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Our observations provide new information on the genotype-phenotype relations of MAOA/B and EFHC2 genes involved in the contiguous deletions of Norrie disease.Based on the case of our observation, contiguous deletion with only one of the MAO genes (MAOB) may not cause psychomotor disability, and deletion of EFHC2may not contribute to epilepsy.
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the mean methylation values of the CpG sites studied in the MAOA gene were related to smoking behavior in women. Similarly, several methylation patterns in the MAOB gene were associated with a smoking history, with each CpG site showing a remarkable sex dependence. Smoking behavior seems to be related to the genetic and epigenetic profile of MAO genes, with considerable individual and sex-related differences
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This study shows that MAO-B levels are increased not only in astrocytes but also in pyramidal neurons in Alzheimer disease brain and also suggests that MAO-B regulates Abeta production in neurons via gamma-secretase
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The findings may suggest that MAO-B is an important sensor in iron-stressed neuronal cells.
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Childhood trauma interacts with haplotypes in COMT, MAOA and MAOB, increasing risk for OCD.
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brain protein levels of MAOB are normal or elevated in the three parkinsonian conditions-with MAOB increase generally associated with elevations in levels of astrocyte markers. Brain MAOA concentrations were, somewhat surprisingly, not decreased in Parkinson's disease, Progressive Supranuclear palsy or multiple system atrophy with the exception of the atrophic putamen in MSA, despite loss of dopamine neurons.
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MAOA and MAOB variants may contribute to the etiology of Attention deficit hyperactivity disorder (ADHD) in the Indo-Caucasoid population and could be responsible for higher occurrence of ADHD in the boys.
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MAOB gene variants are contributing to the etiology of ADHD in the Indo-Caucasoid population
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This study suggests that MAOB increases ASD risk in males, possibly through its sex-specific regulatory effect on 5-HT metabolism and behavior.
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These findings suggest an association of platelet MAO-B activity, but a lack of association of MAOB rs1799836 and MAOA-uVNTR, with selected psychotic symptoms in ethnically homogenous veterans with PTSD.
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No significant association was found between severe agitation and MAOA uVNTR or MAOB rs1799836 polymorphism, revealing that these individual polymorphisms in MAO genes are not related to severe agitation in subjects with schizophrenia and conduct disorder. Higher platelet MAO-B activity was found in subjects with severe agitation vs. non-agitated subjects. Platelet MAO-B activity was not associated with MAOB rs1799836
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we performed a meta-analysis in the Chinese population to provide comprehensive data on the association between the MAOB polymorphism and Parkinson's disease. Overall, no significant association was found between the MAOB A644G polymorphism and Parkinson's disease risk in the Chinese population.
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inhibition of MAO-B using selegiline reversed the cigarette smoke-induced oxidative stress and inflammation in bronchial epithelial cells.
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Monoamine oxidase B levels are highly expressed in gliomas.
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The results of this meta-analysis suggest that people in the Asian population with the MAOB intron 13 A allele have an increased risk of Parkinson disease, especially when combined with the COMT LL genotype.
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Huntington disease neural cells exhibit increased Monoamine oxidase-A and Monoamine oxidases-B expression and activity
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Report isolation of MOA-B inhibitors from Vernonia cinerea.
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These findings demonstrate that regulation of monoamine levels by Mao activity in beta cells is pivotal for physiological insulin secretion and that loss of MaoB expression may contribute to the beta cell dysfunction in type 2 diabetes.
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findings indicate that the low activity of monoamine oxidase gene polymorphisms has a protective effect on smoking cessation and smoking frequency.
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protein environment of MAO-A enhances the polar nucleophilic character of the mechanism compared to that of MAO-B
