ArticleJournal of neural transmission (Vienna, Austria : 1996)2015
Pharmacoepigenetics of depression: no major influence of MAO-A DNA methylation on treatment response.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- The Relationship between DNA Methylation and Antidepressant Medications: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- DNA Methylation as a Biomarker of Treatment Response Variability in Serious Mental Illnesses: A Systematic Review Focused on Bipolar Disorder, Schizophrenia, and Major Depressive Disorder.International journal of molecular sciences · 2018Pooled it
- Association of DNA methylation in BDNF with escitalopram treatment response in depressed Chinese Han patients.European journal of clinical pharmacology · 2018Trial
- Epigenome-Wide DNA Methylation in Unipolar Depression: Predictive Biomarker of Antidepressant Treatment Response?The international journal of neuropsychopharmacology · 2024Article
- Genetic Markers Associated with Postpartum Depression: A Review.Neuropsychiatric disease and treatment · 2024Review
- Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential.Signal transduction and targeted therapy · 2023Review
- The Role of Pharmacogenetics in Personalizing the Antidepressant and Anxiolytic Therapy.Genes · 2023Review
- Review
- Effect of MAOA DNA Methylation on Human in Vivo Protein Expression Measured by [11C]harmine Positron Emission Tomography.The international journal of neuropsychopharmacology · 2023Article
- Can epigenetics shine a light on the biological pathways underlying major mental disorders?Psychological medicine · 2022Review
- Epigenetics in depression and gut-brain axis: A molecular crosstalk.Frontiers in aging neuroscience · 2022Review
- Inclusion of genetic variants in an ensemble of gradient boosting decision trees does not improve the prediction of citalopram treatment response.Scientific reports · 2021Article
- Drug Response-Related DNA Methylation Changes in Schizophrenia, Bipolar Disorder, and Major Depressive Disorder.Frontiers in neuroscience · 2021Review
- Genetic and Epigenetic Consequence of Early-Life Social Stress on Depression: Role of Serotonin-Associated Genes.Frontiers in genetics · 2020Review
- Epigenetic signature of MAOA and MAOB genes in mental disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Monoamine oxidase inhibitors, and iron chelators in depressive illness and neurodegenerative diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Plasticity of Functional MAOA Gene Methylation in Acrophobia.The international journal of neuropsychopharmacology · 2018Article
- Monoamine Oxidase A Gene Methylation and Its Role in Posttraumatic Stress Disorder: First Evidence from the South Eastern Europe (SEE)-PTSD Study.The international journal of neuropsychopharmacology · 2018Article
- Type A monoamine oxidase and serotonin are coordinately involved in depressive disorders: from neurotransmitter imbalance to impaired neurogenesis.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Aberrant CpG Methylation Mediates Abnormal Transcription of MAO-A Induced by Acute and Chronic L-3,4-Dihydroxyphenylalanine Administration in SH-SY5Y Neuronal Cells.Neurotoxicity research · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.