telomere theory of aging
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Introduction
The telomere theory of aging is based on the concept of cellular senescence, derived from the early experiments of Leonard Hayflick who observed the limited proliferative capacity of cultured fibroblasts.
In this case, it turns out, the term cellular senescence was a misnomer.
Hayflick was actually observing terminal differentiation.
The alleged senescent cells* were actually terminally differentiated fibrocytes.
* Mitosis does result in a reduced length of telomeres in the daughter cells
- however, many cells in humans do not divide, & senescent cells has taken a broader scope in some contexts independent of telomere length
Notes
- the early demise of the cloned sheep Dolly has been invoked as support for the telomere theory of aging (see cloning)[1]
- there is no strong evidence (SOE=A) that telomere length plays any role in human aging
- in humans, many (if not most or all) telomere studies on morbidity & mortality use measurements of leukocyte telomere length
- considering the life cycle of neutrophils, isolation of lymphocytes prior to measurement of telomere length would seem prudent (see neutrophil)
- telomere length of lymphocytes in peripheral blood would reflect the number of mature vs naive cells, since the maturation of lymphocytes occurs via mitoses
- thus telomere length of lymphocytes in peripheral blood should be more of a reflection of antigen exposure rather than aging
- the question arises, how does the number of immunizations affect peripheral blood lymphocyte telomere length? (not an anti-vaxxer)
More general terms
References
- ↑ 1.0 1.1 Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022
- ↑ Wang Q, Zhan Y, Pendersen N, et al. Telomere length and all-cause mortality: a meta analysis. Ageing Res Rev. 2018;48:11-20 PMID: https://www.ncbi.nlm.nih.gov/pubmed/30254001 https://www.sciencedirect.com/science/article/pii/S1568163718301235