Mitochondria, which provide energy to cells, have their own set of DNA. Mutations of mitochondrial DNA increase with age, but until now no one knew whether this is a result of aging or a cause of aging. New research findings now indicate that the latter is the case.
Mice with a deficient capacity to correct mutations in mitochondrial DNA acquired an increased number of mutations and proved to age considerably earlier than normal. They lived an average of 10 to 12 months compared with the normal 2 or 3 years. These mice also developed several typical signs of premature aging, such as osteoporosis, weight loss, hair loss, anemia, reduced fertility, and heart muscle disorders.
The findings reveal fundamental biological mechanisms that lie behind the aging process. This knowledge paves the way for the possibility of slowing down aging and treating pathological changes that arise in connection with aging by protecting mitochondrial DNA from damage.
The article is published in Nature, May 27, 2004, pp. 417-423.
It is illustrated by a picture on the cover of Nature and commentated by two scientists from the University of Washington, Seattle.
Premature aging in mice expressing defective mitochondrial DNA polymerase
Nature (2004) 429: 417-423,
Trifunovic A, Wredenberg A, Falkenberg M, Spelbrink JN, Rovio AT, Bruder CE, Bohlooly-Y M, Gidlöf S, Oldfors A, Wibom R, Törnell J, Jacobs HT, Larsson N-G.