MiRNA Differences Related to Treatment-Resistant Schizophrenia

Autor:	Daniel Pérez-Rodríguez, Maria Aránzazu Penedo, Tania Rivera-Baltanás, Tonatiuh Peña-Centeno, Susanne Burkhardt, Andre Fischer, José M. Prieto-González, José Manuel Olivares, Hugo López-Fernández, Roberto Carlos Agís-Balboa
Rok vydání:	2023
Předmět:	p53 drug therapy [Schizophrenia] pharmacology [Antipsychotic Agents] treatment resistant schizophrenia microRNA biomarkers Catalysis genetics [Drug Resistance] Inorganic Chemistry diagnosis [Schizophrenia] Humans genetics [Schizophrenia] genetics [MicroRNAs] therapeutic use [MicroRNAs] Physical and Theoretical Chemistry Molecular Biology Spectroscopy Organic Chemistry General Medicine Computer Science Applications MicroRNAs therapeutic use [Antipsychotic Agents] ddc:540 Schizophrenia Treatment-Resistant Antipsychotic Agents
Zdroj:	International journal of molecular sciences 24(3), 1891 (2023). doi:10.3390/ijms24031891 special issue: "Identifying the Molecular Mechanisms of Psychiatric Disorders to Define New Therapeutic Targets" International Journal of Molecular Sciences; Volume 24; Issue 3; Pages: 1891
ISSN:	1422-0067
DOI:	10.3390/ijms24031891
Popis:	Schizophrenia (SZ) is a serious mental disorder that is typically treated with antipsychotic medication. Treatment-resistant schizophrenia (TRS) is the condition where symptoms remain after pharmacological intervention, resulting in long-lasting functional and social impairments. As the identification and treatment of a TRS patient requires previous failed treatments, early mechanisms of detection are needed in order to quicken the access to effective therapy, as well as improve treatment adherence. In this study, we aim to find a microRNA (miRNA) signature for TRS, as well as to shed some light on the molecular pathways potentially involved in this severe condition. To do this, we compared the blood miRNAs of schizophrenia patients that respond to medication and TRS patients, thus obtaining a 16-miRNA TRS profile. Then, we assessed the ability of this signature to separate responders and TRS patients using hierarchical clustering, observing that most of them are grouped correctly (~70% accuracy). We also conducted a network, pathway analysis, and bibliography search to spot molecular pathways potentially altered in TRS. We found that the response to stress seems to be a key factor in TRS and that proteins p53, SIRT1, MDM2, and TRIM28 could be the potential mediators of such responses. Finally, we suggest a molecular pathway potentially regulated by the miRNAs of the TRS profile.
Databáze:	OpenAIRE
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