Vol. 1, No. 3 , 1995, Page 1 
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Vol. 1, No. 3 , 1995, Page 1 |
Studying a large Dutch family in 1993, H. G. Brunner and colleagues found that all of the male family members with one particular genetic defect had borderline retardation and reacted aggressively when angry, fearful or frustrated. Crimes committed by the affected males included arson, attempted rape, and exhibitionism.
The defect Brunner et al. discovered in the impulsive, aggressive males was a mutation in the gene that codes for an enzyme, monoamine oxidase A (MAOA), which metabolizes the brain chemicals serotonin, dopamine, and norepinephrine. Abnormal levels of all three substances -- and serotonin in particular -- have been implicated in aggression and criminal behavior.
To further investigate Brunner's findings, Olivier Cases et al. have studied mice genetically engineered to lack MAOA. They report that rat pups lacking MAOA show abnormal behavior including trembling, fearfulness, and exaggerated startle reactions. Adult mice deficient in MAOA, on the other hand, show a pattern of enhanced aggression; they attack intruders more quickly than normal mice do, and their mating behavior is more rough and aggressive. These findings, the researchers say, support the theory that the aggressive behavior of Brunner's human subjects is a direct result of MAOA deficiency, rather than other genetic influences or psychosocial factors.
Cases' MAOA-deficient rat pups had serotonin levels up to nine times normal, and both pups and adults had elevated norepinephrine levels. Abnormalities in the mice's somatosensory cortexes were also seen.
"This study shows," the researchers say, "that MAOA-deficient mouse pups have a dramatically altered serotonin metabolism and severe behavioral alterations, both phenomena being linked."
Brunner urges researchers to investigate the frequency of MAOA deficiency in the general population, and to continue animal studies to determine the effects of MAOA abnormalities. "Such studies," he says, "might also suggest possibilities for treatment of the metabolic disturbance caused by the MAOA deficiency state."
"Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A," H. G. Brunner et al., Science, Vol. 262, No. 5133, Oct. 22, 1993.