Pharmacoepigenetics of depression: no major influence of MAO-A DNA methylation on treatment response

The monoamine oxidase A ( MAO - A ) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation p...

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Published inJournal of Neural Transmission Vol. 122; no. 1; pp. 99 - 108
Main Authors Domschke, Katharina, Tidow, Nicola, Schwarte, Kathrin, Ziegler, Christiane, Lesch, Klaus-Peter, Deckert, Jürgen, Arolt, Volker, Zwanzger, Peter, Baune, Bernhard T.
Format Journal Article
LanguageEnglish
Published Vienna Springer Vienna 01.01.2015
Springer Nature B.V
Subjects
Analysis of Variance
Antidepressive Agents - therapeutic use
Cohort Studies
Depressive Disorder, Major - drug therapy
Depressive Disorder, Major - genetics
DNA Methylation - drug effects
DNA Methylation - genetics
Exons - drug effects
Exons - genetics
Female
Genetic Association Studies
Genotype
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Minisatellite Repeats - drug effects
Minisatellite Repeats - genetics
Monoamine Oxidase - genetics
Neurology
Neurosciences
Pharmacogenetics
Psychiatry
Psychiatry and Preclinical Psychiatric Studies - Original Article
Treatment Outcome
Epigenetics
Depression
Monoamine oxidase A
Gender
Methylation
Pharmacoepigenetics
Online AccessGet full text

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Abstract The monoamine oxidase A ( MAO - A ) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO - A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder ( f  = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO - A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO - A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO - A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p  = 0.04; CpG 43.514.684, p  = 0.009), not, however, withstanding correction for multiple testing. MAO - A VNTR genotypes did not influence MAO - A methylation status. The present pilot data do not suggest a major influence of MAO - A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO - A gene hypomethylation—possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability—to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.
AbstractList The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation-possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability-to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.
Issue Title: Special Issue: Personalized therapies in psychiatry: promises, pitfalls and perspectives The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation--possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability--to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.[PUBLICATION ABSTRACT]
The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation-possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability-to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation-possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability-to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.
The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation-possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability-to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.
The monoamine oxidase A ( MAO - A ) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO - A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder ( f  = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO - A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO - A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO - A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p  = 0.04; CpG 43.514.684, p  = 0.009), not, however, withstanding correction for multiple testing. MAO - A VNTR genotypes did not influence MAO - A methylation status. The present pilot data do not suggest a major influence of MAO - A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO - A gene hypomethylation—possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability—to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.
Author Domschke, Katharina
Schwarte, Kathrin
Lesch, Klaus-Peter
Tidow, Nicola
Deckert, Jürgen
Ziegler, Christiane
Arolt, Volker
Baune, Bernhard T.
Zwanzger, Peter
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  organization: Department of Psychiatry, University of Muenster
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  organization: Department of Psychiatry, University of Muenster
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  organization: Department of Psychiatry, University of Muenster
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  givenname: Bernhard T.
  surname: Baune
  fullname: Baune, Bernhard T.
  organization: Department of Psychiatry, Royal Adelaide Hospital, University of Adelaide
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24809685$$D View this record in MEDLINE/PubMed
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IsPeerReviewed true
IsScholarly true
Issue 1
Keywords Epigenetics
Depression
Monoamine oxidase A
Gender
Methylation
Pharmacoepigenetics
Language English
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PMID 24809685
PQID 1641179202
PQPubID 51646
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crossref_citationtrail_10_1007_s00702_014_1227_x
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ProviderPackageCode CITATION
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PublicationCentury 2000
PublicationDate 2015-01-01
PublicationDateYYYYMMDD 2015-01-01
PublicationDate_xml – month: 01
  year: 2015
  text: 2015-01-01
  day: 01
PublicationDecade 2010
PublicationPlace Vienna
PublicationPlace_xml – name: Vienna
– name: Austria
– name: Wien
PublicationSubtitle Translational Neuroscience, Neurology and Preclinical Neurological Studies, Psychiatry and Preclinical Psychiatric Studies
PublicationTitle Journal of Neural Transmission
PublicationTitleAbbrev J Neural Transm
PublicationTitleAlternate J Neural Transm (Vienna)
PublicationYear 2015
Publisher Springer Vienna
Springer Nature B.V
Publisher_xml – name: Springer Vienna
– name: Springer Nature B.V
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Snippet The monoamine oxidase A ( MAO - A ) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive...
The monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive...
Issue Title: Special Issue: Personalized therapies in psychiatry: promises, pitfalls and perspectives The monoamine oxidase A (MAO-A) gene has been suggested...
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StartPage 99
SubjectTerms Analysis of Variance
Antidepressive Agents - therapeutic use
Cohort Studies
Depressive Disorder, Major - drug therapy
Depressive Disorder, Major - genetics
DNA Methylation - drug effects
DNA Methylation - genetics
Exons - drug effects
Exons - genetics
Female
Genetic Association Studies
Genotype
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Minisatellite Repeats - drug effects
Minisatellite Repeats - genetics
Monoamine Oxidase - genetics
Neurology
Neurosciences
Pharmacogenetics
Psychiatry
Psychiatry and Preclinical Psychiatric Studies - Original Article
Treatment Outcome
Title Pharmacoepigenetics of depression: no major influence of MAO-A DNA methylation on treatment response
URI https://link.springer.com/article/10.1007/s00702-014-1227-x
https://www.ncbi.nlm.nih.gov/pubmed/24809685
https://www.proquest.com/docview/1641179202
https://www.proquest.com/docview/1641858342
https://www.proquest.com/docview/1647021708
Volume 122
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