Stem Cell Aging

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Stem cell aging is still a controversial topic among scientists. One of the most popular explanations of stem cell aging is defined by the decrease in ability to proliferate or self-renew. Cell regulation mechanisms that have been related to aging are senescence and apoptosis. Leading evidence has identified the relationship between p16INK4a, a tumor suppressor protein, and aging in neural stem cells. Neural stem cells regenerate neurons and glial cells as required by the organisms, but an increase in p16INK4a declines the ability of the stem cells to function as they were able to do initially. Such relationship has been established, however, the mechanism for how this occurs is currently unknown. In an attempt to address this unidentified…show more content…
These anti cancer mechanisms depend on p53 and p16ink4 activation, which appear to be responsible for aging similarly to how their failure is associated with cancer. Some other possible mechanisms include heritable mutations and environmental changes in stem cell surroundings. These assumptions are so controversial because adequate models to test the function of these cells have yet to be constructed. Therefore, there I no direct way of determining that stem cell aging is the decrease in stem cell function through regeneration degradation. However, it is an idealistic assumption due to the resulting data of stem cells from other tissues that identify the association between proliferating decline in tissue and aging. A study involving rodents identified that a decline in the quantity of neurons being produced by neural stem cells would decrease with telomere dysfunction. Senescence is a form of growth arrest that is induced by stimuli like loss of telomere function, reactive oxygen species, some DNA damage, and tumor suppressor activation. As shown by the study when telomere function is not regulated they lose normal ability to regenerate which, thus far has been presumed as aging. Recent studies on neural stem cells have leading information on the mechanism of aging using p16INK4a overexpression and oppression in mice. The results indicated that an increase in p16INK4a contributes to a decrease in proliferation and function
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