| Background and purposeDepression is a very common mental illness,which has complex and various clinical symptoms with persistently abnormal emotional state and changes of cognitive,physiological and social behavior.It is characterized by high morbidity,suicide,disability rate and low diagnostic rate.With the complexity of the pathogenesis of depression,it has been considered that depression results from the combined effects of biochemical,hereditary,environmental and social psychological factors.The relation of 5-hydroxytryptamine transporter gene linked polymorphic(5-HTTLPR)and depression has been one of the hot topics.Functional magnetic resonance imaging provides a new direction for studying the pathogenesis of depression.Independent component analysis(ICA)is one common methodology for analyzing functional connectivity in resting-state networks(RSNs).From the perspective of gene imaging,this study intends to discuss the changes of functional connectivity in RSNs of first-episode depression patients by fMRI-ICA and the impacts on RSNs of 5-HTTLPR.Materials and methods93 first-episode depression patients and 70 healthy controls were enrolled for undergoing GE Discovery 750 3.0T MRI scanning,with 2 depression patients and 1 healthy control excluded for the head movement.5-HTTLPR genotype data were extracted from 58 first-episode depression patients and 39 healthy controls.Resting-state fMRI images were preprocessed by DPARSFA toolbox based on the Matlab platform.Independent component analysis was proceeded by GIFT toolbox based on the Matlab platform.Between-group comparisons were carried out on SPM toolbox based on the Matlab platform.Comparisons of the functional connectivity in RSNs between first-episode depression group and healthy control group were using two-sample t-tests corrected for AlpahSim with a threshold of P<0.001.Comparisons among 5-HTTLPR genotypes were using two-factor analysis of variance and post-hoc tests corrected for AlpahSim with a threshold of P<0.001.ResultsThere was no significant difference of 5-HTTLPR genotype frequencies between first-episode depression patients and healthy controls(P>0.05).There was higher S allelic frequency in first-episode depression patients with significant difference(P<0.05).There were 13 RSNs obtained through ICA,including anterior default network(aDMN),posterior default network(pDMN),salience network(SN),centralexecutive network(CEN),dorsal attention network(dAN),sensorimotor network(SMN),auditory network(AUN),lateral visual network(lVN),medial visual network(mVN),occipital pole visual networks(pVN),language network(LN),left frontoparietal network(lFPN)and right frontoparietal network(rFPN).Differences of functional connectivity within each RSN(corrected for AlpahSim,P<0.001):(1)aDMN: Compared with healthy controls,the functional connectivity decreased in right superior frontal gyrus in first-episode depression within aDMN(t=-3.4291).Comparing SS genotype carriers with L allele carriers,the functional connectivity of left anterior cingutate decreased(t=-3.5735).(2)pDMN: Compared with healthy controls,the functional connectivity increased in left precuneus in first-episode depression within pDMN(t=2.962).Comparing SS genotype carriers with L allele carriers,the functional connectivity of left posterior cingutate increased(t=2.9896)and right inferior parietal lobule decreased(t=-3.3036).(3)SN: Compared with healthy controls,the functional connectivity decreased in right middle frontal gyrus in first-episode depression within SN(t=-3.6232).Comparing SS genotype carriers with L allele carriers,the functional connectivity of right superior frontal gyrus(t=-3.8313)and left middle frontal gyrus(t=-3.7324)decreased.(4)CEN: Compared with healthy controls,the functional connectivity decreased in left middle frontal gyrus(t=-4.6137)and increased in left inferior parietal lobule(t=3.2683)in first-episode depression within CEN.Comparing SS genotype carriers with L allele carriers,the functional connectivity of left middle temporal gyrus increased(t=3.7654).(5)dAN: Compared with healthy controls,the right superior parietal lobule both had increased(t=3.4507)and decreased(t=-3.6394)functional connectivity regions in first-episode depression within dAN.(6)SMN: Compared with healthy controls,the functional connectivity decreased in right posterior central gyrus in first-episode depression within SMN(t=-4.3926).Comparing SS genotype carriers with L allele carriers,the functional connectivity of right posterior central gyrus increased(t=4.4873).(7)AUN: Compared with healthy controls,the functional connectivity decreased in both sides lentiform nucleus in first-episode depression within AN(left: t= t=-3.7995,right: t=-4.0086).(8)lVN: Compared with healthy controls,the functional connectivity increased in right cuneus in first-episode depression within lVN(t=3.2075).Comparing SS genotype carriers with L allele carriers,the functional connectivity of right superior temporal gyrus increased t=3.2641).(9)mVN: The differences between groups were not significant.(10)pVN: Compared with healthy controls,the functional connectivity increased in right cuneus in first-episode depression within pVN(t=3.5478).(11)LN: Compared with healthy controls,the functional connectivity increased in right precuneus in first-episode depression within LN(t=3.7834).Comparing SS genotype carriers with L allele carriers,the functional connectivity of left middle temporal gyrus decreased(t=-3.6036).(12)lFPN: Compared with healthy controls,the functional connectivity decreased in left middle frontal gyrus in first-episode depression within lFPN(t=-3.1384).(13)rFPN: Compared with healthy controls,the functional connectivity decreased in middle frontal gyrus in first-episode depression within rFPN(t=-3.937).ConclusionsThe S allele of 5-HTTLPR may be the susceptible gene for depression.There are abnormalities of functional connectivity in multiple RSNs in first-episode depression patients.Functional connectivity within RSNs may be affected by 5-HTTLPR through the expression of 5-hydroxytryptamine transporter. |
PDF Full Text Request