Mixed
Defects in DNA repair pathways (specifically NER and BER) and the resulting accumulation of DNA damage are causally linked to premature aging syndromes and neurodegenerative diseases, whereas enhanced DNA repair capacity is associated with increased longevity.
Maintaining genomic integrity is critical for healthy aging. While you cannot directly 'dose' DNA repair, supporting cellular health through lifestyle factors that minimize oxidative stress and support metabolic function may help preserve DNA repair capacity. Avoiding excessive genotoxic stressors (like smoking or extreme UV exposure) is a practical application of this mechanism.
Distinct evidence for a role of imperfect DNA repair in aging is that several premature aging syndromes have underlying genetic DNA repair defects. ... In humans, premature aging and early death are characteristics of several rare heritable diseases linked to defects in DNA repair or the processing of DNA damage ... genetically modified mice with comparable defects in DNA repair show similar disease phenotypes that resemble normal aging, suggesting a causal relationship between DNA repair defects and premature aging
Why this rating
Strong evidence from human genetic disorders (progerias), mouse models, and evolutionary theories, though direct human lifespan extension via repair enhancement is not yet clinically established.
Source
DNA Damage, DNA Repair, Aging, and Neurodegeneration
Scott Maynard et al. · Cold Spring Harbor Perspectives in Medicine · 2015
DOI 10.1101/cshperspect.a025130
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