The interaction of genetics and behavior is complex. Previous information in this area has been largely statistical in nature, but connections at the molecular level are now beginning to emerge.
One interesting case is the association between violent criminal behavior and monoamine oxidase (MAO) activity in the brain. It has been known for many years that there is a statistical correlation between violence and the levels of MAO assayed in blood platelets. Lower MAO activity is found in violent criminals, both male and female. More recently, the underlying genetic defects have been characterized for a small number of extreme cases.
Signals are transmitted between nerve cells by a variety of chemical neurotransmitters that must be degraded once the signal has been received. Monoamine oxidase A is located in the outer membrane of the mitochondria of neurons and initiates degradation of neurotransmitters of the catecholamine family - dopamine, adrenalin (= epinephrine) and noradrenalin (= norepinephrine).
Monoamine oxidase A degrades the neurotransmitters norepinephrine and dopamine by converting the amine group into aldehyde group.
The gene for monoamine oxidase A (MAO-A) is located on the X chromosome and individuals with deletions and point mutations are known. Thus MAO-A defects are sex-linked. Alterations in the MAO-A gene result in marked changes in monoamine metabolism and are associated with variable cognitive deficits and behavioral changes in both humans and transgenic mice.
A monoamine oxidase A defect has been linked to violence among males in a family in the Netherlands. Over a dozen males who showed marginal mental retardation and uncontrolled violent outbursts proved to have a point mutation in the eighth exon of the MAO-A gene. This mutation changed a codon (CAG) for Gln to a stop codon (TAG) and resulted in a truncated protein.
No mutation was found in the MAO-A gene of normal brothers of the violent males. Females who gave birth to violent males were shown to have one normal and one mutant allele, as expected for carriers of a sex-linked defect. In affected individuals neurotransmitter levels would rise well above normal levels, especially under stressful situations. It seems likely that minor stresses trigger an overwhelming response.
The incidence of severe MAO-A defects is extremely low, and unlikely to account for more than a tiny proportion of criminal behavior. On the other hand, it is conceivable that the wider correlation between MAO levels and violent crime is due to genetic alterations that result in moderate reduction of monoamine oxidase activity. This is a matter for further investigation.