Monoamine oxidase polymorphisms

Yoshida, K. et al. (2002). Monoamine oxidase a gene polymorphism, tryptophan hydroxylase gene polymorphism and antidepressant response to fluvoxamine in Japanese patients with major depressive disorder. Prog. Neuropsychopharmacol. Biol. Psychiatry, 26, 1279-83. 

Cusin, C., Serretti, A., Zanardi, R. etal. (2002). Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI antidepressant activity. Int.. Neuropsychopharmacol, 5, 27-35. 

Samochowiec J, Lesch KP, Rottmann M, Smolka M, Syagailo YV, Okladnova O, Rom-melspacher H, Winterer G, Schmidt LG, Sander T (1999) Association of a regulatory polymorphism in the promoter region of the monoamine oxidase A gene with antisocial alcoholism. Psychiatry Res 86 67-72... 

Hamilton SP, Slager SL, Heiman GA, Haghighi F, Klein DF, Hodge SE, Weissman MM, Fyer AJ, Knowles JA (2000b) No genetic linkage or association between a functional promoter polymorphism in the monoamine oxidase-A gene and panic disorder. Mol Psychiatry 5 465-466... 

Muller DJ, Schulze TG, Macciardi F, et al (2002) Moclobemide response in depressed patients association study with a functional polymorphism in the monoamine oxidase A promoter. Pharmacopsychiatry 35 157-158... 

Preisig M, Bellivier F, Fenton BT. Association between bipolar disorder and monoamine oxidase A gene polymorphism results of a multicenter study. Am J Psychiatry 2000 157 948-955. 

Vanyuko r, Michael M., Howard B. Moss, Ling M. Yu, and Ranjan Deka. 1995b. "A Dinucleotide Repeat Polymorphism at the Gene for Monoamine Oxidase A and Measures of Aggressiveness." Psychiatry Research 59 35-41. 

Hyperserotonemia has been a consistent finding in subjects with autism, which may be due to activity of serotonin-associated platelet proteins (Hranilovic et al., 2008, 2009). Interestingly, 99% of blood serotonin is contained in platelets (Anderson et al., 1987) and studies have shown that there is an approximate 50% increase in blood-levels of serotonin in subjects with autism vs. controls (McBride et al., 1998). Hypotheses for increased serotonin include increased synthesis of serotonin by tryptophan hydroxylase (TPHl), increased uptake of serotonin into platelets via serotonin transporters (5-HTT), diminished release of serotonin from platelets via serotonin 2A receptor, and decreased breakdown of serotonin by monoamine oxidase (MAOA) (Hranilovic et al., 2008). A study by Hranilovic et al. (2008) identified polymorphisms of tryptophan hydroxylase and MAOA with increased serum serotonin levels. Similarly, haplotype analysis has shown a significant association between polymorphisms of TPHl and increased serotonin in whole blood (Cross et al., 2008). 

Jonsson EG, Norton N, Gustavsson JF et al (2000) A promoter polymorphism in the monoamine oxidase A gene and its relationships to monoamine metabolite concentrations in CSF of healthy volunteers. J Psychiatr Res 34 239-244... 

Monoamine oxidase A (MAOA) seems to be the principal serotonin degrading enzyme. The gene is located on chromosome Xpll [77]. Recent reports have shown that a low activity genetic variant of monoamine oxidase A (MAOA) is likely to be related to aggressive behavior, but only when paired with abusive experience in childhood. It also has been found that the low activity form of MAOA was associated with more adult symptoms of antisocial alcoholism than the high activity variant [113]. No studies related to autism have been carried out with this polymorphism (for more details see section 5 in Serotonergic innervations). 

HT transporter-linked polymorphic region Monoamine oxidase Magnetic resonance imaging Monozygotic twins... 

Genetic polymorphism exists with pseudocholinesterases ° Example local anesthetics Monoamine oxidases... 

Y.-Yu. Huang et al. An Association between a Functional Polymorphism in the Monoamine Oxidase A Gene Promoter, Impulsive Traits and Early Abuse Experiences. Neuropsychopharmacology, 2004. 

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