Monoamine Oxidase (MAO) is an enzyme found in two forms, A and B. MAO-B is obtained from blood platelets in living organisms and is primarily involved in the metabolism of dopamine, regulating its level in the dopamine neuron
Table 5. Psychopathology and Monoamine Oxidase (MAO)
Low MAO found in:
High normal sensation seekers
Attention-Deficit Hyperactivity Disorder
Relatives of alcoholics
Bipolar Mood Disorder
Relatives of Bipolar Disorders
Zuckerman (1994) Shekim et al. (1986) Lidberg et al. (1985) Klinteberg (1996) Reist et al. (1990) Major & Murphy (1988) Shukitt (1994), Sher (1993) von Knorring et al. (1987) Murphy & Weiss (1972) Leckman et al. (1977) Zureik & Meltzer (1990)
by catabolizing this neurotransmitter after uptake (Murphy, Aulakh, Garrick, & Sunderland, 1987). MAO-A is involved in the intracellular metabolism of serotonin while MAO-B metabolizes extracellular serotonin (Azmitia & Whitaker-Azmtia, 1995). MAO-B is positively correlated with cortisol activity (Schatzberg & Schildkraut, 1995) and with serotonin activity in particular brain areas (Adolfsson, Gottfries, Oreland, Roos, & Winblad, 1978). Twin studies suggest that MAO-B is under nearly total genetic control involving one or two major genes. Behavioral differences between low- and high-MAO babies have been found in the first three days of life consisting of higher activity, motor reactivity and motor maturity in the low MAO babies (Sostek, Sostek, Murphy, Martin, & Born, 1981).
MAO-B has been correlated negatively with sensation seeking in many studies; high sensation seekers tend to have low levels of platelet MAO (Zuckerman, 1994). Although the mean relationship is not high (about .24 for Total SS and the Dis subscale) it was significant in 9 of 13 studies reviewed in 1994). Low MAO found in various disorders also characterized by high levels of sensation seeking, particularly disinhibition, and impulsivity (Table 5). Among alcoholics, low MAO is especially associated with the type II alcoholic characterized by younger onset, more antisocial behavior when intoxicated, and a family history of alcoholism (Pandey et al., 1988). The suggestion that the MAO link with psy-chopathology is genetically transmitted is supported by the finding of low MAO in the relatives of alcoholics and bipolar patients who may not manifest the disorder itself.
Many studies have found associations between low MAO and tobacco, alcohol, and drug use in non-clinical populations. Convictions for felony offenses are not common in a college population, but 37% of students selected from a very low MAO group had such convictions, contrasted with only 6% of the high MAO group (Coursey, Buchsbaum, & Murphy, 1979).
Low MAO monkeys living in a natural environment were more playful, active, social, aggressive, dominant, and sexually active than monkeys with high MAO levels (Redmond, Murphy, & Baulu, 1979). College students with low MAO reported more hours spent socializing than high MAO students (Coursey et al., 1979) but the results with self-report measures of extraversion have been inconsistent.
All of the above studies have used MAO-B from blood platelets. Recent data have implicated MAO type A in antisocial behavior and aggression, and studies on mice have shown a relationship between aggression and the absence of the gene. Caspi et al. (2002) have shown an interaction between childhood maltreatment and alleles of the gene encoding MAO-A. This is a longtudinal study so that the records of childhood maltreatment do not depend on retrospective accounts. Among those with the form of the gene that results in low MAO-A activity those children who also experienced severe maltreatment had a high incidence of conduct disorder during childhood, and antisocial personality disorder with violence at age 26. But among those with the form of the gene producing high MAO-A activity there was no difference in incidence of either of these disorders or in violence between those maltreated and those not maltreated during childhood. Neither the form of the gene nor childhood maltreatment alone were sufficient to produce antisocial personality, but the genetic-experience interaction did so.
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