The cellular senescence unification model and telomerase therapy: To treat all age-related diseases

Abstract

Since the discovery of the telomere by Hermann Muller and Barbara McClintock in years 1938-1940, a great progress has been made in molecular genetics and in the relatively new field, biogerontology. Almost 40 years have passed since the discovery of telomerase by Carol Greider and Elizabeth Blackburn (1984). Since those major discoveries, the scientific community has linked many naturally occurring ageing mechanisms in cells to the shortening of telomeres and the lack of telomerase activity in these cells. A great number of mutagens, radiation, and toxic chemicals negatively impact the length of telomeres with their truncation triggering a fatal cascade of events inside the cell which can lead to the state of senescence and eventually to cell death. Even though cellular and bodily ageing is a complex, multilevel, and highly orchestrated natural process happening at the subcellular level of all multicellular organisms, and a single known mechanism is extremely insufficient to explain all observed molecular and morphological changes, a unified cohesive theory of ageing must exist. The cellular senescence unification (CSU) model, combining the free-radical-mitochondrial and telomeric theories, helps establish a strengthened base for future therapies of all age-related disorders. If the CSU model is strong enough to explain and describe most of all the observed alterations in the ageing cell, a focused and deliberate therapy might be developed. This work introduces telomerase therapy as an efficient, highly effective, and clinically favored treatment for most age-related disorders, which can be elucidated by the CSU model. Gene therapy is the next natural step forward for biogerontology since the discovery of the telomere 80 years ago. Keywords: Telomeres, telomerase therapy, cellular senescence, unified theory of ageing