cafinater said:
I thought I'd ask some of you if it's theoretically possible a genetic mutation could lead to stopped or very slowed aging.
In humans, very unlikely.
The causes of aging are not fully understood. It is a very complex biological phenomenon. The general senescent phenotype is characteristic of each species. There are a variety of model organisms that are used for aging research. Interestingly, the invertebrate organisms -- Drosophila (fruitfly) and C.elegans (nematode worm) -- have shown us that mutations in single genes can result in greatly increased life spans. But this is not as simple as it might seem as this increased longevity can be very dependant on genetic background. When it comes to vertebrates, however, the aging process is considerably more complex as the same single gene mutations recapitulated in mice have no such effect. There are multiple genes and biochemical pathways controlling aging in vertebrates.
One major theory sees our metabolism as the cause of our aging. According to this theory, aging is a by-product of normal metabolism; no mutations are required. Some of the oxygen atoms taken up by the mitochondria are reduced insufficiently to reactive oxygen species (ROS). ROS can oxidize and damage cell membranes, proteins, and nucleic acids.
General wear-and-tear and genetic instability is another theory of aging and are among the oldest hypotheses proposed to account for the general senescent phenotype. As one gets older, small traumas to the body build up. Point mutations increase in number, and the efficiencies of the enzymes encoded by our genes decrease. Moreover, if a mutation occurred in a part of the protein synthetic apparatus, the cell would make a large percentage of faulty proteins. If mutations arose in the DNA-synthesizing enzymes, the rate of mutations would be expected to increase markedly.
The mutation rate in mitochondria is many times faster than the nuclear DNA mutation rate. It is thought that mutations in mitochondria could (1) lead to defects in energy production, (2) lead to the production of ROS by faulty electron transport, and/or (3) induce apoptosis. Age-dependent declines in mitochondrial function are seen in many animals, including humans.
In addition to environmental factors, there is also a genetic aging program involving at least several genes that we know of. This is an aspect to aging that most people of science forums overlook. Most focus on mutations and free radicals and the like but ignore the fact that we are programmed to die as a result of normal gene function. There is a genome wide down regulation of muscle and tissue maintenance genes as we age. I seriously doubt that any technology we develop will ever overcome this genetic programming that is the result of millions of years of evolution. So as human life expectancy increases due to our increased ability to prevent and cure disease, we are still left with a general aging syndrome that is characteristic of our species. This is worth remembering because unless attention is paid to the genetic mechanisms controlling our aging syndrome, we risk ending up like Tithonios - the miserable wretch of Greek mythology to whom the gods awarded eternal life, but not eternal youth.<P>
