DNA Methylation in Depression and Depressive-Like Phenotype: Biomarker or Target of Pharmacological Intervention?

Major depressive disorder (MDD) is a debilitating psychiatric disorder, the third leading global cause of disability. Regarding aetiopathogenetic mechanisms involved in the onset of depressive disorders, the interaction between genetic vulnerability traits and environmental factors is believed to pl...

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Vydáno v:Current neuropharmacology Ročník 20; číslo 12; s. 2267
Hlavní autoři: Paoli, Caterina, Misztak, Paulina, Mazzini, Giulia, Musazzi, Laura
Médium: Journal Article
Jazyk:angličtina
Vydáno: United Arab Emirates 15.11.2022
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ISSN:1875-6190, 1875-6190
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Shrnutí:Major depressive disorder (MDD) is a debilitating psychiatric disorder, the third leading global cause of disability. Regarding aetiopathogenetic mechanisms involved in the onset of depressive disorders, the interaction between genetic vulnerability traits and environmental factors is believed to play a major role. Although much is still to be elucidated about the mechanisms through which the environment can interact with genetic background shaping the disease risk, there is a general agreement about a key role of epigenetic marking. In this narrative review, we focused on the association between changes in DNA methylation patterns and MDD or depressive-like phenotype in animal models, as well as mechanisms of response to antidepressant drugs. We discussed studies presenting DNA methylation changes at specific genes of interest and profiling analyses in both patients and animal models of depression. Overall, we collected evidence showing that DNA methylation could not only be considered as a promising epigenetic biomarker of pathology but could also help in predicting antidepressant treatment efficacy. Finally, we discussed the hypothesis that specific changes in DNA methylation signature could play a role in aetiopathogenetic processes as well as in the induction of antidepressant effect.
Bibliografie:ObjectType-Article-2
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ISSN:1875-6190
1875-6190
DOI:10.2174/1570159X20666220201084536