Negative life events (NLEs) are an important predictor of depressive symptoms (DS). College students experiencing NLEs are at risk of developing DS that could further weaken their academic engagement (AE), while social supports may assuage such negative effect. The aim of this study was to examine the relationship between negative life events, depressive symptoms, and academic engagement, and how the NLE-DS-AE relationship is affected by the level of social support among Chinese college students. To test this hypothesis, we applied data from the Decoding Happiness Gene Cohort Study (DHGCS). Baseline depressive symptoms and academic engagement were measured at the beginning of the first academic year. Approximately 12 months later, negative life events and social support over the past year were assessed retrospectively along with current depressive symptoms and academic engagement. A total of 3629 college students (Age = 18.67 ± 0.82) were included in the study. The prevalence of depressive symptoms was 26.7% and 36.7% in college students at the beginning of the first and second academic year, respectively. Depressive symptoms predicted subsequent academic engagement rather than the reverse based on cross-lagged analyses. Using structural equation modeling analyses, findings revealed a partial mediation effect of social support between negative life events and the development of depressive symptoms, and a partial mediation effect between negative life events and academic engagement. The findings presented negative life events jeopardize the academic engagement via depressive symptoms, while social supports are able to cancel such negative effect among college students under the Chinese cultural context.
Psychiatric disorders are a class of complex disorders characterized by brain dysfunction with varying degrees of impairment in cognition, emotion, consciousness and behavior, which has become a serious public health issue. The NGFR gene encodes the p75 neurotrophin receptor, which regulates neuronal growth, survival and plasticity, and was reported to be associated with depression, schizophrenia and antidepressant efficacy in human patient and animal studies. In this study, we investigated its association with schizophrenia and major depression and its role in the behavioral phenotype of adult mice. Four NGFR SNPs were detected based on a study among 1010 schizophrenia patients, 610 patients with major depressive disorders (MDD) and 1034 normal controls, respectively. We then knocked down the expression of NGFR protein in the hippocampal dentate gyrus of the mouse brain by injection of shRNA lentivirus to further investigate its behavioral effect in mice. We found significant associations of s2072446 and rs11466162 for schizophrenia. Ngfr knockdown mice showed social and behavioral abnormalities, suggesting that it is linked to the etiology of neuropsychiatric disorders. We found significant associations between NGFR and schizophrenia and that Ngfr may contribute to the social behavior of adult mice in the functional study, which provided meaningful clues to the pathogenesis of psychiatric disorders.
Happiness and depression are interlinked and both heritable, while personality, as an important predictor of them, shares the genetic basis with them. We conjecture that genetic factors of depression can affect both depressive symptoms (DS) and subjective well-being (SWB), while personality traits play important roles in mediating this process. In this study, 878 Han Chinese college freshmen and 384 Han Chinese patients with the major depressive disorder (MDD) were included. SNPs were genotyped using AGENA MassARRAY iPLEX technology and we investigated an important MDD variant rs454214. Correlation, association and mediation analysis were employed, aiming to decipher the complex relationship between SWB, DS, personality traits and the genetic variant. Association study indicated that rs454214 was not only associated with both SWB and DS (P < 0.05), but also possibly linked to MDD. Mediational analysis showed that rs454214 had no direct effect on SWB and DS, but had a significant indirect effect through personality traits, i.e., Extraversion, Neuroticism, Agreeableness and Openness to Experience or SWB, Extraversion, Neuroticism and Agreeableness for DS. This study found a shared genetic basis for happiness and depression; the causal process could be better explained if personality traits are taken as mediating factors. Subjective well-being(SWB) is a subjective measure of one's emotion and cognition, consisting of positive and negative affect as well as life satisfaction which stands for happiness 1. In contrast, depression can be a serious disorder with significantly increased risk of physical and mental disabilities 2,3. The depressive symptoms (DS) are warning signals for one's psychological health and if not taken seriously, the individual can easily develop into clinical depression 4. Happiness and depression are negatively correlated with each other 5 ; they both show heritability at a rate from 30% to 40%, according to many twin and family studies 6-8. Single nucleotide polymorphisms (SNPs) that are significantly associated with them were discovered as well 9,10. On the other hand, according to previous studies, personality traits had been widely reported as important predictors of subjective well-being (SWB) 11,12 and depression 10,13,14 , which can usually be illustrated as a five-factor model (FFM), including Extraversion (E), Neuroticism (N), Conscientiousness (C), Agreeableness (A), and Openness to Experience (O) 15. Twin studies suggested it with a heritability of nearly 40% 16 and genome-wide association studies (GWAS) have probed several remarkable associating SNPs 17. In addition, correlation was found between personality and SWB as well as depression 10,12,17 in a genetic level. This complex intrinsic correlation suggested a shared genetic inheritance of happiness and depression and we conjecture that personality traits can play an important role as a mediator. The purpose of this study was to explore the possible shared genetic basis of SWB and DS through the MDD GWAS-supported SNP 9 and the med...
Objective: Cannabis consumption during adolescence has been reported as a risk-factor for psychotic-like experiences (PLEs) and schizophrenia. However, brain developmental processes associated with cannabis-related PLEs are still ill-described. Method: 706 adolescents from the general population that were recruited by the IMAGEN consortium had structural MRI scans both at 14 and 19 years-old. We used deformation-based morphometry to map voxel-wise brain changes between the two time points, using the pairwise algorithm in SPM12b. We used an a-priori region of interest (ROI) approach focusing on the hippocampus/parahippocampus to perform voxel-wise linear regressions. Life time cannabis consumption was assessed using the European School Survey Project on Alcohol and other Drugs (ESPAD) and PLEs were assessed with the Comprehensive Assessment Psychotic-like experiences (CAPE). We first tested whether hippocampus/para-hippocampus development was associated with PLEs. Then, we formulated and tested an a-priori simple mediation model where uncus development mediates the association between lifetime cannabis consumption and PLEs. Results: We found that PLEs was associated with reduced expansion within a specific region of the right hippocampus/para-hippocampus formation, the uncus (p=0.002 at the cluster level, p=0.018 at the peak-level). The partial simple mediation model revealed a significant total effect from lifetime cannabis consumption to PLEs (b=0.069 95CI [0.04-0.1], p=2 x 10-16), as well as a small yet significant, indirect effect of right uncus development (0.004, 95IC [0.0004-0.01], p=0.026).
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