학술논문

Serum 15-d-PGJ2 and PPARγ levels are reduced in manic episode of bipolar disorder while IL-4 levels are not affected
Document Type
article
Source
Psychiatry and Clinical Psychopharmacology, Vol 29, Iss 3, Pp 298-306 (2019)
Subject
bipolar disorder
pparγ
15d-pgj2
cytokine
neuroinflammation
peripheral markers
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Language
English
ISSN
2475-0581
24750573
Abstract
OBJECTIVES: Bipolar disorder (BD) carries a high rate of morbidity and mortality, and the clarification of its aetiology continues to be an important field of research. In recent studies, the clinical characteristics of BDs have been explained through a number of underlying factors, including cytokines, steroids, neurotrophins, mitochondrial energy generation, oxidative stress, and neurogenesis. In this study, we aimed to investigate potential associations between BDs and inflammatory processes. METHODS: Patients with mania or in remission who attended outpatient clinics of the Department of Psychiatry of the Ankara Numune Training and Research Hospital, and who were diagnosed with BD according to the DSM-V criteria, were included in the study. IBM SPSS Statistics 23 software was used for statistical analyses of the data. The normality of the distribution of continuous and discrete numerical variables was tested with a Shapiro–Wilk Test. RESULTS: In this study, the measurements and statistical analyses revealed significantly lower 15-deoxy delta12, 14-prostaglandin J2 (15d-PGJ2) and Peroxisome Proliferator-Activated Receptor-Gamma (PPARγ) levels in patients with mania in comparison to healthy controls and patients in remission. Group comparisons did not reveal any significant differences between IL-4 levels. CONCLUSIONS: This study was not a longitudinal study evaluating the same patients during both relapse and remission periods; no group of patients in a depressive episode of BD were included in the group comparisons either. Although this evidence is not adequate for a definite conclusion, the available evidence suggests that anti-inflammatory markers such as 15d-PGJ2 and IL-4 and nuclear PPARγ receptors are potential biomarkers to clarify the aetiology of BD, and these markers may be included among the therapeutic targets for future pharmacological modulations. Further studies are required in this area.