Bidder's hypothesis revisited. Solution to some key problems associated with general molecular theory of ageing.
In this paper I consider three major difficulties associated with the general molecular theory of ageing, namely: (1) How can molecular damage accumulate in the face of the constellation of repair mechanisms that is found in cells? (2) How can the obvious programmatic nature of ageing be reconciled with underlying stochastic processes? (3) How do some organisms avoid ageing? As a solution to points 1 and 2, I propose that the repair mechanisms themselves deteriorate in a programmed fashion with age. However, I argue that this programming is unlikely to be a result of direct selection for life-shortening but, rather, is more likely to be a result of an indirect selection for other characters. This idea is very similar to the theory of senescence first formulated by Bidder. The solution to point 3 is that the repair mechanisms in systems which avoid ageing, in particular cellular and molecular turnover, are not impaired with age. The rejuvenating capacities of sexual and asexual reproduction are also discussed.
D000375:Aging; D000818:Animals; D002470:Cell Survival; D004260:DNA Repair; D005246:Feedback; D006801:Humans; D008954:Models, Biological; D014176:Protein Biosynthesis; D012098:Reproduction; D014158:Transcription, Genetic