![]() Factors that can damage DNA include ultraviolet radiation, cigarette smoking, and exposure to hydrocarbons, such as auto exhaust and coal (Dollemore, 2006). As DNA damage accumulates with increasing age, it can cause cells to deteriorate and malfunction (Jin, 2010). Scientists believe that this damage, and the body’s inability to fix itself, is an important part of aging (NIA, 2011a). However, some damage cannot be repaired and remains in our DNA. This is usually not a concern as our cells are capable of repairing damage throughout our life. The answer may lead to some important clues about the aging process.ĭNA Damage: Over time DNA, which contains the genetic code for all organisms, accumulates damage. Understanding why cellular senescence changes from being beneficial to being detrimental is still under investigation. When we are young, senescent cells may reduce our risk of serious diseases such as cancer, but as we age they increase our risk of such problems (NIA, 2011a). While they may be turned off, they are not dead, thus they still interact with other cells in the body and can lead to an increase risk of disease. Senescent cells can also create problems. Or, as in the development of cancer, it can continue to divide and become abnormal. It can stop replicating by dying, called apoptosis. It can stop replicating by turning itself off, called cellular senescence. Once it becomes too short the cell does one of three things. With each replication, the telomere gets shorter. ![]() ![]() But what is the mechanism behind this cellular senescence? At the end of each chromosomal strand is a sequence of DNA that does not code for any particular protein, but protects the rest of the chromosome, which is called a telomere. This is known as the Hayflick limit, and is evidenced in cells studied in test tubes, which divide about 40-60 times before they stop (Bartlett, 2014). If these detrimental disorders occurred earlier in the development cycle, they may have been eliminated already (Gems, 2014).įigure 9.10 Telomeres and Cellular SenescenceAdapted from National Institute on AgingĬellular Clock Theory: This theory suggests that biological aging is due to the fact that normal cells cannot divide indefinitely. Consequently, natural selection has not eliminated these damaging disorders from the gene pool. Genes associated with aging, such as Alzheimer Disease, do not appear until after the individual has passed their main reproductive years. Researchers believe that it is most likely a combination of many genes that affect the rate of aging.Įvolutionary Theory: Evolutionary psychology emphasizes the importance of natural selection that is, those genes that allow one to survive and reproduce will be more likely to be transmitted to offspring. For example, a National Institutes of Health study identified genes possibly associated with blood fat levels and cholesterol, both risk factors for coronary disease and early death (NIA, 2011a). To help determine which genes promote longevity and how they operate, researchers scan the entire genome and compare genetic variants in those who live longer with those who have an average or shorter lifespan. For others, some genes may accelerate the rate of aging, while others decrease the rate. Specifically, longevity may be due to genes that better equip someone to survive a disease. Based on animal models, some genes promote longer life, while other genes limit longevity. Genetics: One’s genetic make-up certainly plays a role in longevity, but scientists are still attempting to identify which genes are responsible.
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