As hypocretin can markedly affect neurophysiological and behavioural processes in mood disorders. However, few studies have measured changes in hypocretin levels in patients with mood disorders. We estimated the hypocretin-1 plasma levels in mood disorder patients and controls (CON) using an enzyme-linked immunosorbent assay. Results: (i) The hypocretin-1 plasma level was significantly higher in major depressive disorder (MDD) patients [59.04 (35.78–80.12) pg/ml, P < 0.001] and bipolar disorder (BD) patients [65.50 (58.46–74.57) pg/ml, P < 0.001] patients than in CON [49.25 (28.51–80.40) pg/ml]. Moreover, the plasma hypocretin-1 levels in the BD group were significantly higher than those in the MDD group (P < 0.001). (ii). In the MDD group, patients with higher suicidal ideation had higher hypocretin-1 levels [62.09 (38.23–80.12) pg/ml] than those with lower suicidal ideation [59.63 (35.79–77.37) pg/ml), P = 0.032]. (iii). Plasma hypocretin-1 levels were increased in both female and male mood disorder patients compared to CON [male: MDD 60.51 (35.79–80.12) pg/ml; BD 65.40 (58.76–74.14) pg/ml; CON 45.63 (28.51–62.05) pg/ml; all P < 0.016; female: MDD 57.37 (34.59–80.40) pg/ml; BD 65.61 (58.46–74.57) pg/ml; CON 52.92 (38.23–78.89) pg/ml; all P < 0.015]. (iv). In CON, we found a significant negative correlation between plasma hypocretin-1 levels and age (rho = −0.251, P = 0.032), while this negative correlation was absent in the MDD and BD groups. Limitations may partly arise from the relatively small sample size and the medication history of patients participating in our research. We concluded that the clear changes found in plasma hypocretin-1 levels might be applied in the diagnosis of depression and the differential diagnosis of MDD and BD. The clear suicidal-ideation-related change found in hypocretin-1 levels in depression might be taken into account in the prevention of suicidal behaviour and further study of hypocretin-targeted therapies.
Epidemiological studies have demonstrated that the genetic factors partly influence the development of same-sex sexual behavior, but most genetic studies have focused on people of primarily European ancestry, potentially missing important biological insights. Here, we performed a two-stage genome-wide association study (GWAS) with a total sample of 1478 homosexual males and 3313 heterosexual males in Han Chinese populations and identified two genetic loci (rs17320865, Xq27.3, FMR1NB, Pmeta = 8.36 × 10−8, OR = 1.29; rs7259428, 19q12, ZNF536, Pmeta = 7.58 × 10−8, OR = 0.75) showing consistent association with male sexual orientation. A fixed-effect meta-analysis including individuals of Han Chinese (n = 4791) and European ancestries (n = 408,995) revealed 3 genome-wide significant loci of same-sex sexual behavior (rs9677294, 2p22.1, SLC8A1, Pmeta = 1.95 × 10−8; rs2414487, 15q21.3, LOC145783, Pmeta = 4.53 × 10−9; rs2106525, 7q31.1, MDFIC, Pmeta = 6.24 × 10−9). These findings may provide new insights into the genetic basis of male sexual orientation from a wider population scope. Furthermore, we defined the average ZNF536-immunoreactivity (ZNF536-ir) concentration in the suprachiasmatic nucleus (SCN) as lower in homosexual individuals than in heterosexual individuals (0.011 ± 0.001 vs 0.021 ± 0.004, P = 0.013) in a postmortem study. In addition, compared with heterosexuals, the percentage of ZNF536 stained area in the SCN was also smaller in the homosexuals (0.075 ± 0.040 vs 0.137 ± 0.103, P = 0.043). More homosexual preference was observed in FMR1NB-knockout mice and we also found significant differences in the expression of serotonin, dopamine, and inflammation pathways that were reported to be related to sexual orientation when comparing CRISPR-mediated FMR1NB knockout mice to matched wild-type target C57 male mice.
Dear Editor,Millions of individuals sustain mood disorders, including bipolar disorder (BD) and major depressive disorder (MDD), contributing a heavy burden to society. 1 A previous study suggested dysfunction in the innate immune system underlies the pathophysiology of mood disorders. 2 Meanwhile, certain components, such as natural killer (NK) cells and CD8+ lymphocytes, both belonging to killer lymphocytes, are dysfunctions of innate immunity and might participate in the pathogenesis of MDD and BD. 3,4 To study the characteristics of CD8+ T cells among BD, MDD, and healthy controls (HCs), 10x single-cell RNA and T cell receptor (TCR) sequencing were applied to analyze the peripheral blood mononuclear cells from participants, including 4 BD patients, 4 MDD patients, and 4 HCs. T cells, expressing the TCR on the cell surface, received stimulation from pathogens and subsequently initiated an immune response. 5 TIM-3 has emerged as a critical regulator in T cells, and IL-6, IL-1β, and Caspase 3 have been linked to TIM-3 activity. Hence, we examined plasma levels of these genes in patients with BD prior to and 1-month after treatment with quetiapine.A total of 14,098, 20,701, and 22,206 CD8+ T cells were isolated from patients with BD, MDD, and HCs, respectively. Twelve main clusters (Figure 1A) represented the different cell types (Figure 1B). The main CD8+ cell types were identified by comparing marker genes in various cell types (Figure 1C, Table S1). No significant differences in cell type clusters among the three groups (Figure 1D) were observed. The naiveness and cytotoxicity scores of each cell type were separately evaluated based on a predefined set of genes. Compared with that of other cell types, the naive score of NK cells expressing TIM-3 was relatively low, while the effector score was the highest (Figures 1E and 1F), suggesting high expression levels of TIM-3 from NK cells were related to activated cytotoxic phenotypes.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
PurposeThere is growing evidence showing that inflammatory cytokines and neuropeptides may be involved in the pathophysiology of suicidal behavior. However, studies have yielded contradictory data, and no biological markers that help predict suicide have been identified. This study aimed to identify biological patterns, such as NPY, IL-1β and hypocretin plasma levels, in people who died by suicide.Patients and methodsTwenty-two people who died by suicide compared with 22 controls matched for age and sex were studied. In suicide and control subjects, we estimated the levels of NPY, IL-1β and hypocretin in plasma using enzyme-linked immunosorbent assay. The data are presented as the median (25th–75th percentile).ResultsWe found (1) a significant elevation in plasma NPY levels in suicide subjects versus control subjects (suicide: 11.38 (9.380–16.55); controls: 8.95 (7.590–10.93); P=0.013), and plasma NPY concentrations were approximately 62% higher in suicide subjects than those in control subjects; (2) a significant decrease in plasma IL-1β concentrations between suicide and control subjects (suicide: 121.1 (82.97–143.0); controls: 425.9 (233.1–835.3); P<0.001) as well as a decrease in IL-1β concentrations by almost 80%; and (3) no significant difference in plasma hypocretin levels between suicide and control subjects (suicide: 16.62 (13.62–25.77); controls: 21.63 (14.97–29.72); P=0.356).ConclusionOur results suggest that plasma NPY and IL-1β were related with suicide behavior rather than to suicide causes or suicide method. Specific combinations of plasma biomarkers may discriminate between types of suicidal behaviors and indicate increased risk for future suicide attempts.
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