144 Discussion 



be assumed that Pick's and Alzheimer's diseases may occur in the same 

 family; that is, in a family that ordinarily has the capacity for very long 

 life. It is probable, therefore, that a major mutation has occurred in a 

 gene that ordinarily has a normal function in a longevous person. 



Psychopathological symptoms as such don't mean much unless they 

 are related to chronological age and general metabolic changes. They 

 are known to differ from one person to another, although toward the 

 end of their lives all human beings are apt to be maladjusted. 



Lewis: The difficulty in using the neuropathological criterion is that 

 the brains of old people who showed no psychological evidence of de- 

 terioration are sometimes indistinguishable from those of old people 

 who had considerable dementia. 



Kallmann: Yes, but one does not know the extent of cerebrovascular 

 changes which differentiate them. It may be a greater or lesser supply 

 of oxygen and other things that differentiate persons, rather than 

 differences in the structure of the brain itself. Certainly one should be 

 able to identify a biochemical deficiency factor so clearly defined as in 

 Pick's or in Alzheimer's disease. It is almost unbelievable that we still 

 don't know what this gene does and what kind of a defective state it 

 produces. As long as we don't know that, it is not surprising that even 

 ordinary ageing processes are not sufficiently understood. 



Olbrich: Would you say that the rate of ageing, the rate of decline, is 

 genetically conditioned or controlled in your twin studies? 



Kallmann: Yes, as far as variations in traits are concerned which are 

 measurable by psychometric tests. 



Bourne: Has any study been made of the inheritance of Simmond's 

 disease ? 



Kallmann: I don't think so. 



Danielli: Is it possible to generalize in any way about the deterioration 

 of characteristics controlled by single genes, i.e. major genes, as com- 

 pared with characteristics controlled by polygene sets ? 



Kallmann: In the case of a single-factor trait which is due to the effect 

 of a single major mutant gene, pathological changes are associated with 

 some very specific biochemical deficiency states. As a rule, however, 

 the ageing process takes place in traits that are polygenically deter- 

 mined. I don't know of normal personality traits that one would 

 ascribe to the effect of one specific gene. Only when one deals with the 

 effect of one gene that can express itself as clearly as is true in Alzheimer's 

 or Pick's disease, then the effect is pathological as far as ageing is con- 

 cerned. In the last analysis, ageing must be thought of in terms of the 

 individual ability or inability to utilize ordinary longevity potentials. 



Danielli: That seems to me an extremely arbitrary definition of ageing ! 

 In that case, how would you account for a man who lives twenty years 

 longer than he should do because he has lived in a favourable environ- 

 ment ? Something very peculiar would have to happen in his genetic set-up. 



Kallmann: I don't think it is possible. How could you prove that 

 someone lived twenty years longer than his genes were potentially 

 capable of sustaining? 



Danielli: Well, the question really is: is the present-day span of life 



