scholarly journals Association Analysis of Monoamine Oxidase-A Gene Promoter Polymorphism (MAOA uVNTR) for Antisocial Behavior: Absence of the Counting Number Repeats in Central Iran

2020 ◽  
Vol 7 (4) ◽  
Author(s):  
Maryam Khosravian ◽  
Parvaneh Nikpour ◽  
Modjtaba Emadi-Baygi ◽  
Ali Soleimanpour ◽  
Fereidoun Yadollah Moghadam
Keyword(s):  
Antisocial Behavior ◽  
Violent Behavior ◽  
Variable Number Tandem Repeat ◽  
Promoter Polymorphism ◽  
Variable Number ◽  
Monoamine Oxidase A ◽  
Central Iran ◽  
P Value ◽  
Current Case ◽  
Maoa Gene

Background: The MAOA gene is located on the X chromosome (Xp11.23). Several studies have established a VNTR (Variable Number Tandem Repeat) polymorphism in the upstream of the MAOA gene transcriptional initiation region named uVNTR which is correlated with the risk of antisocial behavior. Objectives: This study aimed to investigate the association between MAOA genotypes and the risk of violent behavior in a cohort of violent and age-matched non-violent individuals. Methods: In the current case-control study, MAOA uVNTR was genotyped in a cohort of 88 violent and 95 age-matched non-violent individuals. Individuals were genotyped for the MAOA uVNTR by performing PCR, gel electrophoresis, and sequencing. Furthermore, a chi-square test was performed using SPSS, and a p-value of less than 0.05 was considered statistically significant. Results: We identified three MAOA uVNTR allelic variants: They were harboring 3.5, 4.5, and 5.5 repeated sequences. Alleles with 2, 3, 4, 5, and 6 repeats were not observed in any of the two examined groups. Conclusions: We did not detect a statistically appreciable association between antisocial behavior and allele frequencies in the studied population in central Iran.

scholarly journals MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study

2011 ◽  
Vol 198 (6) ◽  
pp. 457-463 ◽  
Author(s):  
David M. Fergusson ◽  
Joseph M. Boden ◽  
L. John Horwood ◽  
Allison L. Miller ◽  
Martin A. Kennedy
Keyword(s):  
Longitudinal Study ◽  
Physical Abuse ◽  
Conduct Problems ◽  
Variable Number Tandem Repeat ◽  
Antisocial Behaviour ◽  
Variable Number ◽  
Monoamine Oxidase A ◽  
Original Research ◽  
Violent Offending ◽  
Low Activity

BackgroundRecent studies have raised issues concerning the replicability of gene × environment (G × E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between abuse or maltreatment exposure and antisocial behaviour. This study attempted to replicate the findings in this area using a 30-year longitudinal study that has strong resemblance to the original research cohort.AimsTo test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to abuse exposure.MethodParticipants were 398 males from the Christchurch Health and Development Study who had complete data on: MAOA promoter region variable number tandem repeat genotype; antisocial behaviour to age 30; and exposure to childhood sexual and physical abuse.ResultsRegression models were fitted to five antisocial behaviour outcomes (self-reported property offending; self-reported violent offending; convictions for property/violent offending; conduct problems; hostility) observed from age 16 to 30, using measures of childhood exposure to sexual and physical abuse. The analyses revealed consistent evidence of G × E interactions, with those having the low-activity MAOA variant and who were exposed to abuse in childhood being significantly more likely to report later offending, conduct problems and hostility. These interactions remained statistically significant after control for a range of potentially confounding factors. Findings for convictions data were somewhat weaker.ConclusionsThe present findings add to the evidence suggesting that there is a stable G × E interaction involving MAOA, abuse exposure and antisocial behaviour across the life course.

Post-Stroke Fatigue May Be Associated with the Promoter Region of a Monoamine Oxidase A Gene Polymorphism

2016 ◽  
Vol 43 (1-2) ◽  
pp. 54-58 ◽  
Author(s):  
Smi Choi-Kwon ◽  
Mihye Ko ◽  
Sang-Eun Jun ◽  
Juhan Kim ◽  
Kyung-Hee Cho ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Promoter Region ◽  
Tryptophan Hydroxylase ◽  
Variable Number Tandem Repeat ◽  
Variable Number ◽  
Monoamine Oxidase A ◽  
Potential Contribution ◽  
Female Patients ◽  
Post Stroke ◽  
Mao A

Background: Post-stroke fatigue (PSF) is a common sequela of stroke. Despite reports of serotonergic involvement in the etiology of PSF, the potential contribution of serotonergic genes in the development of PSF needs to be investigated. Methods: A total of 373 patients, who experienced ischemic stroke for PSF, were evaluated 3 months after the stroke. PSF was assessed using the Fatigue Severity Scale. The genomic DNA collected and stored in a -70°C freezer was genotyped for 6 polymorphisms in genes associated with serotonin synthesis (tryptophan hydroxylase 1 (TPH1) A218C, TPH2 rs10879355, and TPH2 rs4641528), transport (the promoter region of the serotonin transporter protein), and catabolism (the 30-bp functional variable number tandem repeat) polymorphism in the promoter region of monoamine oxidase A (MAO-A). Results: Among the 373 patients, 164 (44%) had PSF. All patients were ethnic Koreans. Of the 6 polymorphisms examined, only one marker, that is, low-activity MAO-A was associated with PSF (p < 0.05) in female patients. Multiple logistic regression analyses showed that post-stroke depression (PSD; 95% CI 1.561-14.323, p = 0.006) and low MAO-A activity (95% CI 0.166-0.722, p = 0.005) were factors associated with PSF in female patients, whereas only PSD (95% CI 5.511-65.269, p = 0.000) was associated with PSF in male patients. Conclusions: Our findings suggest that PSF may be associated with a genetic polymorphism involving MAO-A, at least in female stroke patients.

scholarly journals Genetic and epigenetic associations of MAOA and NR3C1 with depression and childhood adversities

2013 ◽  
Vol 16 (7) ◽  
pp. 1513-1528 ◽  
Author(s):  
Philippe A. Melas ◽  
Yabin Wei ◽  
Chloe C. Y. Wong ◽  
Louise K. Sjöholm ◽  
Elin Åberg ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Variable Number Tandem Repeat ◽  
Childhood Adversity ◽  
Variable Number ◽  
Monoamine Oxidase A ◽  
Childhood Adversities ◽  
Epigenetic Programming ◽  
And Control ◽  
Gene Expression Levels

Abstract Monoamine oxidase A (MAOA) harbours a polymorphic upstream variable-number tandem repeat (u-VNTR). The MAOA-L allele of the u-VNTR leads to decreased gene expression levels in vitro and has been found to increase the risk of conduct disorder in males with childhood adversities. Early-life adversities have been associated with hypermethylation of the glucocorticoid receptor (NR3C1). In this study, we first performed a genetic association analysis of the MAOA u-VNTR using individuals with depression (n = 392) and controls (n = 1276). Next, DNA methylation analyses of MAOA and NR3C1 were performed using saliva samples of depressed and control subgroups. Adult MAOA-L females with childhood adversities were found to have a higher risk of developing depression (p = 0.006) and overall MAOA methylation levels were decreased in depressed females compared to controls (mean depressed, 42% vs. mean controls, 44%; p = 0.04). One specific childhood adversity [early parental death (EPD)] was associated with hypermethylation of NR3C1 close to an NGFI-A binding site (mean EPD, 19% vs. mean non-EPD, 14%; p = 0.005). Regression analysis indicated that this association may be mediated by the MAOA-L allele (adjusted R2 = 0.24, ANOVA: F = 23.48, p < 0.001). Conclusively: (1) depression in females may result from a gene × childhood-adversity interaction and/or a dysregulated epigenetic programming of MAOA; (2) childhood-adversity subtypes may differentially impact DNA methylation at NR3C1; (3) baseline MAOA-genotypic variations may affect the extent of NR3C1 methylation.

scholarly journals Identification of Six novel missense single nucleotide polymorphisms in the MAOA gene predisposing to aggressive behavior. Bioinformatics study

2019 ◽  
Author(s):  
Abdelrahman H. Abdelmoenim ◽  
Mujahed I. Mustafa ◽  
Naseem S. Murshed ◽  
Nosiba S. Omer ◽  
Alaa I. Mohammed ◽  
...  
Keyword(s):  
Aggressive Behavior ◽  
Violent Behavior ◽  
Gene Interaction ◽  
Genetic Mutation ◽  
Monoamine Oxidase A ◽  
Individual Choice ◽  
Nucleotide Polymorphisms ◽  
Maoa Gene ◽  
And Behavior ◽  
Recent Experimental Work

AbstractBackgroundAn astonishing observation is that aggressive behavior is actually a highly heritable. Recent experimental work and behavior research has linked individual variation in a functional polymorphism of the monoamine oxidase-A gene (MAOA) to the occurrence of anger-driven aggression. Aggressive antisocial and violent behavior has become a regularly debated topic in the scientific community; the impending question is what is the source of aggressive behavior, is it genetic or environmental or is it just an individual choice. This study aims to analyses the SNPs found in MAOA gene and it is possible association to aggressive behavior.MethodVarious bioinformatics software (SIFT, PolyPhen-2, PROVEAN, SNAP22, SNP&GO and PMut)is used to analyses the SNPs within the MAOA gene to study the structural and functional implication on the associated protein, which is further clarified using chimera software. Then gene-gene interaction is studied with geneMANIA software. Furthermore, conservation and annotation studies were done through the ConSurf server and Variant Effect Predictor (VEP) respectively.ResultSix missense SNPs were found to affect the structural and functional prospect of MAOA protein.ConclusionGenetic mutation within MAOA is likely to be associated with aggressive behavior; this will enrich future management and screening possibilities for this behavior.

scholarly journals Moderate the MAOA-L Allele Expression with CRISPR/Cas9 System

2018 ◽  
Author(s):  
Martin L. Nelwan
Keyword(s):  
Animal Models ◽  
Antisocial Behavior ◽  
X Chromosome ◽  
Violent Behavior ◽  
Behavior Disorder ◽  
Maoa Gene ◽  
Allele Expression ◽  
The Future ◽  
Chromosome Mutations ◽  
Healthy Males

Antisocial behavior is a behavior disorder inherited according to the inheritance of X-linked chromosome. Mutations in the MAOA gene can cause different behaviors in humans. These can comprise violent behavior or antisocial behavior. Low MAOA (MAOA-L) allele activity can cause antisocial behavior in both healthy and unhealthy people. Antisocial from healthy males can originate from maltreatment during childhood. There are no drugs for the treatment of antisocial behavior permanently at this time. MAOA inhibitor can reverse antisocial behavior in animal models. To cure antisocial behavior in the future, the CRISPR/Cas9 system in combination with iPSCs or ssODN methods for instance can be used. This system has succeeded to correct erroneous segments in the F8 gene and F9 gene. Both genes occupy the X chromosome. The MAOA gene also occupies the X chromosome. It seems that CRISPR/Cas9 system may be a beneficial tool to edit erroneous segments in the MAOA gene to treat antisocial behavior.

Association of a functional variant of the nitric oxide synthase 1 gene with personality, anxiety, and depressiveness

2012 ◽  
Vol 24 (4) ◽  
pp. 1225-1235 ◽  
Author(s):  
Triin Kurrikoff ◽  
Klaus-Peter Lesch ◽  
Evelyn Kiive ◽  
Kenn Konstabel ◽  
Sabine Herterich ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Emotional Regulation ◽  
Variable Number Tandem Repeat ◽  
Promoter Polymorphism ◽  
Variable Number ◽  
Short Allele ◽  
The Face ◽  
Nitric Oxide Synthase 1 ◽  
Oxide Synthase

AbstractA functional promoter polymorphism of the nitric oxide synthase 1 gene first exon 1f variable number tandem repeat (NOS1 ex1f-VNTR) is associated with impulsivity and related psychopathology. Facets of impulsivity are strongly associated with personality traits; maladaptive impulsivity with neuroticism; and adaptive impulsivity with extraversion. Both high neuroticism and low extraversion predict anxiety and depressive symptoms. The aim of the present study was to evaluate the effect of the NOS1 ex1f-VNTR genotype and possible interaction with environmental factors on personality, anxiety, and depressiveness in a population-representative sample. Short allele carriers had higher neuroticism and anxiety than individuals with the long/long (l/l) genotype. Male short/short homozygotes also had higher extraversion. In the face of environmental adversity, females with a short allele had higher scores of neuroticism, anxiety, and depressiveness compared to the l/l genotype. Males were more sensitive to environmental conditions when they had the l/l genotype and low extraversion. In conclusion, the NOS1 ex1f-VNTR influences personality and emotional regulation dependent on gender and environment. Together with previous findings on the effect of the NOS1 genotype on impulse control, these data suggest that NOS1 should be considered another plasticity gene, because its variants are associated with different coping strategies.

From Genes to Brain to Antisocial Behavior

2008 ◽  
Vol 17 (5) ◽  
pp. 323-328 ◽  
Author(s):  
Adrian Raine
Keyword(s):  
Prefrontal Cortex ◽  
Antisocial Behavior ◽  
Neural Circuits ◽  
Molecular Genetic ◽  
Brain Structures ◽  
Brain Regions ◽  
Monoamine Oxidase A ◽  
Functional Brain ◽  
Maoa Gene ◽  
Ventral Prefrontal Cortex

This review summarizes recent brain-imaging and molecular-genetic findings on antisocial, violent, and psychopathic behavior. A “genes to brain to antisocial behavior” model hypothesizes that specific genes result in structural and functional brain alterations that, in turn, predispose to antisocial behavior. For instance, a common polymorphism in the monoamine oxidase A ( MAOA) gene has been associated with both antisocial behavior and also reductions in the volume of the amygdala and orbitofrontal (ventral prefrontal) cortex—brain structures that are found to be compromised in antisocial individuals. Here I highlight key brain regions implicated in antisocial behavior, with an emphasis on the prefrontal cortex, along with ways these areas give expression to risk factors for antisocial behavior. Environmental influences may alter gene expression to trigger the cascade of events that translate genes into antisocial behavior. Neuroethical considerations include how responsibility and punishment should be determined given the hypothesis that neural circuits underlying morality are compromised in antisocial individuals.

Sign in / Sign up

Export Citation Format

Share Document