The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity

Guo, Guang; Ou, Xiao-Ming; Roettger, Michael E.; Shih, Jean C.

doi:10.1038/sj.ejhg.5201999

Cited by 141 publications

(116 citation statements)

References 36 publications

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“…While Sabol et al [1998] found that the individuals with the 5-repeat allele have a lower transcriptional efficiency than those with 3.5-or 4-repeat allele. The 2-repeat sequence in the MAOA gene promoter is reported to display the lowest level of transcription activity, as compared with the other alleles [Guo et al, 2008].…”

Section: Neuropsychiatric Geneticsmentioning

confidence: 96%

Study of a possible role of the monoamine oxidase A (MAOA) gene in paranoid schizophrenia among a Chinese population

Sun

Zhang

Yuan

et al. 2011

American J of Med Genetics Pt B

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Monoamine oxidase A (MAOA) is the enzyme responsible for degradation of several monoamines, such as dopamine and serotonin that are considered as being two of the most important neurotransmitters involved in the pathophysiology of schizophrenia. To study a possible role of the MAOA gene in conferring susceptibility to schizophrenia, the present study genotyped the variable number of tandem repeat (VNTR) polymorphism and 41 SNPs across this gene among 555 unrelated patients with paranoid schizophrenia and 567 unrelated healthy controls. Quantitative real-time PCR analysis was employed to quantify expression of MAOA mRNA in 73 drug-free patients. While none of these genotyped DNA markers showed allelic association with paranoid schizophrenia, haplotypic association was found for the VNTR-rs6323, VNTR-rs1137070, and VNTR-rs6323-rs1137070 haplotypes in female subjects. Nevertheless, no significant change of the expression of MAOA mRNA was detected in either female or male patients with paranoid schizophrenia. Our study suggests that the interaction between genetic variants within the MAOA gene may contribute to an increased risk of paranoid schizophrenia, but the precise mechanism needs further investigation.

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Section: Neuropsychiatric Geneticsmentioning

confidence: 96%

Study of a possible role of the monoamine oxidase A (MAOA) gene in paranoid schizophrenia among a Chinese population

Sun

Zhang

Yuan

et al. 2011

American J of Med Genetics Pt B

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“…According to Sabol et al [80] and Decker et al [81], the product of the MAOA-VNTR can be five alleles consisting of 2, 3, 3.5, 4, and 5 30-bp tandem repeats. The relatively rare VNTR allele with 2 repeats displays the lowest expression of the enzyme, corresponding only to 25-30% of the activity of the MAOA promoter in allele 4 [82]. When this allele was present, a two-fold increased level of delinquency and violent delinquency compared to the carriers of other MAOA-VNTR variants in men, and similar although weaker symptoms in women, were observed [82].…”

Section: Monoamine Oxidasementioning

confidence: 97%

“…The relatively rare VNTR allele with 2 repeats displays the lowest expression of the enzyme, corresponding only to 25-30% of the activity of the MAOA promoter in allele 4 [82]. When this allele was present, a two-fold increased level of delinquency and violent delinquency compared to the carriers of other MAOA-VNTR variants in men, and similar although weaker symptoms in women, were observed [82]. It has been known that allele 2 of the MAOA-VNTR represents the most "criminogenic" variant of monoamine oxidase A.…”

Section: Monoamine Oxidasementioning

confidence: 99%

Genetic and non-genetic determinants of aggression in combat sports

2014

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Human aggression/impulsivity-related traits are influenced by complex genetic and non-genetic factors. The aggression/anxiety relationship is controlled by highly conserved brain regions including the amygdala, hypothalamus and periaqueductal gray of the midbrain, which is responsible for neural circuits triggering defensive, aggressive, or avoidant behavioral models. The social behavior network consists of the medial amygdala, medial hypothalamus and periaqueductal gray, and it positively modulates reactive aggression. An important role in the incidence of aggressive behavior is played by secreted factors such as testosterone, glucocorticoids, pheromones, as well as by expression of genes such as neuroligin-2, monoamine oxidase A, serotonin transporters, etc. The authors deliberate whether aggression in sport is advantageous (or even indispensable), or to what extent it can hamper attainment of sport success. Methods of reducing and inhibiting expression of aggression in athletes are indicated.

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“…PCR products consist of five fragment sizes, including 2, 3, 3.5, 4 or 5 copies of the repeated sequence; the 3.5R and 4R copies are transcribed more efficiently than the 2R, 3R or 5R, while 2R exhibits the lowest promoter activity (Sabol et al 1998); an association of the 2R variant with delinquent behavior in adolescence has been suggested (Guo et al 2008). …”

Section: Modulation Of Mao-a Expression In Neuropsychiatric Disordersmentioning

confidence: 99%

Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression

2015

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Monoamine oxidase types A and B (MAO-A, MAO-B) regulate the levels of monoamine neurotransmitters in the brain, and their dysfunction may be involved in the pathogenesis and influence the clinical phenotypes of neuropsychiatric disorders. Reversible MAO-A inhibitors, such as moclobemide and befloxatone, are currently employed in the treatment of emotional disorders by inhibiting the enzymatic degradation of dopamine, serotonin and norepinephrine in the central nervous system (CNS). It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson's and Alzheimer's diseases. This effect, however, is not related to their inhibition of MAO activity; in animal and cellular models, selegiline and rasagiline protect neuronal cells through their anti-apoptotic activity and induction of pro-survival genes. There is increasing evidence that MAO-A activity, but not that of MAO-B, is implicated in the pathophysiology of neurodegenerative disorders, but also in gene induction by MAO-B inhibitors; on the other hand, selegiline and rasagiline increase MAO-A mRNA, protein, and enzyme activity levels. Taken together, these results suggest that each MAO subtype exerts effects that modulate the expression and activity of the other isoenzyme. The roles of MAO-A and -B in the CNS should therefore be re-evaluated with respect to the "type-specificity" of their inhibitors, which may not be unconditional during chronic treatment. Mao-a expression, in particular, may be implicated in pathogenesis and phenotypes in neuropsychiatric disorders. MAO-A expression is modified by mao polymorphisms affecting its transcriptional efficiency, as well as by mutations and polymorphism of parkin, Sirt1, FOXO, microRNA, presenilin-1, and other regulatory proteins. In addition, childhood maltreatment has been shown to have an impact upon adolescent social behavior in children with mao-a polymorphisms of low transcriptional activity. Low MAO-A activity may increase the levels of serotonin and norepinephrine, resulting in disturbed neurotransmitter system development and behavior. This review discusses genetic and environmental factors involved in the regulation of MAO-A expression, in the contexts of neuropsychiatric function and of the regulation of neuronal survival and death.

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The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity

Cited by 141 publications

References 36 publications

Study of a possible role of the monoamine oxidase A (MAOA) gene in paranoid schizophrenia among a Chinese population

Study of a possible role of the monoamine oxidase A (MAOA) gene in paranoid schizophrenia among a Chinese population

Genetic and non-genetic determinants of aggression in combat sports

Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression

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