Anna Liachenko, BSc, MSc
Managing Editor,
Geriatrics & Aging

A number of groundbreaking studies seem to suggest that only a few genes are responsible for the multiple changes in our bodies, which lead to the gradual physiological decline, we call aging. The small number of genes involved in aging supports a thesis that was first proposed by Dr. George Martin of the University of Washington.

Using a new technology called oligonucleotide microarrays (or gene chips), to detect the rates of gene transcription, Dr. Richard A. Lerner together with Dr. Peter G. Schultz and other colleagues, recently examined 6000 genes expressed in human fibroblasts from both young and aging humans. They found that only 61 genes consistently showed changes in levels of expression with aging. More than half of these genes were involved in either cell cycle progression or remodeling of extracellular matrix. These cellular markers of aging may be fibro-blast-specific or at least mitotically-active-tissue specific as they are different from those found in post-mitotic tissues. Indeed, Dr. Tomas A. Prolla, who examined transcription rates in post-mitotic mouse gastrocnemius muscle, found a different (but, interestingly, just as narrow) subset of genes, for which the transcription rates were significantly altered with age.

In light of the small number of genes that presumably are able to cause the decline of multiple physiological systems, it is interesting to look at a group of genetic disorders called progerias. Progeria means early aging, in Greek.