Decreased circulating urokinase plasminogen activator receptor (uPAR) concentration in acute episodes of bipolar disorder; could it be a reflection of axonal injury?

INTRODUCTION

In recent years, the role of inflammation in the pathogenesis of Bipolar Disorder (BD) has been studied thoroughly. Urokinase-type plasminogen activator receptor (uPAR) is one of the molecules, whose concentration is of predictive value with regards to an ongoing inflammation and tissue regeneration, and it is hypothesized that it may also be altered in Bipolar Disorder. In this study, it is aimed to compare the levels of serum soluble uPAR during the manic, depressive and euthymic states of cases diagnosed with bipolar disorder, with healthy individuals.

MATERIALS AND METHODS

Forty-four BD patients at manic state (BD-m), 35 BD patients at depressive state (BD-d), 42 euthymic patients (BD-e) and 41 healthy controls (HC) who were similar with the diseased subjects regarding age and smoking status included in the study. Serum soluble uPAR levels of patients and healthy controls were measured.

RESULTS

The main finding of our study is that serum soluble uPAR levels are lower in patients diagnosed with BD either in depressive (BD-d) or in manic state (BD-m) than in BD patients in euthymic state (BD-e) or in healthy controls (HC). There was no significant difference in serum soluble uPAR concentrations between BD-m and BD-d s or between BD-e and HC with regards to serum soluble uPAR concentrations.

CONCLUSIONS

Urokinase-type plasminogen (uPA) is a molecule which is an element of uPAR system and the molecules collectively take role in inflammation, tissue regeneration and axonal regeneration within the Central Nervous System (CNS). It has previously suggested in some studies that there may be a decrease in axonal density or axonal dysfunction in CNS in bipolar individuals. Accordingly, one may say that the low concentrations of soluble uPAR measured in our bipolar patients either at depressive or at manic state is due to the diminished regulatory role of soluble uPAR on axonal regeneration in CNS of BD cases.