Mitochondrial DNA damage accumulates over time, which might contribute to reduced energy production and aging-related decline.
My query is
what are the latest insights into how mtDNA mutations influence the aging process, and can any known compounds help maintain mitochondrial genome stability?
Regards
Barry Armstrong
Neurodegenerative diseases, related with the aging, are consequences of mtDNA mutations resulting in a decrease in mitochondrial function.
I dnt have enough insight to answer your second query.
Barry
The mitochondrial genome is small (≈ 16.5 kb in humans), lacks conventional histones, is located close to the electron-transport chain (ETC) (a major source of reactive oxygen species, ROS), and undergoes replication independently of the cell cycle. PubMed Central+3MDPI+3DoveMed+3
Repair capacity for mtDNA is limited compared with nuclear DNA: for example, double-strand break repair is less efficient in mitochondria. MDPI+2MDPI+2
Errors during mtDNA replication, oxidative damage (e.g., 8-oxoG) and mitochondrial dynamics (fission/fusion) all contribute to accumulation of mtDNA mutations.
Age‐related increases in mtDNA mutation burden have been documented in human tissues (muscle, colon, heart) and in model organisms.
The downstream effects of mtDNA mutation accumulation include impaired bioenergetics, increased apoptotic signalling, tissue decline (e.g., sarcopenia in skeletal muscle) and increased susceptibility to age-related diseases (neurodegeneration, cardiovascular disease) .