In somatic cells, telomeres shorten with each cell division, eventually reducing the number of repeat sequences [15]. This reduction ultimately renders the chromosomes unstable and the cell is no longer able to replicate [15]; Hence, progressive somatic cell division occurs over a finite period of time, which represents the often-mentioned "biological clock." Eventually, somatic cells will enter a growth-arrested yet viable state called senescence [16].

A key element of this theory is that life span is determined by cell division and not time; it proposes that there is a direct correlation between telomere shortening and aging [17]. Further work has determined that telomerase, the enzyme capable of restoring telomeric ends lost during cell division, is absent in many somatic cells, rendering them incapable of maintaining proper telomeric structure [15]. However, telomerase is present in germ cells [18]; and hence the theory is limited in that it cannot account for aging of these cells, given that telomere length is maintained. Further, many believe the theory to be oversimplified and not fully predictive [14], particularly because much of the work has been done in the murine model, in which telomere biology differs greatly from that of the human [19]. Indeed, it has recently been found that, in sperm, telomere length increases as men age [20] .

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