Elevated Monoamine Oxidase A Levels in the Brain

Meyer, Jeffrey H.; Ginovart, Nathalie; Boovariwala, Anahita; Sagrati, Sandra; Hussey, Doug; García, Armando; Young, Trevor; Praschak-Rieder, Nicole; Wilson, Alan A.; Houle, Sylvain

doi:10.1001/archpsyc.63.11.1209

Cited by 490 publications

(128 citation statements)

References 48 publications

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“…Nevertheless, the results of the present study with higher depression scores in MAOA-H carriers with many SLE make sense considering the monoamine deficiency hypothesis of depression [36]. In fact, Meyer et al [37] present data from a positron emission tomography study showing a substantial increase of MAO-A in depressed subjects supporting this theory. The authors discuss a potential interplay between the amount of MAO-A and the rate of 5-HT reuptake that could help in explaining the opposing findings of the workgroups of Cicchetti and Melas [16, 17] on the one hand and the results of the present study on the other.…”

Section: Discussionsupporting

confidence: 66%

Moderator Effects of Life Stress on the Association between MAOA-uVNTR, Depression, and Burnout

et al. 2019

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Background: The serotonergic and noradrenergic systems have a strong impact on several affective disorders and are key targets for psychopharmacological therapy. With respect to pathogenesis, there is a growing body of evidence showing an influence of a promoter repeat polymorphism (MAOA-uVNTR) altering the expression rate of monoamine oxidase A. However, only a few studies investigate its influence on depression with only 2 of them considering the moderating effects of life stress. For burnout, there are no studies so far investigating the genetic basis. Objectives: The aim of the present study was to replicate an interaction effect of MAOA-uVNTR and life stress on depression, and extend these possible findings to the burnout syndrome. Especially, the latter one might help in understanding the underlying mechanisms of burnout and its association to depression. Method: A total of n = 1,541 participants (n = 1,099 healthy controls, n = 442 inpatients with affective disorders) provided genetic samples and filled in self-report questionnaires measuring depression, burnout, and the extent of experienced stressful life events (SLEs). Results: A life stress x MAOA-uVNTR interaction on depression and burnout was observed in women suggesting that carriers of the high expressing allele (MAO-H) with many SLEs had the highest scores in both burnout and depression. In men, there was only a weak effect of MAOA-uVNTR on depression. Conclusions: The results suggest a more pronounced reactivity to adverse environmental factors in carriers of the MAO-H allele. Especially the effect of life stress and MAOA-uVNTR on burnout should be independently replicated in the future as this is the first study showing this association.

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Section: Discussionsupporting

confidence: 66%

Moderator Effects of Life Stress on the Association between MAOA-uVNTR, Depression, and Burnout

et al. 2019

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“…Molecular-imaging studies of unipolar depression have reported decreased monoamine signaling, which is consistent with functional brain-imaging data suggestive of altered reward processing [254]. In addition to a substantial body of literature on positron emission tomography (PET) addressing serotonin (5-HT) 2 receptor density in depression [255,256], DAT-binding potential has received considerable attention.…”

Section: Reviewmentioning

confidence: 64%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

254

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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“…1,9,40 The ability to image and quantify human brain MAO A with PET has enabled the investigation of relationships between MAO A levels and behavioral and disease phenotypes in healthy volunteers and in patients. [41][42][43] For example, PET studies have revealed elevations in brain MAO A activity in major depressive disorder (MDD) 44 and mood disorders, 43 whereas low MAO A activity has been related to maladaptive behavioral traits, such as aggression. 45 Interestingly, PET imaging has also demonstrated a modulating effect of the environment on brain enzyme levels by showing that current cigarette smokers have reduced brain MAO A.…”

Section: Discussionmentioning

confidence: 99%

Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men

Shumay

Logan

Volkow³

et al. 2012

Epigenetics

109

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Elevated Monoamine Oxidase A Levels in the Brain

Abstract: The sizable magnitude of this finding and the absence of other compelling explanations for monoamine loss during major depressive episodes led to the conclusion that elevated MAO-A density is the primary monoamine-lowering process during major depression.

Cited by 490 publications

References 48 publications

Moderator Effects of Life Stress on the Association between MAOA-uVNTR, Depression, and Burnout

Moderator Effects of Life Stress on the Association between MAOA-uVNTR, Depression, and Burnout

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Evidence that the methylation state of the monoamine oxidase A (MAOA) gene predicts brain activity of MAO A enzyme in healthy men

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