The DNA damage theory of aging proposes that aging is a consequence of unrepaired accumulation of naturally occurring DNA damages. Damage in this context is a DNA alteration that has an abnormal structure. Although both mitochondrial and nuclear DNA damage can contribute to aging, nuclear DNA is the main subject of this analysis. Nuclear DNA damage can contribute to aging either indirectly (by increasing apoptosis or cellular senescence) or directly (by increasing cell dysfunction).
In humans and other mammals, DNA damage occurs frequently and DNA repair processes have evolved to compensate. In estimates made for mice, on average approximately 1,500 to 7,000 DNA lesions occur per hour in each mouse cell, or about 36,000 to 160,000 per cell per day (Vilenchik & Knudson 2000). In any cell some DNA damage may remain despite the action of repair processes. The accumulation of unrepaired DNA damage is more prevalent in certain types of cells, particularly in non-replicating or slowly replicating cells, such as cells in the brain, skeletal and cardiac muscle.
Read more about DNA Damage Theory Of Aging: DNA Damage and Mutation, Age-associated Accumulation of DNA Damage and Decline in Gene Expression, Mutation Theories of Aging, Dietary Restriction, Inherited Defects That Cause Premature Aging, Lifespan in Different Mammalian Species, Conclusions
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