![]() ![]() The few longitudinal studies that do exist suggest that telomere attrition is greatest during early life when growth and development are still occurring ( 17 – 20). ![]() ![]() However, because most of these studies have been cross-sectional (i.e., repeat samples were not collected from the same individuals throughout life) it is not possible to separate within-individual effects from population-level processes such as cohort effects or prior selection events producing sample biases. Other studies have not found such a relationship, and the results in humans in particular have been mixed ( 14 – 16). Individuals with longer telomeres have been reported to have a longer subsequent lifespan in some studies of vertebrate species, with the predictive power of age per se being lower ( 12, 13). Thus, intraspecific variation in age-specific telomere length is expected to be a good indicator of biological age.Īverage telomere length in cell samples has been found to decrease with donor age in a number of cell types in diverse taxa ( 12, 13). Progressive telomere shortening has been linked to both normal aging and to various degenerative diseases in a wide range of studies mainly in humans and mice ( 2), and telomere lengthening has been shown to have a restorative effect ( 11). The pattern in birds is less well understood, but in some species, like the zebra finch Taeniopygia guttata, the pattern is similar to that in long-lived mammals ( 8 – 10). However, in long-lived mammals, after embryogenesis, telomerase is down-regulated in most somatic tissues, which is thought to have evolved as a tumor-suppressing mechanism ( 7). Telomere loss can be prevented by the enzyme telomerase, a ribonucleoprotein that adds telomeric sequences to telomere ends ( 6). The loss of DNA from the telomeric cap protects the coding sequences from attrition and also limits cell replicative potential once telomeres reach a critically shortened length, cells stop dividing and enter a state of replicative senescence ( 3, 5). In the absence of restoration, telomeres shorten during each round of normal somatic cell division because RNA polymerase cannot completely replicate the lagging strand ( 3, 4). Telomeres are highly conserved, noncoding, repetitive sequences of DNA that, together with a number of shelterin proteins, form caps at the ends of eukaryotic chromosomes, enabling chromosome ends to be distinguished from double-stranded breaks ( 3). One cellular mechanism thought to be particularly important in this regard is the attrition of telomeres ( 2). Understanding the physiological processes underlying variation in lifespan is of central importance to evolutionary ecology, biomedical research, and conservation science ( 1). ![]() Our results provide the strongest evidence available of the relationship between telomere length and lifespan and emphasize the importance of understanding factors that determine early life telomere length. Reproduction increased adult telomere loss, but this effect appeared transient and did not influence survival. We found telomere length at 25 d to be a very strong predictor of realized lifespan ( P < 0.001) those individuals living longest had relatively long telomeres at all points at which they were measured. We measured telomere length in zebra finches ( n = 99) from the nestling stage and at various points thereafter, and recorded their natural lifespan (which varied from less than 1 to almost 9 y). Key studies, in which telomere length is tracked from early in life, and actual lifespan recorded, have been lacking. So far, data are based either on simple comparisons of telomere length among different age classes or on individuals whose telomere length is measured at most twice and whose subsequent survival is monitored for only a short proportion of the typical lifespan. Studies of this relationship are hampered by the time scale over which individuals need to be followed, particularly in long-lived species where lifespan variation is greatest. The observed variation in telomere length among individuals of the same age is therefore thought to be related to variation in potential longevity. The attrition of telomeres, the ends of eukaryote chromosomes, is thought to play an important role in cell deterioration with advancing age. ![]()
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