Toward the Systemic Replacement of Mitochondrial DNA with Somatic Mutations

The accumulation of lipofuscin, i.e., indigestible intracellular debris, might be the main cause of age-related diseases that we see today. However, without being able to replace mutated mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) that has suffered epigenetic drift, damage, and mutations, we will still eventually succumb to aging. Thus, we must save copies of mitochondrial and nuclear DNA at as young an age as possible, or at least from cell types with the lowest rates of mutation. MtDNA has a 10-100x higher rate of mutation than nDNA, as mitochondria are sites of free radical production. We may need to replace mtDNA before nDNA that has suffered epigenetic drift, damage, and mutations. If so, we will need a strategy to deliver pristine mtDNA to cells around the body and destroy somatically mutated mtDNA. A strategy for doing so is described herein.