Background: Bipolar Disorder (BD) is a chronic, highly disabling mood disorder. Among the major comorbidities, Panic Disorder (PD) is often associated with BD. This could suggest a common genetic and pathophysiological background between these two conditions, as suggested by previous studies. Despite the widespread diffusion of these conditions, little is still known about the exact pathophysiological dynamics that underlies them. Non-coding RNAs have recently started to gain attention in psychiatry research, with several papers indicating the dysregulation of lncRNAs as a possible key factor in etiopathogenesis of several mental disorders. In the light of the above, the aim of this study is to evaluate the gene expression levels of MALAT1, PANDA, GAS5, HOTAIR lncRNAs and miR-221-5p microRNA, which are highly expressed in the CNS, in drug-naïve/drug-free bipolar and panic patients. Methods: the experimental plan envisaged the recruitment of sixteen patients with a first diagnosis of type one or type two BD and ten patients with PD. Patients with medical and/or psychiatric comorbidities were excluded. Peripheral venous blood was collected both from patients and healthy controls. Each of the patients recruited for the study was prescribed with therapy. Serum ncRNAs levels were remeasured after 5 months of therapy. Results: MALAT-1, GAS-5 and miR-221-5p are significantly up-regulated in BD after therapy, while PD group showed a down-regulation of all the ncRNAs investigated after therapy. Conclusions: gene expression levels of the ncRNAs miR-221, MALAT1, GAS5, which are implicated in inhibitory modulation of the glucocorticoid receptor, are significantly over-expressed in bipolar patients following therapy, while all ncRNAs are significantly over-expressed in the PD T1 patients group compared with healthy controls. Data concerning PD represent, to our knowledge, a novelty.

Gene Expression Analysis of nc-RNAs in Bipolar and Panic Disorders: A Pilot Study

Muscatello, Maria Rosaria Anna;D'Ascola, Angela;Campo, Salvatore
Ultimo
2023-01-01

Abstract

Background: Bipolar Disorder (BD) is a chronic, highly disabling mood disorder. Among the major comorbidities, Panic Disorder (PD) is often associated with BD. This could suggest a common genetic and pathophysiological background between these two conditions, as suggested by previous studies. Despite the widespread diffusion of these conditions, little is still known about the exact pathophysiological dynamics that underlies them. Non-coding RNAs have recently started to gain attention in psychiatry research, with several papers indicating the dysregulation of lncRNAs as a possible key factor in etiopathogenesis of several mental disorders. In the light of the above, the aim of this study is to evaluate the gene expression levels of MALAT1, PANDA, GAS5, HOTAIR lncRNAs and miR-221-5p microRNA, which are highly expressed in the CNS, in drug-naïve/drug-free bipolar and panic patients. Methods: the experimental plan envisaged the recruitment of sixteen patients with a first diagnosis of type one or type two BD and ten patients with PD. Patients with medical and/or psychiatric comorbidities were excluded. Peripheral venous blood was collected both from patients and healthy controls. Each of the patients recruited for the study was prescribed with therapy. Serum ncRNAs levels were remeasured after 5 months of therapy. Results: MALAT-1, GAS-5 and miR-221-5p are significantly up-regulated in BD after therapy, while PD group showed a down-regulation of all the ncRNAs investigated after therapy. Conclusions: gene expression levels of the ncRNAs miR-221, MALAT1, GAS5, which are implicated in inhibitory modulation of the glucocorticoid receptor, are significantly over-expressed in bipolar patients following therapy, while all ncRNAs are significantly over-expressed in the PD T1 patients group compared with healthy controls. Data concerning PD represent, to our knowledge, a novelty.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3277028
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