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Gene Review

MAOA  -  monoamine oxidase A

Homo sapiens

Synonyms: MAO-A, Monoamine oxidase type A

Disease relevance of MAOA

  • Thus, the 5HTTLPR but not the MAOA gene promoter-associated polymorphism may be a risk factor for depression in PD patients, while neither polymorphism increases the risk for development of Parkinson's disease itself [1].
  • In implicating both the MAOA and MOAB variants, however, this study provides the first indication that dopamine availability (as opposed to other effects of MAOA) is involved in human obesity [2].
  • Previous reports have described the accumulation of the 5HT metabolite 5-hydroxyindoleacetic acid and increased activities of the 5HT-metabolizing enzyme MAOA in this same material from patients with hepatic encephalopathy [3].
  • Despite the application of this high-throughput genotyping method, negative results from the two-stage DNA pooling design used to screen loci within the TPH, AADC and MAOA genes did not support their role in migraine susceptibility [4].
  • No significant difference was found in total scores on the Abnormal Involuntary Movement Scale (AIMS) among the subject groups, sorted according to the COMT, MAOA and MAOB genotypes [5].

Psychiatry related information on MAOA

  1. MAOA influence on aggressive behaviors: In a seminal paper, Caspi and colleagues reported that a genotype conferring low levels of MAOA gene expression increases the risk for the development of antisocial problems in the presence of history of maltreatment [6] . To date, this association has been positively replicated in six studies, whereas four others have failed to confirm this association. MAOA polymorphisms have also been found to modulate aggressive behavior related to alcohol abuse [7], substance abuse [8] and testosterone levels in cerebrospinal fluidx [9].
  2. Other associations:

High impact information on MAOA


Chemical compound and disease context of MAOA


Biological context of MAOA

  • The implications of fast acetylation, selective MAO inhibitors, types MAOA and MAOB, and measures of platelet MAO inhibition are discussed in this article [24].
  • To examine whether this genetic variation might contribute to differences in brain activation within the anterior cingulate cortex, we genotyped 16 subjects for the DRD4 and MAOA genes who had been scanned during the ANT [25].
  • Human MAOA and MAOB genes isolated from X chromosome-specific libraries span at least 60 kilobases, consist of 15 exons, and exhibit identical exon-intron organization [26].
  • A maximal multipoint lod score of 3.69 was obtained at the monoamine oxidase type A (MAOA) locus in Xp11.23-11 [27].
  • A pVNTR repeat polymorphism located in the promoter region of the X-linked MAOA gene has been associated with mental disorders [28].

Anatomical context of MAOA


Associations of MAOA with chemical compounds

  • Exon 12 codes for the covalent FAD-binding-site and is the most conserved exon; the MAOA and MAOB exon 12 products share 93.9% peptide identity [26].
  • Monoamine oxidases A and B [MAOA and MAOB; amine:oxygen oxidoreductase (deaminating) (flavin-containing), EC] play important roles in the metabolism of neuroactive, vasoactive amines and the Parkinsonism-producing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) [26].
  • Exon 12 (bearing the codon for cysteine, which carries the covalently bound FAD cofactor) and exon 13 are highly conserved between human MAOA and MAOB genes (92% at the amino acid level) [33].
  • RESULTS: A suggestive association of sequence variations in genes responsible for the synthesis (TPH), recognition (5-HTR2A), and degradation (MAOA) of serotonin with depression symptomatology was found, although the effect was generally restricted to men [34].
  • Noradrenaline (NA) is catabolized by monoamine oxidase A (MAOA) and cathecol-O-methyl transferase (COMT) [35].

Physical interactions of MAOA


Enzymatic interactions of MAOA


Regulatory relationships of MAOA

  • Cys5 and Cys266 were identified as the only residues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inactivated MAO B, respectively [40].
  • Estrogenic control of monoamine oxidase A activity in human neuroblastoma cells expressing physiological concentrations of estrogen receptor [41].
  • Specifically, there was a significantly lower rate of CCK-4-induced panic attacks in female subjects who had MAO-A longer alleles or 5-HTTLPR short allele gene variants [42].

Other interactions of MAOA

  • All three complementary approaches employed (family-based, case-control and quantitative trait design) suggest a role for the MAO A promoter-region polymorphism in conferring risk for ADHD in our patient population [43].
  • When comparing specific response to nonspecific response, we found significant negative associations in three SNPs in the HTR2A gene (P=0.001-0.03) and two SNPs in the MAOA gene (P=0.03-0.05) [44].
  • Concentrations of MHPG in plasma are determined mainly by MAO-A activity because COMT inhibition did not have an additional effect on the moclobemide-induced decrease in plasma MHPG [45].
  • In both cases, contingency table analysis revealed previously unreported gene-gene interaction between the MAOA and SLC6A2 genes (P=0.019 and 0.019, respectively) [46].
  • In this study, we performed linkage analysis of MRX9 with a panel of 43 polymorphic DNA markers dispersed over chromosome X. Two-point linkage analysis revealed lod scores of 3.52 and 3.82 at 0% recombination for OATL1 and MAOA, both located in Xp11.2-p11 [47].
  • In our sample, the effects of COMT on the release of adrenocorticotrophin hormone (ACTH) depend on the presence of the low-expression MAOA variant in the same individual [48].

Analytical, diagnostic and therapeutic context of MAOA

  • Restriction mapping of the YAC indicates that it contains both MAOA and MAOB genes in addition to the DXS7 locus [49].
  • Allelic mRNA expression of X-linked monoamine oxidase a (MAOA) in human brain: dissection of epigenetic and genetic factors [28].
  • It has been shown from pulsed-field gel electrophoresis (PFGE) that the monoamine oxidase genes A and B (MAOA & MAOB) and DXS7 loci are physically very close [49].
  • In total, 26.0% of cluster B patients were hemi- or homozygous for the low-activity variant of the MAOA genotype, compared to 16.4% in the control group [14].
  • In the present study variations in the coding sequence of the MAOA gene were evaluated by RT-PCR, SSCP, and sequencing a mRNA or genomic DNA in 40 control males with > 100-fold variations of MAO-A activity, as measured in cultured skin fibroblasts [50].


  1. Allelic variation of serotonin transporter expression is associated with depression in Parkinson's disease. Mössner, R., Henneberg, A., Schmitt, A., Syagailo, Y.V., Grässle, M., Hennig, T., Simantov, R., Gerlach, M., Riederer, P., Lesch, K.P. Mol. Psychiatry (2001) [Pubmed]
  2. Obesity is associated with genetic variants that alter dopamine availability. Need, A.C., Ahmadi, K.R., Spector, T.D., Goldstein, D.B. Ann. Hum. Genet. (2006) [Pubmed]
  3. Alterations of [3H]8-OH-DPAT and [3H]ketanserin binding sites in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy. Rao, V.L., Butterworth, R.F. Neurosci. Lett. (1994) [Pubmed]
  4. A genetic analysis of serotonergic biosynthetic and metabolic enzymes in migraine using a DNA pooling approach. Johnson, M.P., Griffiths, L.R. J. Hum. Genet. (2005) [Pubmed]
  5. Polymorphisms of dopamine degradation enzyme (COMT and MAO) genes and tardive dyskinesia in patients with schizophrenia. Matsumoto, C., Shinkai, T., Hori, H., Ohmori, O., Nakamura, J. Psychiatry research. (2004) [Pubmed]
  6. Role of genotype in the cycle of violence in maltreated children. Caspi, A., McClay, J., Moffitt, T.E., Mill, J., Martin, J., Craig, I.W., Taylor, A., Poulton, R. Science. (2002) [Pubmed]
  7. Different allele distribution of a regulatory MAOA gene promoter polymorphism in antisocial and anxious-depressive alcoholics. Schmidt, L.G., Sander, T., Kuhn, S., Smolka, M., Rommelspacher, H., Samochowiec, J., Lesch, K.P. J. Neural. Transm. (2000) [Pubmed]
  8. Analysis of monoamine oxidase A (MAO-A) promoter polymorphism in male heroin-dependent subjects: behavioural and personality correlates. Gerra, G., Garofano, L., Bosari, S., Pellegrini, C., Zaimovic, A., Moi, G., Bussandri, M., Moi, A., Brambilla, F., Mameli, A., Pizzamiglio, M., Donnini, C. J. Neural. Transm. (2004) [Pubmed]
  9. A non-additive interaction of a functional MAO-A VNTR and testosterone predicts antisocial behavior. Sjöberg, R.L., Ducci, F., Barr, C.S., Newman, T.K., Dell'osso, L., Virkkunen, M., Goldman, D. Neuropsychopharmacology. (2008) [Pubmed]
  10. Increased stress response and beta-phenylethylamine in MAOB-deficient mice. Grimsby, J., Toth, M., Chen, K., Kumazawa, T., Klaidman, L., Adams, J.D., Karoum, F., Gal, J., Shih, J.C. Nat. Genet. (1997) [Pubmed]
  11. Pathological gambling and DNA polymorphic markers at MAO-A and MAO-B genes. Ibañez, A., de Castro, I.P., Fernandez-Piqueras, J., Blanco, C., Saiz-Ruiz, J. Mol. Psychiatry (2000) [Pubmed]
  12. Family-based association studies support a sexually dimorphic effect of COMT and MAOA on genetic susceptibility to obsessive-compulsive disorder. Karayiorgou, M., Sobin, C., Blundell, M.L., Galke, B.L., Malinova, L., Goldberg, P., Ott, J., Gogos, J.A. Biol. Psychiatry (1999) [Pubmed]
  13. An association between a functional polymorphism in the monoamine oxidase a gene promoter, impulsive traits and early abuse experiences. Huang, Y.Y., Cate, S.P., Battistuzzi, C., Oquendo, M.A., Brent, D., Mann, J.J. Neuropsychopharmacology (2004) [Pubmed]
  14. Cluster B personality disorders are associated with allelic variation of monoamine oxidase A activity. Jacob, C.P., Müller, J., Schmidt, M., Hohenberger, K., Gutknecht, L., Reif, A., Schmidtke, A., Mössner, R., Lesch, K.P. Neuropsychopharmacology (2005) [Pubmed]
  15. Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA. Cases, O., Seif, I., Grimsby, J., Gaspar, P., Chen, K., Pournin, S., Müller, U., Aguet, M., Babinet, C., Shih, J.C. Science (1995) [Pubmed]
  16. Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Brunner, H.G., Nelen, M., Breakefield, X.O., Ropers, H.H., van Oost, B.A. Science (1993) [Pubmed]
  17. Mapping human brain monoamine oxidase A and B with 11C-labeled suicide inactivators and PET. Fowler, J.S., MacGregor, R.R., Wolf, A.P., Arnett, C.D., Dewey, S.L., Schlyer, D., Christman, D., Logan, J., Smith, M., Sachs, H. Science (1987) [Pubmed]
  18. Human liver MAO-A and MAO-B separated by immunoaffinity chromatography with MAO-B-specific monoclonal antibody. Denney, R.M., Fritz, R.R., Patel, N.T., Abell, C.W. Science (1982) [Pubmed]
  19. Genetic associations with clinical characteristics in bipolar affective disorder and recurrent unipolar depressive disorder. Ho, L.W., Furlong, R.A., Rubinsztein, J.S., Walsh, C., Paykel, E.S., Rubinsztein, D.C. Am. J. Med. Genet. (2000) [Pubmed]
  20. Direct analysis of candidate genes in impulsive behaviours. Goldman, D., Lappalainen, J., Ozaki, N. Ciba Found. Symp. (1996) [Pubmed]
  21. Immunological uniqueness of human monoamine oxidases A and B: new evidence from studies with monoclonal antibodies to human monoamine oxidase A. Kochersperger, L.M., Waguespack, A., Patterson, J.C., Hsieh, C.C., Weyler, W., Salach, J.I., Denney, R.M. J. Neurosci. (1985) [Pubmed]
  22. Glucocorticoid and androgen activation of monoamine oxidase A is regulated differently by R1 and Sp1. Ou, X.M., Chen, K., Shih, J.C. J. Biol. Chem. (2006) [Pubmed]
  23. A reversible monoamine oxidase A inhibitor (moclobemide) facilitates smoking cessation and abstinence in heavy, dependent smokers. Berlin, I., Saïd, S., Spreux-Varoquaux, O., Launay, J.M., Olivares, R., Millet, V., Lecrubier, Y., Puech, A.J. Clin. Pharmacol. Ther. (1995) [Pubmed]
  24. Monoamine oxidase inhibitors. A review of antidepressant effectiveness. Quitkin, F., Rifkin, A., Klein, D.F. Arch. Gen. Psychiatry (1979) [Pubmed]
  25. Mapping the genetic variation of executive attention onto brain activity. Fan, J., Fossella, J., Sommer, T., Wu, Y., Posner, M.I. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  26. Human monoamine oxidase A and B genes exhibit identical exon-intron organization. Grimsby, J., Chen, K., Wang, L.J., Lan, N.C., Shih, J.C. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  27. X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. Brunner, H.G., Nelen, M.R., van Zandvoort, P., Abeling, N.G., van Gennip, A.H., Wolters, E.C., Kuiper, M.A., Ropers, H.H., van Oost, B.A. Am. J. Hum. Genet. (1993) [Pubmed]
  28. Allelic mRNA expression of X-linked monoamine oxidase a (MAOA) in human brain: dissection of epigenetic and genetic factors. Pinsonneault, J.K., Papp, A.C., Sadée, W. Hum. Mol. Genet. (2006) [Pubmed]
  29. Turner syndrome and Xp deletions: clinical and molecular studies in 47 patients. Ogata, T., Muroya, K., Matsuo, N., Shinohara, O., Yorifuji, T., Nishi, Y., Hasegawa, Y., Horikawa, R., Tachibana, K. J. Clin. Endocrinol. Metab. (2001) [Pubmed]
  30. Association between monoamine oxidase A activity in human male skin fibroblasts and genotype of the MAOA promoter-associated variable number tandem repeat. Denney, R.M., Koch, H., Craig, I.W. Hum. Genet. (1999) [Pubmed]
  31. Increased activities of MAOA and MAOB in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy. Rao, V.L., Giguère, J.F., Layrargues, G.P., Butterworth, R.F. Brain Res. (1993) [Pubmed]
  32. Telomeric length varies with age and polymorphisms of the MAOA gene promoter in peripheral blood cells obtained from a community in Taiwan. Lung, F.W., Fan, P.L., Chen, N.C., Shu, B.C. Psychiatr. Genet. (2005) [Pubmed]
  33. Structure of the human gene for monoamine oxidase type A. Chen, Z.Y., Hotamisligil, G.S., Huang, J.K., Wen, L., Ezzeddine, D., Aydin-Muderrisoglu, N., Powell, J.F., Huang, R.H., Breakefield, X.O., Craig, I. Nucleic Acids Res. (1991) [Pubmed]
  34. Candidate gene polymorphisms in the serotonergic pathway: influence on depression symptomatology in an elderly population. Christiansen, L., Tan, Q., Iachina, M., Bathum, L., Kruse, T.A., McGue, M., Christensen, K. Biol. Psychiatry (2007) [Pubmed]
  35. Gene-gene interaction between MAOA and COMT in suicidal behavior. De Luca, V., Tharmalingam, S., Sicard, T., Kennedy, J.L. Neurosci. Lett. (2005) [Pubmed]
  36. An X chromosome inactivation assay based on differential methylation of a CpG island coupled to a VNTR polymorphism at the 5' end of the monoamine oxidase A gene. Hendriks, R.W., Chen, Z.Y., Hinds, H., Schuurman, R.K., Craig, I.W. Hum. Mol. Genet. (1992) [Pubmed]
  37. Studies of the in vitro oxidation of 1-methyl-4-(1-methylpyrrol-2-yl)-4-piperidinol and its dehydration product 1,2,3,6-tetrahydro-1-methyl-4-(methylpyrrol-2-yl) pyridine by human monoamine oxidases A and B. Bembenek, M.E. Life Sci. (1990) [Pubmed]
  38. Human monoamine oxidase A and B genes map to Xp 11.23 and are deleted in a patient with Norrie disease. Lan, N.C., Heinzmann, C., Gal, A., Klisak, I., Orth, U., Lai, E., Grimsby, J., Sparkes, R.S., Mohandas, T., Shih, J.C. Genomics (1989) [Pubmed]
  39. The relative contribution of monoamine oxidase and cytochrome p450 isozymes to the metabolic deamination of the trace amine tryptamine. Yu, A.M., Granvil, C.P., Haining, R.L., Krausz, K.W., Corchero, J., Küpfer, A., Idle, J.R., Gonzalez, F.J. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  40. Structural comparison of human monoamine oxidases A and B: mass spectrometry monitoring of cysteine reactivities. Hubalek, F., Pohl, J., Edmondson, D.E. J. Biol. Chem. (2003) [Pubmed]
  41. Estrogenic control of monoamine oxidase A activity in human neuroblastoma cells expressing physiological concentrations of estrogen receptor. Ma, Z.Q., Violani, E., Villa, F., Picotti, G.B., Maggi, A. Eur. J. Pharmacol. (1995) [Pubmed]
  42. Association between serotonin-related genetic polymorphisms and CCK-4-induced panic attacks with or without 5-hydroxytryptophan pretreatment in healthy volunteers. Maron, E., Tasa, G., Tõru, I., Lang, A., Vasar, V., Shlik, J. World J. Biol. Psychiatry (2004) [Pubmed]
  43. Family-based and association studies of monoamine oxidase A and attention deficit hyperactivity disorder (ADHD): preferential transmission of the long promoter-region repeat and its association with impaired performance on a continuous performance test (TOVA). Manor, I., Tyano, S., Mel, E., Eisenberg, J., Bachner-Melman, R., Kotler, M., Ebstein, R.P. Mol. Psychiatry (2002) [Pubmed]
  44. Investigation of serotonin-related genes in antidepressant response. Peters, E.J., Slager, S.L., McGrath, P.J., Knowles, J.A., Hamilton, S.P. Mol. Psychiatry (2004) [Pubmed]
  45. Simultaneous inhibition of catechol-O-methyltransferase and monoamine oxidase A: effects on hemodynamics and catecholamine metabolism in healthy volunteers. Illi, A., Sundberg, S., Ojala-Karlsson, P., Scheinin, M., Gordin, A. Clin. Pharmacol. Ther. (1996) [Pubmed]
  46. Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype). Urwin, R.E., Bennetts, B.H., Wilcken, B., Lampropoulos, B., Beumont, P.J., Russell, J.D., Tanner, S.L., Nunn, K.P. Eur. J. Hum. Genet. (2003) [Pubmed]
  47. Localization of a gene responsible for nonspecific mental retardation (MRX9) to the pericentromeric region of the X chromosome. Willems, P., Vits, L., Buntinx, I., Raeymaekers, P., Van Broeckhoven, C., Ceulemans, B. Genomics (1993) [Pubmed]
  48. Convergent genetic modulation of the endocrine stress response involves polymorphic variations of 5-HTT, COMT and MAOA. Jabbi, M., Korf, J., Kema, I.P., Hartman, C., van der Pompe, G., Minderaa, R.B., Ormel, J., den Boer, J.A. Mol. Psychiatry (2007) [Pubmed]
  49. Characterization of a YAC containing part or all of the Norrie disease locus. Chen, Z.Y., Sims, K.B., Coleman, M., Donnai, D., Monaco, A., Breakefield, X.O., Davies, K.E., Craig, I.W. Hum. Mol. Genet. (1992) [Pubmed]
  50. Mutational analysis of the human MAOA gene. Tivol, E.A., Shalish, C., Schuback, D.E., Hsu, Y.P., Breakefield, X.O. Am. J. Med. Genet. (1996) [Pubmed]
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