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Open AccessJournal ArticleDOI

Monoamine oxidase: from genes to behavior.

TLDR
MAO A and B knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders and show increased reactivity to stress.
Abstract
Cloning of MAO (monoamine oxidase) A and B has demonstrated unequivocally that these enzymes are made up of different polypeptides, and our understanding of MAO structure, regulation, and function has been significantly advanced by studies using their cDNA. MAO A and B genes are located on the X-chromosome (Xp11.23) and comprise 15 exons with identical intron-exon organization, which suggests that they are derived from the same ancestral gene. MAO A and B knock-out mice exhibit distinct differences in neurotransmitter metabolism and behavior. MAO A knock-out mice have elevated brain levels of serotonin, norephinephrine, and dopamine and manifest aggressive behavior similar to human males with a deletion of MAO A. In contrast, MAO B knock-out mice do not exhibit aggression and only levels of phenylethylamine are increased. Mice lacking MAO B are resistant to the Parkinsongenic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine. Both MAO A and B knock-out mice show increased reactivity to stress. These knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders.

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Relationship of monoamine oxidase A binding to adaptive and maladaptive personality traits.

TL;DR: A new continuum describing the relationship between personality and MAOA is proposed: deliberate/thoughtful contrasting aggressive/impulsive, and higher MAOA binding is associated with an adaptive personality facet.
Journal ArticleDOI

Transcription Factor E2F-Associated Phosphoprotein (EAPP), RAM2/CDCA7L/JPO2 (R1), and Simian Virus 40 Promoter Factor 1 (Sp1) Cooperatively Regulate Glucocorticoid Activation of Monoamine Oxidase B

TL;DR: It is reported that dexamethasone, a synthetic glucocorticoid hormone, stimulates MAO B (an isoform of MAOs) promoter and catalytic activities via both the fourth glucoc Corticoid response element (GRE) and simian virus 40 promoter factor 1 (Sp1) binding sites inMAO B promoter.
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Division of labor in the honey bee (Apis mellifera) : the role of tyramine β-hydroxylase

TL;DR: The results show that the transcription of this neurotransmitter synthetic enzyme is associated with regulation of social behavior in honey bees, but other factors may be involved.
Journal ArticleDOI

Platelet MAO-B, personality, and psychopathology.

TL;DR: It was hypothesized that low platelet MAO-B activity does not directly predispose individuals to psychopathology but is related to specific personality traits, which in turn represent a vulnerability factor for psychopathology.
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Comparative Neuroprotective Effects of Rasagiline and Aminoindan with Selegiline on Dexamethasone-Induced Brain Cell Apoptosis

TL;DR: The greater neuroprotective effect of rasagiline may be associated with the combination of the parent drug and its metabolite, R-aminoindan, with selegiline (Deprenyl) in prevention of dexamethasone-induced brain cell death.
References
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Journal ArticleDOI

Mutation in the α-synuclein gene identified in families with Parkinson's disease

TL;DR: A mutation was identified in the α-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype.
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Some observations upon a new inhibitor of monoamine oxidase in brain tissue.

TL;DR: The hypothesis that in the enzyme prepared, the MAO is a binary system of enzymes each of which has a detectably different sensitivity to this particular inhibitor, is put forward and evidence after dialysis supports this hypothesis.
Journal ArticleDOI

Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A

TL;DR: Analytical results indicate that isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.
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Aggressive Behavior and Altered Amounts of Brain Serotonin and Norepinephrine in Mice Lacking MAOA

TL;DR: Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine, and adults manifested a distinct behavioral syndrome, including enhanced aggression in males.
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