MAO deficiency

The 1960 s and 1970 s saw several other hypotheses proposed and dis-proven. The monoamine oxidase (MAO) deficiency hypothesis was based on the observation of diminished activity of platelet MAO-B in schizophrenia, although this was likely to be an artifact of drug treatment and the small deficits could not, in any case, account for changes in monoamine transmitters. Other hypotheses relating to, among other transmitter molecules, noradrenaline and enkephalin/endorphin have also been proposed. Each of these have had propo-... 

In addition to the aforementioned inborn errors of metabolism, deficiencies in the catabolism of dopamine and serotonin would also be expected to result in decreased concentrations of HVA and 5HIAA (e.g. MAO deficiency and COMT deficiency). 

Described defects in biogenic amine metabolism include deficiencies of tyrosine hydroxylase (TH) (EC 1.14.16.2) [1, 2], aromatic L-amino acid decarboxylase (AADC) (EC 4.1.1.28) [3], dopamine jff-hydroxylase (DjffH) (EC 1.14.17.1) [4, 5] and monoamine oxidase (MAO) (EC 1.4.3.4). MAO deficiency has been described as an isolated defect of MAO-A [6] and as a deficiency of either MAO-A or MAO-B, or both, in association with Norrie disease [7]. Inheritance in all of these disorders is thought to be autosomal recessive. 

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