Turkish Journal of
GERIATRICS

Hacettepe Üniversitesi Fen Fakültesi Biyoloji Bölümü Genel Biyoloji Anabilim Dalı Beytepe/Ankara Why do we get old? The basic theme of our inquiry concerns the answer of this question which have been asked by the people themselves for a long time. In our review, the cell of younger people are compared with those of elderly, as well as the cells of organisms with shorter and longer life - span are compared. In addition, the hypothesis of "telomere lost" is reviewed in detail as it is supposed to be one of the fundamental cause of ageing. Telomer loss hypothesis states that the telomeres which are specific nucleotide repeats at the eucaryotic chromosome tips are reduced per division and hence are a causal factor in ageing. Again this hypothesis also observes that telomeres have crucial function for chromosomal integrity by reducing recombination, being a signal for cellular recognition preventing nonfunctional chromosome fusion and attaching chromosomes to nuclear membrane. Our review gives an interspecific account of the repeated structures (e. g. TTAGGG in human and TTGGGG in unicellular Tetrahymena). We also provide mechanistic explanations about how gaps left after replication are filled up by specific action of the enzyme, telomerase. Further on, the structure and function of telomerase enzyme and its tissue expression are explicated especially for humans. Above all, the relationship between ageing and telomere length is discussed. Few important general definitions of "ageing" are given and specifically it is emphasized that cellular ageing in human occurs at two steps, M1 and M2, and additionally which events take place in these two steps are explained. Artificial telomere induction and the presence of human telomerase reverstranscriptase (hTERT) in cells are discussed in relation to their possible effects. In the end, the review is completed by considerations of future concern. Keywords : Telomere, End Replication Problem, Telomerase, Ageing