An inhibited neural response to reward is typical of clinical depression and can predict an individual's overall depressive symptoms. However, the mechanism underlying this are unclear. Previous studies have found that anhedonia and inattention may mediate the relationship between reward sensitivity and depressive symptoms. Therefore, this study aimed to verify the relationship between reward sensitivity and overall depressive symptoms in a depressive tendency sample as well as to explore the mechanism underlying the ability of neural responses to reward to predict overall depressive symptoms via a mediation model. Sixty-four participants (33 with depressive tendencies and 31 without; dichotomized by BDI-II) finished simple gambling tasks while their event-related potential components (ERPs) were recorded and compared. Linear regression was conducted to verify the predictive effect of ERPs on overall depressive symptoms. A multiple mediator model was used, with anhedonia and distractibility as mediators reward sensitivity and overall depressive symptoms. The amplitude of reward positivity (ΔRewP) was greater in healthy controls compared to those with depressive tendencies (p = 0.006). Both the gain-locked ERP component (b = − 1.183, p = 0.007) and the ΔRewP (b = − 0.991, p = 0.024) could significantly negatively predict overall depressive symptoms even after controlling for all anxiety symptoms. The indirect effects of anhedonia and distractibility were significant (both confidence intervals did not contain 0) while the direct effect of reward sensitivity on depressive symptom was not significant (lower confidence interval = − 0.320, upper confidence interval = 0.065). Individuals with depressive tendencies display impaired neural responses to reward compared to healthy controls and reduced individual neural responses to reward may reflect the different biotypes of depression such as anhedonia and inattention.

Post-traumatic stress disorder (PTSD) is a severe and heterogenous psychiatric disorder that was first defined as a mental disorder in 1980. Currently, the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5) and the International Classification of Diseases 11th Edition (ICD-11) offer the most widely accepted diagnostic guidelines for PTSD. In both diagnostic categories, experiencing a traumatic event (TE) is the necessary criterion for diagnosing PTSD. The TEs described in the DSM-5 include actual or threatened death, serious injury, sexual violence, and other extreme stressors, either directly or indirectly. More than 70% of adults worldwide are exposed to a TE at least once in their lifetime, and approximately 10% of individuals develop PTSD after experiencing a TE. The important features of PTSD are intrusion or re-experiencing fear memories, pervasive sense of threat, active avoidance, hyperarousal symptoms, and negative alterations of cognition and mood. Individuals with PTSD have high comorbidities with other psychiatric diseases, including major depressive disorder, generalized anxiety disorder, and substance use disorder. Multiple lines of evidence suggest that the pathophysiology of PTSD is complex, involving abnormal neural circuits, molecular mechanisms, and genetic mechanisms. A combination of both psychotherapy and pharmacotherapy is used to treat PTSD, but has limited efficacy in patients with refractory PTSD. Because of the high prevalence, heavy burden, and limited treatments, PTSD is a psychiatric disorder that requires urgent attention. In this review, we summarize and discuss the diagnosis, prevalence, TEs, pathophysiology, and treatments of PTSD and draw attention to its prevention.