6 



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THE MECHANISMS OF SENESCENCE 



All theories of senescence are at present based on unwarrant- 

 able assumptions, in the absence of concrete answers to the 

 essential questions of fact. The formulation which would re- 

 ceive, perhaps, the widest assent, at least in the matter of human 

 senescence, is that morphogenetic processes lead to the differ- 

 entiation of cells which have lost the capacity for division, such 

 as neurones and skeletal muscle fibres, and to a suspension of 

 division in others, and that processes of 'wear and tear', 

 chemical, mechanical, or of a degree of biophysical subtlety 

 depending on the taste of the investigator, thereafter bring 

 about the decline of some or all of the tissues thus deprived of 

 the power of self-renewal. This is plausible and probably true. 

 On the other hand (1) it has been shown already that we do 

 not know whether all vertebrates, in spite of their apparently 

 similar degree of histological complexity, are susceptible to 

 senescence, and there is some ground to suspect that they are 

 not; (2) no satisfactory technique has been devised for the study 

 of cell populations in situ, apart from the search for mitotic 

 figures in sections: we do not, therefore, know the life-span of 

 any tissue cell in its natural situation; (3) many of the descrip- 

 tions of senile change in fixed postmitotics, especially neurones, 

 are based upon the assumption that the life-span of cells 

 specialized to this extent is limited by their incapacity for 

 division, as appears to be the case in rotifer and Anguillula cells. 

 The striking differences in specific age between related species 

 do not disprove the contribution of cell ageing to general sen- 

 escence, but they cast a great deal of doubt on any assumption 

 that the effect of wear and tear upon neurones (Bab, 1948; 

 Vogt and Vogt, 1946) or any similar process is the prime mover 



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