Is serum complement C1q related to major depressive disorder?

被引:9
作者
Yang, Jing [1 ,2 ]
Li, Ruibo [1 ,2 ]
Shi, Yuanhong [2 ]
Jiang, Siyu [1 ,2 ]
Liu, Jing [1 ,2 ]
机构
[1] Dalian Med Univ, Dept Clin Psychol, Dalian, Peoples R China
[2] Yangzhou Univ, Dept Clin Psychol, SuBei Hosp, Affiliated Hosp, 98 Nan Tong Xi Lu, Yangzhou 225000, Jiangsu, Peoples R China
关键词
Complement C1q; inflammation; major depressive disorder; STRESSORS;
D O I
10.4103/psychiatry.IndianJPsychiatry_394_19
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Background: Major depressive disorder (MDD) has a high global incidence. While the pathogenesis of depression remains unknown, accumulating evidence has implicated inflammatory changes. Aim: The aim of the study is to compare the serum complement C1q levels in patients with MDD and healthy controls. Setting and Design: The design was a case-control study. Materials and Methods: Blood samples were collected from the patients with MDD and healthy controls to assess the serum C1q levels using an immunotransmission turbidimetric method. Statistical Analysis: Differences in complement C1q levels between patients with MDD and the controls, as well as between sexes among patients with MDD and the controls, were assessed using Mann-Whitney U-test. Spearman correlations were obtained between complement C1q levels and age. Results: In total, 1016 participants (508 MDD and 508 controls) were recruited. Differences in the sex ratio (male/female among controls, 181/327; and MDD, 178/330) and age (controls, 47.0 +/- 14.9 years; MDD, 46.5 +/- 16.5 years) were not significant. The C1q level in the patients with MDD was significantly higher than that in the healthy controls (P < 0.05). In the MDD group, C1q level correlated significantly with age. Conclusion: Elevation of the serum complement C1q levels in MDD may support the use of C1q as a potential biomarker for diagnosing depression, but further research is needed.
引用
收藏
页码:659 / 663
页数:5
相关论文
共 21 条
[1]   Neuroimmune and Inflammatory Signals in Complex Disorders of the Central Nervous System [J].
Clara Liberman, Ana ;
Trias, Emiliano ;
Chagas, Luana da Silva ;
Trindade, Pablo ;
Pereira, Marissol dos Santos ;
Refojo, Damian ;
Hedin-Pereira, Cecilia ;
Serfaty, Claudio A. .
NEUROIMMUNOMODULATION, 2018, 25 (5-6) :246-270
[2]   The GLP-1 analog, liraglutide prevents the increase of proinflammatory mediators in the hippocampus of male rat pups submitted to maternal perinatal food restriction [J].
Diz-Chaves, Y. ;
Toba, L. ;
Fandino, J. ;
Gonzalez-Matias, L. C. ;
Garcia-Segura, L. M. ;
Mallo, F. .
JOURNAL OF NEUROINFLAMMATION, 2018, 15
[3]   Specific inhibition of the classical complement pathway with an engineered single-chain Fv to C1q globular heads decreases complement activation by apoptotic cells [J].
Duvall, Marcus R. ;
Hwang, Hee Young ;
Boackle, Robert J. .
IMMUNOBIOLOGY, 2010, 215 (05) :395-405
[4]   Depressive symptoms and adipokines in women: Study of women's health across the nation [J].
Everson-Rose, Susan A. ;
Clark, Cari J. ;
Wang, Qi ;
Guo, Hongfei ;
Mancuso, Peter ;
Kravitz, Howard M. ;
Bromberger, Joyce T. .
PSYCHONEUROENDOCRINOLOGY, 2018, 97 :20-27
[5]   C1q Differentially Modulates Phagocytosis and Cytokine Responses during Ingestion of Apoptotic Cells by Human Monocytes, Macrophages, and Dendritic Cells [J].
Fraser, Deborah A. ;
Laust, Amanda K. ;
Nelson, Edward L. ;
Tenner, Andrea J. .
JOURNAL OF IMMUNOLOGY, 2009, 183 (10) :6175-6185
[6]  
Idonije O B, 2012, Niger J Physiol Sci, V27, P19
[7]   Depressive disorders and immunity: 20 years of progress and discovery [J].
Irwin, Michael R. ;
Miller, Andrew H. .
BRAIN BEHAVIOR AND IMMUNITY, 2007, 21 (04) :374-383
[8]   Astroglial correlates of neuropsychiatric disease: From astrocytopathy to astrogliosis [J].
Kim, Ronald ;
Healey, Kati L. ;
Sepulveda-Orengo, Marian T. ;
Reissner, Kathryn J. .
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, 2018, 87 :126-146
[9]   C1q: structure, function, and receptors [J].
Kishore, U ;
Reid, KBM .
IMMUNOPHARMACOLOGY, 2000, 49 (1-2) :159-170
[10]   In animal models, psychosocial stress-induced (neuro)inflammation, apoptosis and reduced neurogenesis are associated to the onset of depression [J].
Kubera, Marta ;
Obuchowicz, Ewa ;
Goehler, Lisa ;
Brzeszcz, Joanna ;
Maes, Michael .
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, 2011, 35 (03) :744-759