Abnormal functional connectivity of the nucleus accumbens subregions mediates the association between anhedonia and major depressive disorder.

BACKGROUND: The nucleus accumbens (Nac) is a crucial brain region in the pathophysiology of major depressive disorder (MDD) patients with anhedonia. However, the relationship between the functional imaging characteristics of Nac subregions and anhedonia remains unclear. Thus, this study aimed to investigate the role of resting-state functional connectivity (rsFC) of the Nac subregions between MDD and anhedonia. METHODS: We performed resting-state functional magnetic resonance imaging (fMRI) to measure the rsFC of Nac subregions in 55 MDD patients and 30 healthy controls (HCs). A two-sample t test was performed to determine the brain regions with varying rsFC among Nac subregions between groups. Then, correlation analyses were carried out to investigate the relationships between the aberrant rsFC of Nac subregions and the severity of anhedonia. Furthermore, we constructed a mediation model to explain the role of the aberrant rsFC of Nac subregions between MDD and the severity of anhedonia. RESULTS: Compared with the HC group, decreased rsFC of Nac subregions with regions of the prefrontal cortex, insula, lingual gyrus, and visual association cortex was observed in MDD patients. In the MDD group, the rsFC of the right Nac shell-like subregions with the middle frontal gyrus (MFG)/superior frontal gyrus (SFG) was correlated with consummatory anhedonia, and the rsFC of the Nac core-like subdivisions with the inferior frontal gyrus (IFG)/insula and lingual gyrus/visual association cortex was correlated with anticipatory anhedonia. More importantly, the functional alterations in the Nac subregions mediated the association between anhedonia and depression. CONCLUSIONS: The present findings suggest that the functional alteration of the Nac subregions mediates the association between MDD and anhedonia, which provides evidence for the hypothesis that MDD patients have neurobiological underpinnings of reward systems that differ from those of HCs.

Correlation of clinical features with hs-CRP in TRD patients.

Correlation of clinical features with hypersensitive C-reactive protein (hs-CRP) in patients with treatment-resistant depression (TRD) was investigated. The severity of disease in 103 TRD patients and 103 non-TRD patients was evaluated using the Hamilton Depression Scale (HAMD)-17. The levels of hs-CRP in both groups were detected via immunofluorescence. Clinical features and differences in hs-CRP before and after treatment in both groups were analyzed, and correlation of baseline hs-CRP level with clinical features of TRD patients was also analyzed. Moreover, the relationship between hs-CRP and occurrence of TRD was analyzed using logistic regression analysis, and the diagnostic value of hs-CRP in TRD was evaluated using the receiver operating characteristic (ROC) curve. The onset age in the TRD group was lower than that in the non-TRD group, the education in the TRD group was shorter than that in the non-TRD group, the total course of disease in the TRD group was longer than that in the non-TRD group, and both baseline and post-treatment hs-CRP level in the TRD group (12.05±5.79 and 9.02±3.71 mg/l) were higher than those in the non-TRD group (7.85±2.85 and 6.10±2.74 mg/l) (p<0.05). The HAMD score (r=0.338, p=0.031), anxiety/somatization factor score (r=0.465, p=0.015) and sleep disorder (r=0.387, p=0.029) of TRD patients were positively correlated with the hs-CRP level, but the onset age (r=-0.59, p=0.009) was negatively correlated with the hs-CRP level. Logistic regression analysis revealed that the baseline hs-CRP was included into the TRD regression equation [odds ratio (OR) =2.834, 95% confidence interval (CI) =1.723-4.886], and the area under the ROC curve was 0.893 (p<0.05, 95% CI=0.852-0.933). In the TRD group, the course of TRD in patients was longer, the onset of disease was earlier and the educational level was lower than that in the non-TRD group. Therefore, the level of hs-CRP can serve as a reference for the diagnosis of TRD.

The analog of Ginkgo biloba extract 761 is a protective factor of cognitive impairment induced by chronic fluorosis.

Ginkgo biloba extract EGb761 is widely used to treat patients with learning and memory impairment in Alzheimer's disease and Parkinson's disease in China. However, it is not yet clear whether the analog of EGb761 (EGb) has a protective effect on the learning and memory damage induced by chronic fluorosis. In this study, 30 Wistar rats were randomly divided into three groups: a control group, a sodium fluoride (NaF) + EGb group, and a NaF group. The rats were administered 0.5 ml water containing NaF (100 mg/l) and EGb (120 mg/kg) per day via gavage. After 3 months, the rats' capacity for learning and memory was tested using a Y-maze. Damage to hippocampal neurons was evaluated by histological examination of the CA3 area. Superoxide dismutase (SOD) activity and the levels of glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were measured. Furthermore, the expression levels of Bcl-2 and Bax and the levels of cleaved Caspase3 in the hippocampus were evaluated by RT-PCR and Western blotting. The results showed that EGb could improve learning and memory abilities, enhance the activities of SOD and GSH-Px, attenuate the level of MDA, upregulate the ratio of Bcl-2/Bax, and downregulate the level of cleaved Caspase3.