488 DAVID H. DOLLEY * 



manner as before, but either type can grow again, though as in 

 the norm, only under the functional stimulus. 



A final statement concerns the relation of the senescence of the 

 nerve cell to its differentiation. The differentiation of the nerve* 

 cell is such that it does not appear in. continuous progressive 

 relationship with senescence, though this statement does not 

 contraindicate the fact that its potentiality of senescence de- 

 pends upon its peculiar status quo of differentiation. For the 

 quantitative nature of the dynamic reactions of that cell pred- 

 icates that differentiation is determined at the moment the 

 quantitative principle of function becomes operative. In the 

 Purkinje cell of the dog that moment is as close to birth as ten 

 days and probably earlier, and it is at least sure that the differ- 

 entiation remains a constant factor through adult life and senes- 

 cence. Thus within that quantitative principle, the nerve cell 

 is insusceptible to dedifferentiation (compare Child, '15, p. 281). 

 It regresses, of course, but this is the functional atrophy, and a 

 quantitative regression ; it may again go forward in renewed func- 

 tional growth, but there is no rejuvenation in the manner of 

 certain other cells. All of this connects up with established 

 knowledge. Let it be understood that this is not written in 

 antagonism to the princif^le of dedifferentiation, without which 

 the pathologist would face an insuperable barrier to intelligent 

 interpretations. 



Child ('15, p. 288) makes a place for such a degree of speciali- 

 zation, as follows: 



Atrophy in the higher animals differs from reduction in the lower 

 forms in that, while decrease in size occurs, there is little or no dedif- 

 ferentiation. The cell has apparently become so highly differentiated 

 that it has lost the capacity for synthesizing a substratum adequate in 

 quantity or constitution to carry on metabolism. Consequently the 

 losses from degradation and breakdown of the existing substratum are 

 not compensated by the synthesis of new substratal substance, and 

 sooner or later the fundamental mechanism of the cell is destroyed and 

 degeneration and death occur. The atrophj^ of old age in organs of 

 such fundamental importance as the nervous system indicates that 

 there is some truth in the statement, so often made, that the later 

 stages of senescence are a 'wearing out' of the physiological mechanism 

 or some essential part of it. Apparently the nerve cells or some of 

 them do wear out because they are no longer able to synthesize the 

 substratum necessary for their continued function. 



