Depression is a relatively common psychosomatic disease in clinical practice. It is mainly characterized by significant and lasting depression. It generally manifests as depression, loss of interest, impaired cognitive function, etc. Some patients are accompanied by somatization symptoms such as insomnia or lethargy, Loss of appetite, fatigue, loss of libido, etc. In severe cases, self-injury or even suicide may occur. According to research, depression has become the third leading cause of disability and death. At present, the pathogenesis of depression has not been definitively concluded, but a large number of studies have shown that it is related to biochemical, neuroendocrine, and neuroimmunological factors. At present, selective 5-HT reuptake inhibitors are routinely used in clinical treatment, such as sertraline, citalopram, Prozac, etc., but they often have slow onset and obvious side effects, making it difficult to achieve satisfactory therapeutic effects. Traditional Chinese medicine has gradually begun to be accepted by doctors and patients in the treatment of refractory diseases due to its multi-component and multi-target characteristics. This article mainly discusses the research progress of Chinese herbal extracts, Chinese herbal medicine pairs, Chinese herbal compound prescriptions, and Chinese patent medicines in the treatment of depression, and provides references for the clinical application of Chinese medicines in the treatment of depression.

Chronic kidney disease (CKD) is a common chronic disease, often accompanied by cognitive impairment (CI), which can progress to dementia. CKD-induced cognitive impairment (CKD-CI) seriously affects the patient's quality of life and disease self-management. From the perspective of kidney-brain axis, this article elaborates on the damage of vascular endothelial function, oxidative stress, endoplasmic reticulum stress, and inflammation caused by brain nerve damage, brain structure and function changes, cerebral hemodynamic imbalance, brain metabolic disorders and renal replacement therapy affect cognition mechanisms from pathophysiological, neuroimmunological and neuroimaging. This is a review of recent advance in the mechanism of cognitive impairment in CKD.

Objective To explore the relationship between anhedonia,alexithymia and self-efficacy in college students.Methods 260 college students were tested with Snaith-Hamilton Pleasure Scale (SHAPS),Temporal Experience of Pleasure Scale (TEPS),20-item Toronto Alexithymia Scale (TAS-20)and General Self-Efficacy Scale (GSES).Results (1) Males showed obviously higher level of SHAPS scores (24.91±5.14) and lower level of anticipatory pleasure of TEPS (TEPS-ANT) scores(31.81±5.79)than females (22.97±5.34 and 33.36±5.71,respectively).(2)Significant difference existed between the high-scoring,the middle-scoring and the low-scoring anhedonia group in TAS factor 1 (difficulty in identifying feelings) and GSES (F=3.11,5.30,P＜0.05 or 0.01),the scores of TAS factor 1 (difficulty in identifying feelings) in high-scoring anhedonia group were higher than that in low-scoring anhedonia group (20.24±4.94 vs 18.10±5.07,P＜0.01),and the scores of GSES in high-scoring anhedonia group were lower than that in low-scoring anhedonia group (24.97±6.72 vs 27.90±4.37,P＜0.01).(3)The SHAPS scores were positively related to TAS factor 2 (difficulty in describing feelings) and factor 3 (externally oriented thinking) (r =0.18,0.27,both P＜0.01),negatively related to GSES scores(r=-0.33,P＜0.01).Both TEPS-ANT and consummatory pleasure of TEPS (TEPS-CON) were negatively related to TAS factor1 (difficulty in identifying feelings)scores (r=-0.22,P＜ 0.01;r =-0.15,P＜ 0.05),positively related to GSES scores (r =0.28,0.26,both P＜0.01).(4)Layer multivariate linear regression analysis showed that the SHAPS scores were significant predictors of the general self-efficacy(β=-0.33,P＜0.01).Conclusions The anhedonia in college students has a closely relationship with alexithymia and self-efficacy,college students with high anhedonia have high level of alexithymia and low level of self-efficacy.

Objective To determine how genetic polymorphisms in norepinephrine transporter (NET) gene influence the response of antidepressant treatment and how they interact with childhood trauma and recent life stress in a Chinese depressive patients.Methods 281 Chinese Han depressive patients received single antidepressant drugs for 6 weeks.Hamilton Depression Scale-17 (HAMD-17),the Childhood Trauma Questionnaire short term (CTQ-SF) and the Life Events Scale (LES) were used to evaluate severity of depressive symptoms and the occurrence of stressful life events respectively.Three single nucleotide polymorphisms (SNPs) in norepinephrine transporter were genotyped.Associations of single locus and haplotypes with antidepressant treatment response were analyzed using UNPHASED 3.0.13.The interaction of gene and life stress was analyzed by SPSS13.0 software.Results One NET SNP rs2242446 was significantly associated with antidepressant response in this Chinese male sample(0.4118vs0.2375,x2=7.046,P=0.0079,OR=0.445,95％ CI (0.243-0.815)),as was the haplotype CG(rs2242446 and rs5569;x2 =5.886,P=0.0153,OR=0.457,95％ CI (0.198-1.054)) and another haplotype CG-G(rs2242446,rs1532701 and rs5569;x2=5.360,P=0.0206,OR=0.530,95％ CI (0.202-1.386)) of NET in male samples.The NET SNPs rs5569 demonstrated interaction with childhood trauma to influence antidepressant response(β=-2.727,SE =1.195,P=0.023,OR=0.065,95％ CI (0.006-0.681)).Conclusion Antidepressant drug response was influenced by not only NET genetic polymorphisms in norepinephrine transporter gene but also interaction between the NET genetic polymorphisms and early life stress.

Post-stroke fatigue is a common symptom after stroke independent of depression. It impacts functional recovery of limbs, psychological rehabilitation and quality of life, and has been linked w ith a higher mortality rate. Identifing the risk factors of post -stroke fatigue and clarifying the diagnosis and conducting effective intervention may contribute to the early rehabilitation. This article review s the advances in research on the incidence, risk factors, mechanisms, diagnosis and treatment of post -stroke fatigue.

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 explore the relationships between angiotensin converting enzyme (ACE) gene polymorphism of insertion/deletion(I/D) and cognition function in senile depressive patients in Chinese Han population.Methods 97 patients with major depression were recruited according to the Diagnostic and Statistical Manual of Mental Disorders,Fourth Edition criteria,and 103 healthy persons were used as controls.The Hamilton Depression Scale (HAMD) and neuropsychological tests were used to assess depressive severity and cognitive function in all patients and 44 healthy controls,respectively.The intron 16 I/D polymorphism of ACE gene was detected by polymerase chain reaction (PCR).Results The performances of neuropsychological tests in case group except TMT B were significantly poorer than those in control group (P＜ 0.001).Correlation analysis indicated that the total scores of HAMD were negatively associated with Digit Span Test forward score in senile depressive patients (r=-0.213,P=0.040).There were no significant differences between case and controls on genotype and allele frequencies of ACE gene(x-2 =1.745,P=0.418 ; x2 =0.700,P=0.403).And there were no significance in different sex,respectively (P ＞ 0.05).Furthermore,no significant differences of neuropsychological test performances were found between ACE genotypes of senile depressive patients (P ＞ 0.05).Conclusion Senile depressive patients have extensive cognitive impairments in the acute phase of illness,and working memory performance is correlated with depression severity.ACE gene Ⅰ/D polymorphism may not significantly associate with cognitive function in senile patients.

Objective To investigate the relation of serum leptin level in senile depressive patients with type 2 diabetes and polymorphisms of leptin receptor gene 3057 G/A.Methods 10 senile depressive patients with type 2 diabetes and 47 senile depressive patients without type 2 diabetes were selected for the study.Leptin levels were determined by radioimmunoassay.Genomitic DNA were obtained by phenol/chloroform method.Leptin receptor gene 3057 G/A polymorphisms and allele frequencies were determined with the polymerase chain reaction and restricted fragment length polymorphism assay.Results (1) The differences of leptin receptor genotypes and allele distribution in the 3 groups were not found (all P ＞ 0.05).(2) Serum leptin level in senile depressive patients with type 2 diabetes and without type 2 diabetic patients ((41.65 ± 28.19) ng/ml,(25.56 ± 21.04) ng/ml) were significantly higher than the normal people ((10.84 ± 9.16) ng/ml) (all P ＜ 0.05).Serum leptin level in senile depressive patients with type 2 diabetes were significantly higher than without type 2 diabetic patients(P＜ 0.05).(3) The serum leptin level in genotype AA senile depressive patients with type 2 diabetes were significantly higher than genotype AA patients without type 2 diabetes.The differences of the serum leptin levels in genotype AA senile depressive patients without type 2 diabetes and genotype AG/GG patients without type 2 diabetes were not found(P ＞ 0.05).The differences of the serum leptin level in genotype AA and genotype AG/GG in normal groups were not found (P＞ 0.05).Conclusion Senile depressive patients have higher serum leptin level.The serum leptin level is higher,especially with type 2 diabetes.Serum leptin level is related to type 2 diabetes.Serum leptin level is not related to the polymorphisms of leptin receptor gene 3057 G/A.Type 2 diabetes are not related to polymorphisms of leptin receptor gene 3057 G/A.

Objective To investigate outcome and cognitive changes of amnestic mild cognitive impairment (aMCI) in a follow-up study. Methods A cross-sectional and longitudinal parallel cohort study design was conducted among 109 aMCI patients and 104 matched normal controls. Multi-dimension neuropsychologic tests were used to extensively assess the cognitive function. Results The scores of neuropsychologic tests in aMCI patients were significantly lower than those in the normal controls( all P＜0.01 ) ,with the largest impairment on 20minutes delayed recall of the auditory verbal memory test ( AVMT), which reflects episodic memory ( aMCI pa-tients :2.50 ± 1.48, normal controls :7.85 ± 1.59, Z = - 12.697, P ＜ 0.01 ); AD was diagnosed in 15 of the 69aMCI patients with a prevalence rate of 22% ,but none was converted to AD in the normal controls. The cognitivechanges of performance in AVMT, CDT, MMSE of the patients in aMCI group (( 3.77 ± 60.83 )%, (6.89 ±28.24) %, (6.13 ± 16.89) % respectively) were significantly poorer than those of the controls group(( - 10.75 ±27.46) %, ( - 5.23 ± 14.05 ) %, ( - 1.11 ± 8.26 ) % respectively) ( all P ＜ 0.05 ). At baseline, demented aMCIperformed poorer in AVMT, CFT, TMT, SDMT, CDT, MMSE when compared to stable. During the follow-up, demented aMCI groups performed significantly poorer than did stable subjects in AVMT, CFT, DST, VFT, SDMT,MMSE ( all P ＜ 0.05 ). Conclusion aMCI is a prodromal period of AD and characterized by episodic memory impairment. The neuropsychologic test is a predictive factor for aMCI to develop AD.

Objective To explore the effect of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism,environmental factor and their interactions on antidepressant treatment.Methods 340 patients of major depressive disorder (MDD) who met the diagnosis criteria of MDD ( DSM-Ⅳ Axis Ⅰ) were recruited.280 patients of them were finished 12 weeks antidepressant treatment.The severity of depression was measured with the Hamilton Depression Rating Scale (HDRS) before and after 12 weeks antidepressant treatment.Childhood Trauma Questionnaire,28-item Short Form (CTQ-SF) and Life Events Scale (LES) were used to evaluate childhood adverse and life stress before onset.Genotyping of BDNF Val66Met polymorphism was detected by Illumina GoldenGate assays.Results Male patients proportion were significantly higher in non-remitters than remitters (P =0.008 ).After adjusting by gender, the frequencies of genotype and allele for the BDNF Val66Met polymorphism were no significant difference between remitters (AA: AG: GG = 28: 79: 40, A:G = 135:159 ) and non-remitters (AA: AG: GG = 29:81:23 ,A: G = 139:127 ) (P ＞0.05 ).There was no significant difference of CTQ scores and LES scores between the two groups (P＞0.05 ).The regression analysis showed that social intercourse problem and age were the risk factor for the severity of depression.The gender, HDRS baseline scores and mental disorder family history were associated with the efficacy of 12 weeks antidepressant.However,there was no significantly relationship between the interaction of BDNF Val66Met polymorphism and environment with the antidepressant treatment.Conclusion The older men with the mental disorder family history, severe depression symptom would be less-response to antidepressant treatment.However, BDNF Val66Met polymorphism, childhood trauma, life events stress and the interaction of BDNF Val66Met polymorphism and environment have no significantly effect on the 12 weeks antidepressant treatment.