Age-damaged mitochondria are age-damaged because they have lost genes necessary to produce proteins they need to function. This damage causes a good degree of age-related degeneration. There are a number of approaches here: fix the mitochondrial DNA, or provide the proteins some other way. New reseach suggests a novel way to accomplish the latter goal: "Scientists have determined that human cells are able to shift important gene products into their own mitochondria ... The gene products, known as tRNAs, assemble amino acids for the production of proteins within mitochondria. If the mitochondrial tRNA genes are defective or missing, and proteins are not manufactured, the mitochondria are unable to generate adequate energy. ... This was totally unexpected, to find an innate, built-in mechanism that we humans have ... If you have a mutation in a tRNA that you suspect is involved in disease, you theoretically should be able to bring a healthy tRNA from the cytoplasm into the mitochondria and correct the malfunction."