Search

BackgroundThe etiopathogenesis of major depressive disorder （MDD） is strongly associated with neuroinflammation. MDD is a highly heterogeneous psychiatric disorder， and the disease subtyping is an essential step for the identification of biological markers. The presence of psychomotor retardation seriously affects the prognosis of MDD， whereas the underlying mechanism is not yet completely clear. A potential involvement of granulocyte colony-stimulating factor （G-CSF） and macrophage colony-stimulating factor （M-CSF） in the pathogenesis of MDD with psychomotor retardation has been suggested in previous studies， but little detailed research has been completed.ObjectiveTo analyze the correlation of plasma G-CSF and M-CSF levels with psychomotor retardation in patients with MDD， and to explore the potential biological underpinnings of psychomotor retardation in MDD.MethodsA total of 50 MDD patients who met the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders， fifth edition （DSM-5） and attended the outpatient clinics of Shanghai Mental Health Center from April 2018 to April 2019 were included. The severity of symptoms was assessed using the Hamilton Depression Scale-17 item （HAMD-17）. According to the retardation factor in HAMD-17， patients with a score of ≥8 were included in retardation group （n=22）， and those with a score below 8 were included in non-retardation group （n=28）. Another 22 age- and sex-matched healthy controls were concurrently recruited. Plasma G-CSF and M-CSF levels were measured in all subjects using Luminex liquid suspension chip technology. Spearman correlation analysis was adopted to verify the correlation of retardation factor score in HAMD-17 with plasma G-CSF and M-CSF levels in MDD patients.ResultsPlasma G-CSF levels were decreased in MDD patients compared with healthy controls ［57.34（39.24， 83.15）pg/mL vs. 71.47（61.20， 79.99）pg/mL， Z=-2.098， P

People with an evening chronotype have an increased risk of experiencing a major depressive disorder (MDD). It is unclear if this effect is predominantly related to the initial development of MDD or also present in recurrent episodes. The current study aimed to investigate if the association between chronotype and depressive severity in MDD patients is comparable in MDD patients with first and recurrent episodes. 386 MDD patients, 70.7% females and aged between 16 and 64, participated in the study. The Morningness – Eveningness Questionnaire (MEQ), Pittsburgh Sleep Quality Index (PSQI), Multidimensional Fatigue Inventory (MFI20), and Quick Inventory of Depressive Symptomatology (QIDS-SR16) were administered to participants to determine chronotype, sleep quality, fatigue level, and depressive severity, respectively. Multivariate regression models were utilized to analyze how chronotype influences depressive severity. The study showed that chronotype, sleep quality, and fatigue level were all associated with depressive severity. Eveningness significantly predicted an increase in depressive severity independently of sleep quality and fatigue level only in patients with the first episode (−0.068, p = 0.010), but not in patients with recurrent episodes (0.013, p = 0.594). Circadian-focused treatment should be considered in first-episode depression only. [ABSTRACT FROM AUTHOR]

Sleep deprivation (SD) has been suggested to have a rapid antidepressant effect. There is substantial evidence that neuroinflammation and neuroplasticity play critical roles in the pathophysiology and treatment of depression. Here, we investigated the mechanisms of SD to alleviate depression-like behaviors of mice, and the role of neuroinflammation and neuroplasticity in it. Adult male C57BL/6 J mice were subjected to chronic restraint stress (CRS) for 6 weeks, and 6 h of SD were administrated. Behavioral tests were performed to measure depression-like behaviors. RNA-sequencing and bioinformatic analysis were performed in the anterior cingulate cortex (ACC). The differentially expressed genes were confirmed by quantitative real-time polymerase chain reaction (RT-qPCR). Neuroinflammation and neuroplasticity were measured by western blotting and immunofluorescence staining. Behavioral tests demonstrated that SD swiftly attenuated the depression-like behaviors induced by CRS. RNA-sequencing identified the upregulated immune and inflammatory pathways after CRS exposure were downregulated by SD. Furthermore, SD reversed the levels of immune and inflammation-related mRNA, pro-inflammatory factors and microglia activation in ACC. Additionally, the impaired neuroplasticity elicited by CRS in the prefrontal cortex (PFC) and ACC were improved by SD. More in-depth studies are required to determine the role of different SD protocols in depressive symptoms and their underlying mechanisms. Our study revealed the rapid antidepressant effect of SD on CRS mice through the reduction of the neuroinflammatory response in ACC and the improvement of neuroplasticity in PFC and ACC, providing a theoretical basis for the clinical application of SD as a rapid antidepressant treatment. • Six hours of SD rapidly alleviated depression-like behaviors in CRS mice. • SD reversed the upregulation of immune inflammation-related genes of ACC in CRS mice. • SD ameliorated neuroinflammation by targeting pro-inflammatory factors and microglia. • SD increased neuroplasticity and synaptic function in the PFC and ACC of CRS mice. [ABSTRACT FROM AUTHOR]