Possible candidates that have been discussed in the past included DRD2 and MAO-A. DRD2 was a possibile candidate for non-sanguinity because of its reported relation to substance abuse and to susceptibility to schizophrenia in a non-sanguine habitancy. MAO-A was a possibility for either inhibition of aggression or for non-sanguinity because of its reported relation to violence and antisocial behavior ("the warrior gene"). However, we noted that in itself MAO-A could not by itself be the locus for non-sanguinity in the NPA model (the N locus) because it is X-linked. In X-linkage there can not be father-to-son transmission of a dominant trait, and this would be inconsistent with our observations that a non-sanguine male can indeed acquire the trait from his father.
The study (link below) from Finland raises the possibility that MAO-A is nevertheless involved in the coding for inhibition of trait N, but that a second gene, CDH13, is primarily required for the transmission of non-sanguinity in a quasi-dominant mechanism.
Finland's being geographically adjacent to a non-sanguine area, we think that it is highly probable that the cohort of violent individuals in the study contained a high preponderance of (non-sanguine) A types. Thus, the comparison between the two groups (violent and non-violent) was likely, at least in part, a comparison between sanguinity and non-sanguinity, i.e., different alleles of the primary locus that determines the presence or absence of the N trait.
Thus, we propose cadherin 13 (CDH13) as a not unreasonable primary candidate gene for the N locus of the NPA model, coding for the inhibition of sanguinity,
The cadherin 13 gene has previously been mentioned in behavioral studies, iand interestingly enough, in the susceptibility to schizophrenia.
So, CDH13 is a gene to watch.
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