Potential Roles of microRNAs in the Regulation of Monoamine Oxidase A in the Brain
Open accessAbstract
Monoamine oxidase A (MAO-A) is an enzyme that regulates the levels of monoamine neurotransmitters, such as serotonin, noradrenaline and dopamine and it has been used as a therapeutic target for depression. However, MAO-A inhibitors, which directly acts on MAO-A protein, have limited use due to their adverse effects. microRNAs (miRNAs) are 18-22 nucleotide long, small non-coding RNAs, which have recently emerged as regulators of protein levels that could potentially be new therapeutic targets for psychiatric disorders. This review article aims to discuss the current status of the treatment for depression with MAO-A inhibitors and the regulatory factors of MAO-A. Further, the review also proposes possible regulatory mechanisms of MAO-A by miRNAs, which leads to better understanding of the pathology of depressive disorders and their potential use as therapeutic agents.
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miR-142, miR-34a, and miR-34c indirectly regulate MAO-A, potentially impacting monoamine neurotransmitters.
“miR-142, miR-34a, and miR-34c indirectly regulate MAO-A, potentially impacting monoamine neurotransmitters.284”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [284]
The figure caption presents a proposed indirect pathway: miR-142, miR-34a and miR-34c target SIRT1, which activates MAO-A expression. The miR-142 section reports experimental evidence for that pathway, but the miR-34 Family section does not establish that miR-34a or miR-34c regulates MAO-A; it frames the connection as a possibility. The Introduction supports the potential relevance to monoamine neurotransmitters by reporting that MAO-A inhibition elevates brain serotonin. (LLM, conf=0.84)
Experimental — accuracy not yet measuredmiRNA-mediated disturbance of neurotransmitters including glutamate, dopamine, serotonin, and norepinephrine can lead to neuronal damage and loss of trophic effects and thereby potentially contribute to the pathogenesis of depression.
“miRNA-mediated disturbance of neurotransmitters, including glutamate, dopamine, serotonin and norepinephrine, can lead to neuronal damage, and loss of trophic effects and thereby potentially contribute to the pathogenesis of depression.271–274”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [273]
The Abstract and Conclusion link miRNAs, MAO-A regulation, and depression; the Abstract identifies serotonin, noradrenaline, and dopamine as neurotransmitters regulated by MAO-A. The paper does not establish the claimed chain from miRNA-mediated disturbance of those transmitters and glutamate to neuronal damage, loss of trophic effects, and depression. No page numbers are available in our copy. (LLM, conf=0.85)
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Regulatory Pathways of Monoamine Oxidase A during Social Stress
Higuchi, Y., Soga, T., & Parhar, I. S. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00604 · Cited by 57 · see citing works
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The Path to microRNA Therapeutics in Psychiatric and Neurodegenerative Disorders
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Valproic Acid Induces Monoamine Oxidase A via Akt/Forkhead Box O1 Activation
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miR-22 inhibits mouse ovarian granulosa cell apoptosis by targeting SIRT1
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Safety and tolerability of combined treatment with moclobemide and SSRIs
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Rines E3 Ubiquitin Ligase Regulates MAO-A Levels and Emotional Responses
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Epigenetic silencing of Kruppel like factor-3 increases expression of pro-metastatic miR-182
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A Neuronal Transcriptome Response Involving Stress Pathways is Buffered by Neuronal microRNAs
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Structure and Mechanism of Monoamine Oxidase
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Not miR-ly aging: SIRT1 boosts memory via a microRNA-dependent mechanism
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Flagged first, then by citations
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Monoamine oxidases in age-associated diseases: New perspectives for old enzymes
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Role of non-coding RNA in the pathogenesis of depression
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Regulatory Pathways of Monoamine Oxidase A during Social Stress
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Restraint Stress in Mice Alters Set of 25 miRNAs Which Regulate Stress- and Depression-Related mRNAs
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- Authors
- Higuchi, Y., Soga, T., & Parhar, I. S.
- Affiliations
- Monash University Malaysia (MY)
- Corresponding author
- Parhar, Ishwar S.
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-09-14
- Volume
- 11
- Pages
- 339-339
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC6149293
- OpenAlex
- W2891362468
- Cited by
- 22
- References
- 113
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 6 · 2019: 2 · 2017: 1
- FWCI
- 0.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Monash University Research Portal (Monash University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Monash University
- Monash University Malaysia
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- microRNA, monoamine oxidase A, depression, MAO-A inhibitors, monoamines, non-coding RNA, therapeutic target, depressive disorders
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