Monoamine oxidase (MAO) A and B are enzymes that catalyze the oxidative deamination of biogenic amines, playing key roles in neurotransmitter metabolism and behavior. The genes for MAO A and B are located on the X chromosome and share a similar exon-intron structure, suggesting they originated from a common ancestral gene. MAO A and B knockout mice exhibit distinct changes in neurotransmitter levels and behavior. MAO A knockout mice show elevated serotonin, norepinephrine, and dopamine levels and display aggressive behavior, similar to human males with MAO A deficiency. In contrast, MAO B knockout mice do not show aggression and have increased phenylethylamine levels. Both MAO A and B knockout mice are more reactive to stress. These mice are valuable models for studying the role of monoamines in psychoses and neurodegenerative disorders. MAO A and B differ in substrate specificity, with MAO A preferring serotonin, norepinephrine, and dopamine, while MAO B prefers phenylethylamine and benzylamine. MAO A is predominantly found in catecholaminergic neurons, while MAO B is abundant in serotonergic and histaminergic neurons and glial cells. MAO A is most concentrated in the locus coeruleus, and MAO B is most concentrated in the raphe nuclei. The distribution of MAO in peripheral tissues varies, with MAO B mainly in human platelets and bovine liver and kidney, and MAO A in human placenta and bovine thyroid. The MAO A and B genes have been cloned and characterized, showing high conservation among species. Their promoters have been studied, revealing distinct regulatory elements. MAO A and B have different tissue-specific expression patterns, with MAO B activity increasing with age. MAO A is present in most tissues before MAO B, and its activity increases with aging. MAO B is predominantly located in glial cells, and its activity increases with aging due to glial cell proliferation. MAO A and B knockout mice have been generated, showing distinct behavioral and metabolic changes. MAO A knockout mice have elevated serotonin levels and aggressive behavior, while MAO B knockout mice have increased phenylethylamine levels. These mice are useful for studying the role of MAO in neurodegenerative and stress-related disorders. MAO B is involved in Parkinson's disease, as increased MAO B activity is associated with the loss of dopaminergic neurons. MAO B also converts MPTP to MPP+, which selectively destroys dopaminergic neurons. MAO B knockout mice are resistant to MPTP toxicity, indicating its role in Parkinson's disease pathogenesis. MAO A and B are involved in smoking and alcoholism, with reduced MAO activity in smokers and alcoholics. MAO inhibition by cigarette smoke is not fully understood, but may involve reactive adducts with MAO.Monoamine oxidase (MAO) A and B are enzymes that catalyze the oxidative deamination of biogenic amines, playing key roles in neurotransmitter metabolism and behavior. The genes for MAO A and B are located on the X chromosome and share a similar exon-intron structure, suggesting they originated from a common ancestral gene. MAO A and B knockout mice exhibit distinct changes in neurotransmitter levels and behavior. MAO A knockout mice show elevated serotonin, norepinephrine, and dopamine levels and display aggressive behavior, similar to human males with MAO A deficiency. In contrast, MAO B knockout mice do not show aggression and have increased phenylethylamine levels. Both MAO A and B knockout mice are more reactive to stress. These mice are valuable models for studying the role of monoamines in psychoses and neurodegenerative disorders. MAO A and B differ in substrate specificity, with MAO A preferring serotonin, norepinephrine, and dopamine, while MAO B prefers phenylethylamine and benzylamine. MAO A is predominantly found in catecholaminergic neurons, while MAO B is abundant in serotonergic and histaminergic neurons and glial cells. MAO A is most concentrated in the locus coeruleus, and MAO B is most concentrated in the raphe nuclei. The distribution of MAO in peripheral tissues varies, with MAO B mainly in human platelets and bovine liver and kidney, and MAO A in human placenta and bovine thyroid. The MAO A and B genes have been cloned and characterized, showing high conservation among species. Their promoters have been studied, revealing distinct regulatory elements. MAO A and B have different tissue-specific expression patterns, with MAO B activity increasing with age. MAO A is present in most tissues before MAO B, and its activity increases with aging. MAO B is predominantly located in glial cells, and its activity increases with aging due to glial cell proliferation. MAO A and B knockout mice have been generated, showing distinct behavioral and metabolic changes. MAO A knockout mice have elevated serotonin levels and aggressive behavior, while MAO B knockout mice have increased phenylethylamine levels. These mice are useful for studying the role of MAO in neurodegenerative and stress-related disorders. MAO B is involved in Parkinson's disease, as increased MAO B activity is associated with the loss of dopaminergic neurons. MAO B also converts MPTP to MPP+, which selectively destroys dopaminergic neurons. MAO B knockout mice are resistant to MPTP toxicity, indicating its role in Parkinson's disease pathogenesis. MAO A and B are involved in smoking and alcoholism, with reduced MAO activity in smokers and alcoholics. MAO inhibition by cigarette smoke is not fully understood, but may involve reactive adducts with MAO.