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The authors studied platelet monoamine oxidase (MAO) activity in 29 schizophrenic inpatients and 26 schizophrenic outpatients during a 4-week double-blind trial of chlorpromazine with imipramine or thiothixene with placebo. The found that significantly more schizophrenic patients than normal control subjects had low platelet MAO activity after 4 weeks. Outpatients with low MAO activity were distinguished by increased behavioral activity and reduced social apathy. Inpatients with low MAO activity were distinguished by severity of illness and symptoms. Hallucinations were significantly more frequent among patients with low MAO activity. The authors suggest that platelet MAO activity might decline in some actively schizophrenic patients as part of the psychotic process.

Monoamine oxidase (MAO), a mitochondrial enzyme involved in the degradation of biogenic amines, has been associated with psychiatric morbidity. Although twin and family studies have indicated that MAO activity is familial, the exact mode of transmission is unclear. We performed segregation analysis on 154 nuclear families containing 419 individuals using the mixed model, which allows for a single major locus with a polygenic background. We were able to reject a dominant and additive locus with or without a heritable background and a recessive locus without background. The acceptable models were: (1) a codominant model without background where the mean of the heterozygote distribution was 30% of the distance from the low to the high homozygote distributions, and (2) a recessive locus with heritable background. In both cases, the gene frequency for the high-MAO allele is approximately .25--at odds with suggestions that low-MAO represents a genetic marker for a disorder such as schizophrenia with a lifetime risk of only 0.85%. To ensure that results were not artifacts from a familial, skewed distribution, the data were also analyzed after power transformation. In addition, hypotheses were tested using both the joint and conditional likelihoods to examine for possible misspecification of the model with respect to intergenerational differences. Finally, we allowed for non-Mendelian transmission probabilities to provide another class of alternatives against which to test the hypothesis of a major locus. All these approaches provided additional confirmation for the presence of a major locus segregating within these families.

Platelet MAO activity (tryptamine as substrate) was assessed in 44 hospitalized men alcoholics to examine the relationships between MAO levels and variables related to alcohol misuse and physiological status. Mean MAO levels were lower in this population than in normal controls and hospitalized psychiatric patients. MAO activity correlated with age but was independent of variables derived from self-reported drinking histories and scales of alcohol dependence. Similarly, platelet MAO activity was not related to the misuse of other drugs. Of the variance in MAO activity, 38% could be accounted for by age, and the values of Mg++, low density lipoproteins and eosinophil combined. The significance of low platelet MAO activity in alcoholics is discussed.

Blood platelet monoamine oxidase (MAO) activity was evaluated in twenty-four anergic, schizophrenic outpatients during a double-blind study comparing a chlorpromazine-imipramine combination to thio-thixeneplacebo. Platelet MAO activity was determined on blood samples drawn after a two-week drug-free washout and once weekly over a four-week on-drug period. Schizophrenic patients could be classified according to their blood platelet MAO activity into either a low-MAO or a high-MAO group. In neither group of this population of schizophrenics did blood platelet MAO activity correlate with any of the primary or secondary symptoms of schizophrenia. Ten alcoholics and seven volunteer non-patients could similarly be divided into low- and high-MAO groups. Mean blood platelet MAO activity for these groups was not significantly different from the mean values of the low and high-MAO groups of the schizophrenics. These findings do not support published reports of low blood platelet activity as a genetic marker for schizophrenia. Discriminate function analysis of symptomatology ratings at baseline was used to characterize the low- and high-MAO schizophrenic patient groups. Individuals in the low-MAO group were distinguished by hyperactivity, anergia and sleep disturbance.

Ascorbic acid levels are commonly reported to be decreased in alcoholics. Although this deficiency could be due to dietary factors, there is evidence that ascorbic acid may be involved in the metabolism and acute effects of ethanol, possibly related to the pathogenesis of alcoholism. Therefore, we examined ethanol preference in guinea pigs receiving an ascorbate deficient vs a normal diet. Brain and spleen ascorbic acid levels were dramatically decreased, but ethanol preference was not altered by the acute dietary deficiency of this vitamin. In addition, an acute stressor (cold water swim), alone or in combination with ascorbate deficiency, had no effect on ethanol preference. At termination of the experiment, two measures of brain aminergic function (MAO activity and 3H-spiroperidol binding), purportedly altered by ethanol or ascorbic acid or both, were not associated with tissue ascorbate levels.

As part of a prospective, psychosocial, and biochemical study of infectious mononucleosis, platelet monoamine oxidase (MAO) activity has been evaluated as a host factor. It was found that platelet MAO activity may be a possible predisposing host factor but not a precipitating factor. The results on infectious mononucleosis, a viral disease which involves the host's cell-mediated immune system, are compared with an evaluation of platelet MAO activity in dengue, a viral disorder involving the host's humoral immune system. The platelet MAO activity in these disorders has been compared to that in schizophrenia, a disease for which low platelet MAO activity has been postulated, from retrospective and twin studies, to be a risk factor. One hypothesis suggests that low platelet MAO activity predisposes to development of schizophrenia, but also increases cell-mediated immune system responses.

The distribution of platelet monoamine oxidase (MAO) activity is examined in a large cohort of 18-year-olds from a college setting. A mixture of three distributions is needed to describe the data, even when a power transformation is used to remove skewness in the distribution. This is compatible with MAO activity being controlled by a single major locus with a gene frequency of 0.02 for high-MAO activity. Accordingly, it is unlikely that such a locus could serve as a genetic marker for a disorder which is associated with low activity. However, this finding does not rule out the possibility that MAO activity is an associated risk factor in disease.