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Objective:To explore the association between the spontaneous neural activity and memory function in depressive patients with different sleep quality.Methods:Totally 58 patients with depressive disorder and 58 gender-, age-, education-matched healthy controls (HC) completed 3.0 T MRI Scanning and clinical assessment including Wechsler memory scale (WMS), 24 Hamilton depression scale(HAMD-24) and Pittsburgh sleep quality index (PSQI). According to the score of PSQI, patients were divided into poor sleep quality group (PS, n=38) and good sleep quality group (GS, n=20). Amplitude of low frequency fluctuations (ALFF) were calculated and compared among three groups.Correlation analyses between the brain activity and the score of WMS were conducted as well. Results:Memory quotient of WMS showed differences among three groups( F=14.163, P<0.01), and the lowest score was found in patients with low sleep quality.The brain areas showed significant differences among three groups located in the left medial superior frontal gyrus (lmSFG, MNI: x=-10, y=30, z=58; K=56), right orbital inferior frontal gyrus (roIFG, MNI: x=26, y=20, z=-26; K=24) and left middle frontal gyrus (lMFG, MNI: x=-40 y=32, z=42; K=25) (voxel size P<0.001, cluster size P<0.05, GRF corrected). Compared with GS group, the ALFF of PS group showed significantly increased in the lmSFG, which was negatively correlated with memory quotient ( r=-0.327, P=0.045) and short term memory( r=-0.388, P=0.016). Compared with HC group, the ALFF of PS group showed increased in the lmSFG and lMFG, GS group showed increased ALFF in the roIFG. Conclusion:The impairment of memory function is more serious in patients with depression of low sleep quality, and the activity of frontal lobe is abnormally increased, which is related to memory function.Their association suggests that poor sleep quality in depressive patients may impair memory function by disrupting neural plasticity and synaptic pruning in the frontal lobes.
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Objective To explore the relationship of miR-34b/c gene polymorphisms and event-related potential P300 in major depressive disorder.Methods The design of case-control research was used,and 302 major depressive patients and 327 normal controls who were in age and gender matched with patients were measured auditory event-related potential P300 on the day when two groups were collected.Polymerase chain reaction(PCR) and direct DNA sequencing technology were used to detect miR-34b/c gene polymorphisms.Results (1) In the single locus analysis,the rs4938723,rs2187473 and rs28757623 had no significant difference in allele frequency and genotype frequency between depressive patients and controls (P＞ 0.05);Haplotype C-C-C in rs4938723-rs2187473-rs28757623 was statistically significant different in depressive patients and controls(x2 =3.96,P=0.046).The odds ratio (OR) was 1.322(95％CI=1.004-1.740).(2) Compared with normal controls,P300 of the patients with major depressive disorder had longer latency of N2 (P＜0.01),P3a (P＜0.01) and P3b (P＜0.05).(3) The P300 targets of major depressive disorder had statistical difference(P＜0.05)in rs28757623 between the individuals with the G allele genotype and C/C genotype.The latency of N1 ((90.80±28.62) ms),P3a((281.79±37.89) ms),P3b((323.87±41.17) ms) were longer thanC/C genotype ((77.40 ± 20.96) ms,(253.00 ± 34.36) ms,(297.30± 23.70) ms).Conclusion Rs4938723-rs2187473-rs28757623 haplotype CCC in miR-34b/c gene might be risk factor for the onset of depression,miR-34b/c gene rs28757623 polymorphism is associated with the principal component of P300 latency in patients with Major depressive disorder which suggest that genetic factors may have a certain impact on cognitive function in the patients with major depressive disorder.
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Objective To investigate the relevance of brain-derived neurotrophic factor (BDNF) gene polymorphisms and the effects of citalopram antidepressant.Methods The subjects comprised 280 patients according to the diagnostic and statistical manual of mental disorders in the fourth edition (DSM-Ⅳ) criterion for major depressive disorder (MDD).Severity of depression were assessed by 17 Hamilton depression scale (HAMD) at the baseline and 1,2,4,6 weekend.Citalopram were selected for treatment.Polymerase chain reaction (PCR) and DNA sequencing analysis were used to detect the genotype of SNPs rs7124442 and rs6265 of BDNF.SPSS17.0 software was used for statistical analysis.Results (1) There were 280 patients (242 responders and 38 nonresponders;175 remissioners and 105 nonremissioners) accomplished 6 weeks of treatment.No association was found between the polymorphisms and antidepressant drug response or remission (the reduction rate of HAMD score ≥ 50％ was defined as response,conversely,defined as nonresponse;HAMD score more than 7 was named as remission,in contrast,named as nonremission) (P＞0.05).(2) Repeated measures analysis of variance was adopted to compare the change of HAMD scores among the genotypes at different time points.There was a significant difference in rs6265 polymorphism between the GA +AA genotype (the scores of HAMD at 2,4,6 weeks were(9.98±4.97),(8.02±4.50),(5.83±3.49) respectively) and the GG genotype groups (the scores of HAMD at 2,4,6 weeks were(11.90±6.55),(9.34± 4.71),(7.07±4.28) respectively) (P=0.031).Conclusion The results suggest that BDNF rs6265 polymorphisms in part determine the antidepressant response to citalopram.