Objective:To test the validity and reliability of the Chinese version of the Snaith-Hamilton Pleasure Scale (SHAPS).Methods:Totally 166 patients with major depression completed the Chinese version of SHAPS,Beck Depression Inventory (BDI-Ⅰ) and Hamilton Depression Scale (HAMD-17).The validity was tested by using correlation analysis and exploratory factor analysis.The reliability was tested by using internal consistency coefficient and Pearson correlation analysis.Results:The ICCs between three different Scale score were 0.90 and 0.91(Ps ＜ 0.001).Exploratory factor analysis identified 2 common factors,which explained 62.8％ of total variancel.The Cronbach coefficient of SHAPS was 0.94.The test-retest coefficient was 0.91 (P ＜ 0.001).The intercorrelations of 14 items ranged from 0.30 to 0.93 and item-total correlations ranged from 0.61 to 0.79.Conclusion:The Chinese version of SHAPS has good validity and reliability,it could be used to assess anhedonia in Chinese patients with major depression.

OBJECTIVE: The pathogenesis of depression is not fully understood yet, but studies have suggested higher circulating C reactive protein (CRP) level might relate to depression occurrence. However, due to high variability of patients’ individual condition, the results to date are inconsistent. Considering CRP single-nucleotide polymorphisms (SNPs) could also regulate plasma CRP levels, in the present study, we hypothesized that inherited CRP allelic variations may co-vary with depressive symptomatology. METHODS: We recruited 60 depression patients with family depression history and 60 healthy control volunteers into this project. We detected circulation CRP level as well as genome CRP SNPs from participants of this project. RESULTS: We have found a significantly higher circulating CRP level in patients with a positive family history. Furthermore, we also identified some certain inherited CRP SNPs (A allele in rs1417938 and C allele in rs1205) could up regulate serum CRP level and distributed more in depression patients with family history. CONCLUSION: Our finding may raise new evidence that genetically increased serum CRP level through SNPs variation is likely to induce family inherited depression.
Alleles ; C-Reactive Protein* ; Depression* ; Genome ; Humans ; Plasma ; Polymorphism, Single Nucleotide ; Volunteers

OBJECTIVETo assess the association of BDNF gene Val66Met polymorphism with efficacy of antidepressant treatment and plasma BDNF level.

METHODSTwo hundred and forty-nine ethnic Han Chinese patients with depression(study group), who have met the diagnostic criteria of DSM-IV, were prescribed with venlafaxine or paroxetine. Two hundred and two healthy individuals were recruited as the control group. General demographic information such as gender, age, educational status, occupation, and marriage status were collected. HAMD-17 was adopted as the primary rating tool to evaluate the severity of depression on the baseline and at the end of 1st, 2nd, 4th, 6th week of treatment. PCR-restriction fragment length polymorphism was applied to determine the Val66Met polymorphism of the BDNF gene in the two groups. Plasma BDNF concentration was measured with ELISA before and after 6 weeks of treatment.

RESULTSNo significant differences have been found in HAMD scores and reduction of HAMD scores on the baseline and at the end of 1 st, 2nd, 4th, 6th weeks of treatment for each genotype. Nor were significant differences found in the Val66Met genotypes and allelic frequency between patients who achieved remission or not after 6 weeks' treatment as well as the healthy volunteers. The plasma BDNF level in depression patients was lower than that in healthy controls. The BDNF level has increased significantly after 6 weeks' treatment with both venlafaxine and paroxetine, but was still lower than the healthy controls. The BDNF level in the patients achieved remission who were treated with venlafaxine was similar to the normal controls, while those treated with paroxetine was still lower than normal controls. The BDNF level in patients who have not achieved remission was lower than normal controls. The BDNF level was not associated with the Val66Met polymorphism on the baseline and the end of 6th week.

CONCLUSIONNo association has been found between the efficacy of venlafaxine or paroxetine and the BDNF Val66Met polymorphism. The BDNF level of patients with depression is significantly lower than healthy controls on the baseline, and can be enhanced with the treatment. Particularly, the BDNF level in patients who achieved remission after the treatment of venlafaxine can rise to normal. The level of BDNF has certain value in the forecasting of efficacy in the anti-depression therapy. BDNF level is not associated with the Val66Met polymorphism of the BDNF gene.

Adolescent ; Adult ; Aged ; Antidepressive Agents ; therapeutic use ; Brain-Derived Neurotrophic Factor ; blood ; genetics ; Depression ; blood ; drug therapy ; genetics ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic

Objective To observe the effect of risperidone on serum brain derived neurotrophic factor ( BDNF) in first-episode schizophrenic patients. Methods In the treatment group, 90 first-episode schizophrenics were treated with risperidone for 16 weeks, and the dose of risperidone was (3.79±0.88) mg·d-1. Serum BDNF levels were measured before treatment, at 2, 8, and 16 weeks after treatment. The severity of schizophrenia symptoms was assessed by the positive and negative symptom scale ( PANSS) before and after sixteen weeks of treatment. Serum BDNF concentrations were measured in 90 healthy controls. Results BDNF in the control group was (22.867±6.051) ng·mL-1. The serum BDNF levels before treatment and at the end of week 2, 8, 16 after the treatment in the treatment group were (14.256±4.096), (13.078±3.462), (18.001±5.753), (21.089± 6.692) ng·mL-1 , and the serum BDNF level was significantly lower in the treatment group than that in the control group ( P<0.01) . After the treatment, the level of BDNF in the treatment group decreased at first and then increased, compared with that before treatment, the difference was significantly ( P<0.05 or P<0.01) . The level of BDNF in the treatment group at the end of week 16 was not significantly different from that of the control group ( P>0.05) . After treatment, the total score of PANSS scale and its subscales decreased, the difference was significantly (P<0.01). At the end of week 16, the PANSS subscale reduction rate was positively correlated to the serum BDNF concentration change (r=0.499, P=0.001). The change rate of serum BDNF concentration at the end of week 16 was not correlated with the dose of risperidone (r=0.103, P=0.335). Conclusion BDNF is abnormal in the first episode of schizophrenia, which can be improved by risperidone treatment.