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https://doi.org/10.24869/psyd.2021.314

SERUM TNF- RELATED WEAK INDUCER OF APOPTOSIS (TWEAK), TNF- RELATED APOPTOSIS-INDUCING LIGAND (TRAIL) LEVELS IN PATIENTS WITH BIPOLAR DEPRESSION, MAJOR DEPRESSION AND A HEALTHY CONTROL GROUP

Hasan Karadag ; University of Health Science,Diskapy Training and Research Hospital, Psychiatry Department, Ankara, Turkey
Gorkem Saygili ; Cognitive Science and Artifical Intelligence Department Tilburg University, Tilburg, Netherlands
Rabia Yuksel ; Ankara City Hospital, Psychiatry Department, Ankara, Turkey
Mirac Baris Usta ; Ondokuz Mayis University, Child and Adolescent Psychiatry and Mental Health Department, Ankara, Turkey
Canan Topcuoglu ; Ankara City Hospital, Biochemistry Department, Ankara, Turkey
Gamze Erzin ; University of Health Science,Diskapy Training and Research Hospital, Psychiatry Department, Ankara, Turkey


Puni tekst: engleski pdf 154 Kb

str. 314-319

preuzimanja: 240

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Sažetak

Background: A low-grade inflammation is presumed to be related to the etiopathogenesis of major depressive disorder (MDD)
and bipolar disorder. Tumor necrosis factor (TNF) superfamily members have roles in the pathogenesis of neuropsychiatric disorders
because of the relationship with inflammation and neurogenesis. The aim of this study was to investigate the serum TNFrelated
weak inducer of apoptosis (TWEAK) and TNF-related apoptosis-inducing ligand (TRAIL) levels in patients with bipolar
depression (BD), MDD and a healthy control (HC) group to determine any differences between MDD and BD in terms of inflammation
biomarkers.
Subjects and methods: After a 12-hour overnight fast, 5 milliliter (mL) samples of fasting blood were obtained from the
participants. The TWEAK and TRAIL plasma levels were calculated using ELISA kits.
Results: The TWEAK levels were found to be higher in the BD group than in the HC group (p=0.03). No statistically significant
differences were determined between the BD vs MDD and MDD vs HC groups (p=0.17, p=0.37, respectively). There were no
statistically significant differences between the three groups (BD vs HC; BD vs MDD; MDD vs HC) in terms of TRAIL levels
(p=0.21).
Conclusion: To the best of our knowledge, this study is the first to have explored TWEAK levels in patients with BD. The higher
TWEAK levels in BD than in the control group is compatible with the inflammation hypothesis of BD. Limitations of the study were
the differences in medications of the patient groups and that it was a cross-sectional study. There is a need for further longitudinal
studies with larger sample size and medication-free patients.

Ključne riječi

major depressive disorder; bipolar disorder; tumor necrosis factor; inflammation; neurogenesis

Hrčak ID:

266014

URI

https://hrcak.srce.hr/266014

Datum izdavanja:

22.11.2021.

Posjeta: 559 *