The role of telomerase in age-related degenerative disease and cancer

Abstract

Abstract Aging is caused by cell senescence and an altered pattern of gene expression in the context of complex interdependencies of the multitude of tissues and organs that constitute the human body. All cells do not senesce. Those that do are responsible for the pathology that we associate with aging, even in cells that do not themselves senesce. Cell senescence is, without intervention at the genetic level, unavoidable, but both cell senescence and its clinical outcome (age-related disease) can be slowed or hastened through non genetic means including, but not limited to, behavioral changes, environmental exposures, diet, drugs, infections, genetic inheritance, and concurrent diseases. In the same manner, such interventions can slow or hasten the overall process of aging in the body. Although it can be slowed or hastened, aging cannot be prevented, stopped, or reversed by any intervention that does not affect cell senescence and specifically senescence associated gene expression. Although many other approaches might be feasible, the most efficient means of either treating age-related diseases, cancer, or the fundamental process of aging itself will almost certainly be the reversible control of native telomerase activity by induction of expression and, in the case of cancer, by telomerase inhibitors. Such intervention is currently, although within strict technical limits, possible. Within the next decade, we will likely be capable of therapeutic modulation of telomerase; with telomerase therapy will come not only effective control for age-related diseases and cancer, but an unprecedented alteration of the genetic controls on life span. The fiscal, social, and personal implications of such therapy are almost impossible to predict, but likely to be stunning.