Can we learn about aging from a study of Werner's syndrome?

Werner's syndrome, a rare genetic condition, has many features suggestive of rapid, premature aging. However, it differs from normal aging in several important respects. Cultured skin fibroblast-like cells have markedly reduced growth potential and a characteristic pattern of multiple, variable, stable structural chromosomal rearrangements that are non-constitutional. Since Werner's syndrome is inherited in an autosomal recessive fashion, there is presumably a single gene defect or a multi-gene deletion that accounts for its multiple progeroid features. The identification of this defective protein (or proteins) would be of great interest to both basic gerontologic and clinical geriatric research, since it would shed light on the mechanisms underlying the normal aging process and the development of geriatric diseases. It is evident that such a protein(s) is not the sole determinant of youth or longevity, but the many progeroid manifestations of Werner's syndrome indicate that the basic molecular defect resides in or affects some central pathway of cellular control or homeostatic interaction.