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MITOTIC CLOCK. “Hayflick first described the limited replicative capacity of normal human fibroblasts more than 30 years ago. Since then, numerous other somatic cell types, including epithelial cells, endothelial cells, myoblasts, astrocytes, and lymphocytes, have also shown evidence of a mitotic clock which limits their division capacity.” https://lnkd.in/dFjeJA3 View in LinkedIn

RANGE OF LONGEVITY. “Different species vary dramatically in how long they life. The dome-shelled Galápagos giant tortoise (Geochelone elephantopus) can reach an age of about 180 years, whereas some mayfly species (belonging to the insect order Ephemeroptera) die after about 30 minutes. Even older than giant tortoises are certain trees, such as the yew (Taxus baccata), with some specimens between 4,000 and 5,000 years old. A few other organisms, such as freshwater polyps of the genus Hydra, are thought to age at a negligible rate or to be even potentially immortal, although this is still somewhat controversial.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

TELOMERASE. “A current hypothesis gaining prominence proposes that activation of the enzyme telomerase is necessary for cells to become immortal, or capable of proliferating indefinitely. The theory suggests that almost all cancer cells must attain immortality for progression to malignant states and, hence, require activation of telomerase.” http://jnci.oxfordjournals.org/content/87/12/884.short View in LinkedIn

TWO AGING MODELS. “The classical evolutionary theory of aging has therefore two fundamental cornerstones: MA and AP. However, it is worth noting that both models are conceptually very similar: under MA, aging evolves through the accumulation of effectively neutral mutations with deleterious late-life effects, whereas, under AP, aging occurs due to mutations with beneficial early- and deleterious late-life effects. In reality, probably both types of mutations occur in populations, yet their relative frequencies remain unknown.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

CYCLE ARREST. “Cellular senescence is an irreversible cell cycle arrest caused by intrinsic or extrinsic stress, such as shortened telomeres, DNA damage, induced oncogenes, or chromatin perturbation.” https://lnkd.in/dKvxxVz View in LinkedIn

RESOURCE BUDGETS. “Investment into reproduction – or early fitness components in general – might withdraw limited resources that could otherwise be used for somatic maintenance and repair. Such resource allocation trade-offs can thus been seen as a physiological extension of Williams' AP model.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

NO AGING GENES. “Many confuse aging with longevity determination, which is indirectly driven by genes. There are no genes for aging. There are genes to maintain the biological functionality of an organism up to and including reproductive success. There is no mechanism that immediately causes death after reproductive maturation; it’s too costly. Longevity determination asks ‘Why do we live as long as we do?’ Aging research asks ‘Why does everything ultimately fail?’ and that is a huge difference.” https://lnkd.in/dQMB4k7 View in LinkedIn

ENTROPY AND PATHOLOGY. “When molecular disorder occurs in dividing cells in vivo, post mitotics may also be affected and both may then reveal increasing vulnerability to pathology and subsequent death of the individual well before species maximum longevity is reached.” https://lnkd.in/esfPTAR View in LinkedIn

YOUTH YIELDS TO AGE. “The number of population doublings that a cell strain is capable of undergoing and that is determined by telomere length, may be the in vitro expression of maximum potential longevity. The hundreds of molecular disorders that herald the approaching loss of replicative capacity, and diminution of telomere length, are age changes.” https://lnkd.in/esfPTAR View in LinkedIn

CELLULAR ENTROPY. “Hundreds of biological changes occur in normal cells as they replicate in vitro resulting in increasing molecular disorder and loss of cell function.” https://lnkd.in/esfPTAR View in LinkedIn