Damage to our mitochondrial DNA is one of the root causes of aging, and here is a specific example of such damage associated with an age-related condition - all the more reason to aggressively fund repair strategies such as protofection and mitoSENS. From the paper: "Mitochondrial DNA damage may be associated with age-related diseases, such as age-related macular degeneration (AMD). The present study was designed to test whether the frequency of mitochondrial DNA (mtDNA) damage, heteroplasmic mtDNA mutations, and repair capacity correlates with progression of AMD. ... Macular and peripheral RPE cells were isolated and cultured from human donor eyes with and without AMD history. The stages of AMD were graded according to the Minnesota Grading System. ... To test the mtDNA repair capacity, cultured RPE cells were allowed to recover for 3 and 6 hours after exposure to H(2)O(2) and then repair assessed by quantitative PCR. The levels of human OGG1 protein, which is associated with mtDNA repair, were analyzed by Western Blot. ... Our study showed that mtDNA damage increased with aging, and more lesions occurred in RPE cells from the macular region relative to the periphery. Furthermore, mtDNA repair capacity decreased with aging, with less mtDNA repair capacity in the macular region compared with the periphery in samples from aged subjects. Most interestingly, the mtDNA damage is positively correlated with the grading level of AMD, while repair capacity is negatively correlated. In addition, more mitochondrial heteroplasmic mutations were detected in eyes with AMD. ... Our data show macula-specific increases in mtDNA damage, heteroplasmic mutations and diminished repair that are associated with aging and AMD severity."