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MOLECULAR AND CELULLAR MEDICINE ADVANCES = ETERNAL YOUTH?

© Juan C. Mendible

Part v. Genes

In my previous articles I have told you about the ways they think life will be extended in the near future. They deal with the replacement of cells, organs or disease-related genes. However, those are solutions to the consequences of accidents, diseases and aging. Now I want to tell you about a series of experimental results that strongly indicates that the fountain of youth lies in a set of genes that regulate how we age. Thus, life could be extended if and when the molecular doctors learn how to modulate the action of those genes.

Lets analyze some of the evidence that indicates the existence of such genes.

1.- Worms. Dr. Cynthia Kenyon at UCSF has been able to more than double the life span of a worm known as C. elegans by altering just one gene.

2.- Flies. Researchers at the University of Guelph, Ontario, Canada injected fruit flies with a human gene called SOD1 and the flies lived an average of 40% longer than the normal ones. For what follows (see item 3), it is important to know that the protein coded for by SOD1 functions as an antioxidant 3.- Before going into the next clue, I must tell you that one hypothesis suggests that we age because one very reactive and toxic form of oxygen, called free radical reacts with DNA, damaging it and causing mutations.

The hypothesis sustains that when we are young the free radicals damage is prevented by a set of enzymes that inactivates or detoxifies the free radicals. As we age the activity of these antioxidant enzymes decreases and the aging caused by the free radicals accelerates.

Thus, the next evidence comes from research on a particularly nasty condition called Progeria, a disease whose cause is unknown and that accelerates aging, people with progeria suffers hear attacks before they are 20 years old. Thus, it seems obvious that understanding what is wrong in progeria must shed some light on the aging process, and Larry Oberley from the University of Iowa reported last year that in progeria patients two of the antioxidant enzymes are up to 50% less active than in normal people, which indicates that there is something wrong with its genes.

The hypothesis is also supported by the results of Giussepe Attardi, who using mitochondrial DNA from individuals whose age ranged from 20 weeks of gestation to 101 years old, found that, while there were few mutations in the samples that were under 65, after this age the mutations accumulated. Thus, it seems that when we hit the 65 years mark, our energy producing machinery, the mitochondrion, start to fail and in consequence so do our cells and organs.

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