Cognitive impairment, characterized by impaired attention function, is widely recognized as one of the core symptoms of schizophrenia, significantly impacting the quality of life for individuals with this disorder. The objective of this cross-sectional study is to investigate the characteristics of attentional behavior and related brain structure and gene expression of schizophrenia, aiming to provide new trans-scale evidence. A total of 137 participants were enrolled in this study, including 65 patients with schizophrenia and 72 healthy controls. All participants underwent magnetic resonance imaging scans and completed cognitive tests. The results revealed that patients required more time (all p < 0.05) to complete key responses in attention-related tasks compared to the control group. Moreover, significant structural brain alterations were observed in patients with schizophrenia, including enlarged bilateral pallidum, smaller right hippocampus, and reduced cortical thickness in relevant brain regions (all p < 0.05). Further analysis demonstrated a correlation between alertness during Attention Network Test performance and pallidum volume among patients (r = 0.42, p = 4.30 × 10-4), and this correlation was associated with a specific pattern of gene expression in the patients' brain but not observed among controls. Our study reveals that decreased attentional ability in schizophrenia is accompanied by abnormal changes in pallidum along with specific transcriptional profile among patients with schizophrenia; these findings hold clinical significance for precise diagnosis and treatment strategies targeting schizophrenia.

Empathic pain is defined as the experience of vicarious pain resulting from the observation of another person’s suffering, and it involves complex neurobiological pathways that parallel those involved in direct pain perception. The intricate link between nonsuicidal self-injury (NSSI) and empathic pain lies in the fact that they share certain neurobiological mechanisms, particularly in the areas of emotion regulation and pain perception, and both phenomena involve brain networks involved in pain processing, emotion regulation, and social cognition. This review examines the current understanding of these mechanisms, including cellular and molecular pathways, changes in neural networks, and factors that influence the development of empathic pain. It also explores potential therapeutic strategies to address the complex interactions between empathic pain and NSSI, focusing on psychological interventions, pharmacological approaches, and novel neurostimulation techniques.

ABSTRACT Purpose Repetitive transcranial magnetic stimulation (rTMS) represents a potential clinical tool in treating bipolar disorder (BD). However, the intervention of rTMS combined with pharmacotherapy on the plasma fatty acids (FAs) in patients with bipolar depression has not been reported yet. Method In this study, we assessed the clinical symptoms and evaluated plasma FAs from 30 inpatients with bipolar depression at baseline phase (BD group), after 2 weeks of treatment with rTMS combined with quetiapine and mood stabilizer (BD‐2w group), and 32 healthy controls (HCs). Finding We found that acetic acid, propionic acid, isovaleric acid, isobutyric acid, and valeric acid, as well as levels of total short‐chain fatty acids (SCFAs), were decreased in both BD and BD‐2w groups, and levels of several medium‐ and long‐chain fatty acids (MLCFAs) were altered in BD when compared with HC. Moreover, 2 weeks of treatment increased the levels of various MLCFAs. Finally, we developed combinational FAs panels that could distinguish BD from HC (area under the curve [AUC] = 0.961), BD‐2w from HC (AUC = 0.978), and BD from BD‐2w (AUC = 0.891) effectively. Conclusion These findings might provide a basis for developing diagnostic methods and reveal the potential relationship between bipolar depression and plasma FAs.

This study employed a multi-omics approach to investigate the molecular and functional underpinnings of schizophrenia by integrating blood transcriptomic profiles, neuroimaging-derived brain phenotypes, and clinical symptomatology. RNA sequencing of blood samples from 43 patients with schizophrenia and 60 healthy controls identified 994 differentially expressed genes (DEGs), the vast majority of which were downregulated (n = 921, |FC| > 1.5, P < 0.05), with enrichment in pathways related to neuronal development and inflammation. Concurrent neuroimaging analyses revealed altered functional activation in key brain regions, including the prefrontal and anterior cingulate cortices. A Partial Least Squares correlation analysis demonstrated significant cross-modal relationships among gene expression, neuroimaging patterns, and clinical presentation. Furthermore, we identified six genes—GRK2, KLF3, TAOK2, ARFGAP45, AP1M1, and GPAT2—that were shared across gene sets associated with both brain function and clinical symptoms, suggesting a common transcriptional basis for these features of schizophrenia. Collectively, these findings provide novel insights into the integrated molecular and functional changes in schizophrenia, highlighting the value of a comprehensive multi-omics strategy to decipher its pathophysiology and potentially inform improved diagnostic and therapeutic strategies.

Background Invasive vagus nerve stimulation therapy has been approved for the adjunctive treatment of treatment-resistant depression,which may contribute to the anti-inflammatory properties of vagus nerve stimulation(VNS),whereas the efficacy of non-invasive transcutaneous cervical vagus nerve stimulation(tcVNS)in treating major depressive disorder(MDD)and its impact on plasma inflammatory factors remain unclear.Objective To observe the effect of escitaloprom combined with tcVNS on the status of depression,anxiety and sleep quality as well as the plasma levels of interleukin-6(IL-6)and interleukin-10(IL-10)in MDD patients,in order to provide references for the recovery and treatment of MDD patients.Methods From August 21,2019 to April 17,2024,45 patients who met the diagnostic criteria for MDD in the Diagnostic and Statistical Manual of Mental Disorders,fifth edition(DSM-5)were recruited from the psychosomatic outpatient clinic of the First Affiliated Hospital of Air Force Military Medical University.Subjects were divided into study group(n=23)and control group(n=22)using random number table method.All patients were treated with escitalopram.On this basis,study group added a 30-minute tcVNS therapy once a day for 4 weeks.While control group was given corresponding sham stimulation,and the duration of each stimulation lasted 30 seconds.Before and after 4 weeks of treatment,Hamilton Depression Scale-17 item(HAMD-17)was used to assess depressive symptoms,and HAMD-17 anxiety/somatization subfactor and insomnia subfactor were used to assess patients' anxiety/somatization symptoms and sleep quality.Levels of plasma IL-6 and IL-10 were measured by enzyme-linked immunosorbent assay(ELISA).Results The generalized estimating equation model yielded a significant time effect for HAMD-17 total score,anxiety/somatization subfactor score and insomnia subfactor score in both groups(Wald χ2=315.226,495.481,82.420,P<0.01).After 4 weeks of treatment,HAMD-17 total score and anxiety/somatization subfactor score of study group were lower than those of control group,with statistically significant differences(Wald χ2=4.967,32.543,P<0.05 or 0.01),while no statistically significant difference was found in the insomnia subfactor score between two groups(Wald χ2=0.819,P=0.366).Significant time effects were reported on plasma IL-6 and IL-10 levels in both groups(Wald χ2=21.792,5.242,P<0.05 or 0.01).Compared with baseline data,a reduction in plasma IL-6 levels was detected in both groups(Wald χ2=22.015,6.803,P<0.01),and an increase in plasma IL-10 levels was reported in study group(Wald χ2=5.118,P=0.024)after 4 weeks of treatment.Conclusion Escitalopram combined with tcVNS therapy is effective in improving depressive symptoms,anxiety/somatization symptoms and sleep quality in patients with MDD.Additionally,it helps reduce plasma IL-6 levels and increase IL-10 levels.

Small‐world networks are of great significance in the field of neuroscience. As the universal nature of the human brain network, their heterogeneous pattern of change in patients with different diseases may satisfy the need for auxiliary objective diagnostic tests. In recent years, combining non‐invasive neuroimaging techniques (e.g., magnetic resonance imaging, electroencephalography, and magnetoencephalography) with graph‐theory‐based brain network topology analysis has provided a new direction for exploring neuroscience. In addition, researchers found more possible features for studying the diagnosis and treatment of neurological or psychiatric disorders based on the human brain's structural and functional connectivity patterns. Therefore, this review introduces the importance of small‐world networks in neuroscience and the contribution of brain network topology analysis in treating and diagnosing mental and neurological disorders. It also summarizes the effects of lifestyle habits, the environment, and some novel therapeutic modalities on small‐world brain networks. It concludes by discussing head‐movement errors in the brain network topology analysis.

Background Major depressive disorder (MDD) is a leading cause of disease burden in adolescents, with persistently rising prevalence. Anhedonia, core symptom of adolescent MDD, is associated with suicidality and poor clinical outcomes. Impaired sleep quality is proven to be a significant risk factor for adolescent MDD and potentially influence anhedonia symptoms. Understanding the interplay between sleep quality and anhedonia is crucial for early intervention and treatment. Methods This cross-sectional study recruited 200 drug-naïve adolescent MDD patients from Xijing Hospital. Depression, anhedonia and sleep quality were assessed during outpatient visits, using the Hamilton Depression Rating Scale, Snaith-Hamilton Pleasure Scale, and Pittsburgh Sleep Quality Index, respectively. Network analysis was applied to construct sleep quality network and its co-occurrence network with anhedonia. Centrality indices were computed to indicate central symptoms. Results Adolescent MDD patients exhibited moderate depression and anhedonia levels, and are heavily accompanied with sleep complaints. The sleep quality network identified “subjective sleep quality” as the most central factor, mainly due to prolonged “sleep latency” and shortened “sleep duration”. In the co-occurrence network, “sleep disturbances” had prominent bridging connection with anhedonia, suggesting its critical role in activating anhedonia symptoms. Conclusions Subjective sleep quality was the most central sleep complaints in adolescent MDD, while sleep disturbances were prominently associated with anhedonia. These findings underscore the importance of reducing sleep disturbances to alleviate anhedonia symptoms under clinical settings. Network analysis provides a nuanced understanding of the complex relationship of sleep quality and its association with anhedonia in adolescent MDD.

Understanding the relationship between genetic variations and brain abnormalities is crucial for uncovering the cross-scale pathophysiological mechanisms underlying schizophrenia. This cross-sectional study identifies brain structural correlates of individual variation in gene expression in schizophrenia and its clinical implication. RNA-sequencing data from blood samples, magnetic resonance imaging scans and clinical assessments were collected from 43 patients with schizophrenia, together with data from 60 healthy controls. Using RNA-sequencing data we show alterations in both gene-level and isoform-level expression between patients with schizophrenia and healthy controls (1,836 genes and 1,104 isoforms, false-discover-rate-adjusted P < 0.05). We also show differential gene expression to be associated with schizophrenia-related genomic variations (based on genome-wide association study data on 76,755 patients and 243,649 controls; regression coefficient (beta) = 0.211, P = 0.001) and differential brain gene expression (P < 0.001, hypergeometric test). Multivariate correlation analysis combining gene expression and brain imaging shows that transcriptional levels of differentially expressed genes significantly correlate with gray matter volume in the frontal and temporal regions of cognitive brain networks in patients with schizophrenia (P < 0.001, permutation test). Findings show a significant association between gene expression, gray matter volume and cognitive performance in patients (P = 0.031, permutation test). Our results suggest that genomic variants in individuals with schizophrenia are associated with alterations in the transcriptome, which plays a role in individual variations in macroscale brain structure and cognition, contributing to building a comprehensive, multi-omics marker for the assessment of schizophrenia.

Major depressive disorder (MDD) is a highly prevalent mental disorder with devastating consequences that often first manifest during adolescence. Anhedonia has emerged as one of the most promising symptoms of adolescent MDD, which means a longer time to remission， fewer depression-free days, and also increased risk of suicide ideas or actions. Research has shown that at least two-thirds of depressed adolescents have significant sleep-onset or sleep-maintenance problems. However, the association between sleep disorder and anhedonia, and the potential mediators are less understood. This is a cross-sectional study that includes 200 adolescents suffered from MDD between the ages of 12–17. We use Spearman’s test to explore the relationship among main variables. To evaluate the mediating effects of stress, we applied regression models and used bootstrap method to validate the significance of effects. Significant correlation exists among sleep disorder, stress, and anhedonia (P<0.05).The direct effect of sleep disorder on anhedonia was 0.214 (95

Objective To explore the impact of sluggish cognitive tempo(SCT)on the efficacy of atomoxetine in the treatment of attention-deficit/hyperactivity disorder(ADHD).Methods A prospective study was conducted.Pediatric patients aged 6-12 years with a diagnosis of ADHD were selected from the Department of Psychiatry,Xijing Hospital,Air Force Military Medical University from May 2020 to May 2023.All the patients were treated with atomoxetine for 8 weeks.ADHD symptoms and SCT symptoms were assessed by Swanson,Nolan,and Pelham-Ⅳrating scale(SNAP-Ⅳ)and SCT rating scale at baseline(before treatment),4 weeks and 8 weeks after treatment.Pearson correlation analysis was used to analyze the correlation between SCT and SNAP-Ⅳscores.Results A total of 61 pediatric patients were enrolled,including 10 cases of inattentive type and 51 cases of mixed type.Baseline SCT score was positively correlated with baseline SNAP-Ⅳscore(r=0.490,P＜0.001)and reduction rate of SNAP-Ⅳscore at week 8(r=0.670,P＜0.001).The total SCT score at week 8 was positively correlated with total SNAP-Ⅳscore at baseline(r=0.320,P=0.012).The baseline SCT score of patients with mixed type was positively correlated with reduction rate of SNAP-Ⅳscore at week 8(r=0.578,P＜0.001).Conclusions The severity of SCT symptoms is positively correlated with the SNAP-Ⅳreduction rate 8 weeks after atomoxetine treatment,which could be a predictor of the efficacy of atomoxetine.

Major psychiatric disorders create a significant public health burden, and mental disorders such as major depressive disorder, bipolar disorder, and schizophrenia are major contributors to the national disease burden. The search for biomarkers has been a leading endeavor in the field of biological psychiatry in recent decades. And the application of cross-scale and multi-omics approaches combining genes and imaging in major psychiatric studies has facilitated the elucidation of gene-related pathogenesis and the exploration of potential biomarkers. In this article, we summarize the results of using combined transcriptomics and magnetic resonance imaging to understand structural and functional brain changes associated with major psychiatric disorders in the last decade, demonstrating the neurobiological mechanisms of genetically related structural and functional brain alterations in multiple directions, and providing new avenues for the development of quantifiable objective biomarkers, as well as clinical diagnostic and prognostic indicators.

Abstract Background Inflammation has been implicated in the pathology of schizophrenia and may cause neuronal cell death and dendrite loss. Neuroimaging studies have highlighted longitudinal brain structural changes in patients with schizophrenia, yet it is unclear whether this is related to inflammation. We aim to address this question, by relating brain structural changes with the transcriptional profile of inflammation markers in the early stage of schizophrenia. Methods Thirty-eight patients with first-episode schizophrenia and 51 healthy controls were included. High-resolution T1-weighted magnetic resonance imaging (MRI) and clinical assessments were performed at baseline and 2 ~ 6 months follow-up for all subjects. Changes in the brain structure were analyzed using surface-based morphological analysis and correlated with the expression of immune cells-related gene sets of interest reported by previous reviews. Transcriptional data were retrieved from the Allen Human Brain Atlas. Furthermore, we examined the brain structural changes and peripheral inflammation markers in association with behavioral symptoms and cognitive functioning in patients. Results Patients exhibited accelerated cortical thickness decrease in the left frontal cortices, less decrease or an increase in the superior parietal lobule and right lateral occipital lobe, and increased volume in the bilateral pallidum, compared with controls. Changes in cortical thickness correlated with the transcriptional level of monocyte across cortical regions in patients (r = 0.54, p < 0.01), but not in controls (r = − 0.05, p = 0.76). In addition, cortical thickness change in the left superior parietal lobule positively correlated with changes in digital span-backward test scores in patients. Conclusions Patients with schizophrenia exhibit regional-specific cortical thickness changes in the prefrontal and parietooccipital cortices, which is related to their cognitive impairment. Inflammation may be an important factor contributing to cortical thinning in first-episode schizophrenia. Our findings suggest that the immunity-brain-behavior association may play a crucial role in the pathogenesis of schizophrenia.

How genetic risk variants may relate to brain abnormalities is crucial for understanding cross-scale pathophysiological mechanisms underlying schizophrenia. The present study identifies brain structural correlates of variation in gene expression in schizophrenia and its clinical significance. Of 43 patients with schizophrenia, RNA-seq data from blood samples, MRI, and clinical assessments were collected, together with data from 60 healthy controls. Gene expression differentiation between schizophrenia and health controls was assessed and cross-referenced to schizophrenia-related genomic variations (GWAS on 76,755 patients and 243,649 controls and GWAS on 22,778 East Asian patients) and brain gene expressions (samples from 559 patients and 175 individuals). Multivariate correlation analysis was employed to examine associations across gene expression, brain volume, and clinical assessments. Differentially expressed genes in blood samples from patients with schizophrenia were significantly enriched for genes previously reported in genome-wide association studies on schizophrenia ( P = 0.002, false discovery rate corrected) and were associated with gene expression differentiation in the brain ( P = 0.016, 5,000 permutations). Transcriptional levels of differentially expressed genes were found to significantly correlate with gray matter volume in the frontal and temporal regions of cognitive brain networks in schizophrenia ( q < 0.05, false discovery rate corrected). A significant correlation was further observed between gene expression, gray matter volume, and performance in the Wechsler Adult Intelligence Scale test ( P = 0.031). Our findings suggest that genomic variations in schizophrenia are associated with differentiation in the blood transcriptome, which further plays a role in individual variations in macroscale brain structure and cognition.

目的 探讨首发精神分裂症大学生患者的认知损害程度及其对相应教育策略的提示.方法 纳入40名首发精神分裂症大学生以及45名人口学特征匹配的健康大学生为研究对象.采用阳性与阴性症状量表(PANSS)评估首发精神分裂症大学生患者的临床症状严重程度.采用数字广度(顺背、倒背)、数字符号评估所有大学生的认知功能,并进行症状严重程度与认知功能间的相关性分析.结果 首发精神分裂症大学生患者的PANSS总积分、阳性症状积分、阴性症状积分、一般精神病理积分分别为(84.3±14.6)、(20.9±5.1)、(20.3±8.4)、(43.1±8.3)分.首发精神分裂症大学生患者的数字广度顺背与倒背原始分、数字符号的原始分、数字广度量表分、数字符号量表分均显著低于健康大学生(P<0.05).Pearson相关性分析未见首发精神分裂症大学生患者的认知功能与临床症状严重程度之间的相关性.结论 首发精神分裂症大学生患者存在工作记忆、注意、信息处理速度等方面的认知损害.探寻基于上述改变的患病学生针对性教育策略有助于降低病耻感,减少被歧视,促进患病学生的全程管理和早期及时干预,以期恢复其社会功能.

Objective:This study explored the impacts of repetitive transcranial magnetic stimulation (rTMS) on spontaneous brain activity in patients with major depressive disorder (MDD).Methods:This study was a randomized controlled study. First-episode, drug-na?ve patients with MDD ( n=27) and healthy controls ( n=30) were enrolled. The left dorsolateral prefrontal region was the stimulation target, and all participants received rTMS treatment for fifteen successive days. Hamilton Depression Rating Scale (HAMD 17) and resting-state functional magnetic resonance imaging (rs-fMRI) data were collected at baseline and the 15th day of the treatment. Changes in the spontaneous brain activity before and after the treatment were compared using the paired samples t-test or the independent sample t-test. The two indices of the amplitude of the low-frequency fluctuation (ALFF) and regional homogeneity(ReHo) were applied to reflect the spontaneous brain activity. Results:After treatment, the score of HAMD 17 (9.4±4.3) in MDD patients was significantly lower than that before the treatment (21.1±6.0), the average score decreased by (11.7±3.6), the remission rate was 40.74%, and the response rate was 74.07%. fMRI results: Before treatment, patients with MDD had significantly lower ALFF in the left superior frontal gyrus ( t=-8.14, P<0.001), higher ALFF in the left middle frontal gyrus and left precuneus ( t=5.79, 6.24, P<0.001), and lower ReHo in the left middle frontal and left middle occipital gyri ( t=-5.17, -6.11, P<0.001) than the corresponding values observed in healthy controls; After the rTMS treatment, the ALFF significantly increased in the left superior frontal gyrus ( t=7.32, P<0.001) and decreased in the left middle frontal gyrus and left precuneus ( t=-4.96,-5.14, P<0.001). Furthermore, ReHo significantly increased in the left middle frontal and left middle occipital gyri ( t=4.25,4.19, P<0.001) in patients with MDD. The score of HAMD 17 after treatment was significantly and negatively correlated with ALFF value of left superior frontal gyrus after treatment ( r=-0.390, P=0.044). Conclusion:Successive 15-day rTMS treatment could efficiently and effectively alleviate individual′s depressive symptoms. The left middle frontal gyrus may play an important role in abnormal spontaneous brain activity in MDD patients; and left superior frontal gyrus function may be essential in improving depressive symptoms.

INTRODUCTION:Gut microbial disturbance has been established as potential pathogenesis of mental disorders. However, the signatures and differences regarding patients with schizophrenia (SCH) or bipolar disorder (BD) in emerging adulthood as well as their subtypes have been poorly addressed.METHODS:In the present study, stool samples obtained from 63 emerging adult patients with schizophrenia (SCH), 50 with bipolar disorder (BD), and 40 healthy controls (HC) were analyzed by 16 S rRNA gene sequencing; psychiatric symptoms and psychological, social, and professional functioning were also assessed.RESULTS:We found that gut microbiota composition was remarkably changed in the patients with SCH and BD. Moreover, the distinct gut microbiome signatures and their potential function in bipolar depression (BP-D) and SCH with predominantly negative symptoms (SCH-N) as well as bipolar mania (BP-M) and SCH with predominantly positive symptoms (SCH-P) were also observed. Furthermore, we identified diagnostic potential biomarkers that can distinguish BD from HC (38 genera, AUC = 0.961), SCH from HC (32 genera, AUC = 0.962), and BD from Scheme (13 genera, AUC = 0.823). Potential diagnostic biomarkers that can distinguish BD-D from SCH-N (16 genera, AUC = 0.969) and BD-M from SCH-P (31 genera, AUC = 0.938) were also identified.CONCLUSION:This study provides further understanding of abnormal gut microbiome in emerging adulthood patients with SCH and BD and lay the potential foundation for the development of microbe-based clinical diagnosis for BD and SCH.

Introduction: Cognitive decline is the core schizophrenia symptom, which is now well accepted. Holding a role in various aspects of cognition, lentiform nucleus (putamen and globus pallidus) dysfunction contributes to the psychopathology of this disease. However, the effects of lentiform nucleus function on cognitive impairments in schizophrenia are yet to be investigated.Objectives: We aim to detect the fractional amplitude of low-frequency fluctuation (fALFF) alterations in patients with schizophrenia, and examine how their behavior correlates in relation to the cognitive impairments of the patients.Methods: All participants underwent magnetic resonance imaging (MRI) and cognitive assessment (digit span and digit symbol coding tests). Screening of brain regions with significant changes in fALFF values was based on analysis of the whole brain. The data were analyzed between Jun 2020 and Mar 2021. There were no interventions beyond the routine therapy determined by their clinicians on the basis of standard clinical practice.Results: There were 136 patients (75 men and 61 women, 24.1 ± 7.4 years old) and 146 healthy controls (82 men and 64 women, 24.2 ± 5.2 years old) involved in the experiments seriatim. Patients with schizophrenia exhibited decreased raw scores in cognitive tests (p < 0.001) and increased fALFF in the bilateral lentiform nuclei (left: 67 voxels; x = −24, y = −6, z = 3; peak t-value = 6.90; right: 16 voxels; x = 18, y = 0, z = 3; peak t-value = 6.36). The fALFF values in the bilateral lentiform nuclei were positively correlated with digit span-backward test scores (left: r = 0.193, p = 0.027; right: r = 0.190, p = 0.030), and the right lentiform nucleus was positively correlated with digit symbol coding scores (r = 0.209, p = 0.016).Conclusion: This study demonstrates that cognitive impairments in schizophrenia are associated with lentiform nucleus function as revealed by MRI, involving working memory and processing speed.

目的:探讨经颅直流电刺激(tDCS)联合盐酸舍曲林对老年抑郁症患者的疗效及对认知功能和血清脑源性神经营养因子(BDNF)水平的影响.方法:62例老年抑郁症患者随机分为tDCS组和伪tDCS组;两组在舍曲林治疗基础上分别给予真、伪tDCS治疗4周.分别于治疗前及治疗后1、2、4周末进行汉密尔顿抑郁量表(HAMD)、治疗中出现的症状量表(TESS)评估;治疗前后采用数字广度测验(DST)及威斯康星卡片分类测试(WCST)评估认知功能;治疗前后测定两组血清BDNF水平.结果:治疗前两组各项评估及检查结果比较差异无统计学意义.治疗后,两组HAMD评分均明显低于治疗前,且tDCS组明显低于伪tDCS组(P均<0.05);两组认知功能均较治疗前明显改善,其中tDCS组DST中的正序评分及总分明显高于伪tDCS组;两组血清BDNF水平均较前明显升高且tDCS组明显高于伪tDCS组(P均<0.05);两组不良反应发生率差异无统计学意义.结论:盐酸舍曲林联合tDCS治疗老年抑郁症疗效以及认知功能改善更优,可能与联合治疗提高了血清BDNF水平有关.

The protective effects of repetitive transcranial magnetic stimulation (rTMS) on myelin integrity have been extensively studied, and growing evidence suggests that rTMS is beneficial in improving cognitive functions and promoting myelin repair. However, the association between cognitive improvement due to rTMS and changes in brain lipids remains elusive. In this study, we used the Y-maze and 3-chamber tests, as well as a mass spectrometry-based lipidomic approach in a CPZ-induced demyelination model in mice to assess the protective effects of rTMS on cuprizone (CPZ)-induced cognitive impairment and evaluate changes in lipid composition in the hippocampus, prefrontal cortex, and striatum. We found that CPZ induced cognitive impairment and remarkable changes in brain lipids, specifically in glycerophospholipids. Moreover, the changes in lipids within the prefrontal cortex were more extensive, compared to those observed in the hippocampus and striatum. Notably, rTMS ameliorated CPZ-induced cognitive impairment and partially normalized CPZ-induced lipid changes. Taken together, our data suggest that rTMS may reverse cognitive behavioral changes caused by CPZ-induced demyelination by modulating the brain lipidome, providing new insights into the therapeutic mechanism of rTMS.

重复经颅磁刺激(rTMS)作为一种治疗精神分裂症(SZ)的方法,已被越来越多地应用于精神分裂症的病理生理机制及局部神经调节的研究之中.rTMS对治疗SZ的阳性症状(包括幻觉、妄想等)具有较好的疗效,而且对SZ的阴性症状也有一定改善作用.然而,如何精确定位和刺激强度的选择以及哪些SZ患者最适合rTMS治疗等问题尚未明确.运用MRI等影像学方法,从脑结构、功能和代谢等角度去探究rTMS的治疗作用机制及疗效预测,对于rTMS定位和评估治疗结果等具有重要价值.本文复习国内外相关文献,旨在就SZ患者进行rTMS治疗前后的头颅MRI研究进展进行综述,并阐述了rTMS的潜在作用机制、疗效预测手段和神经导航定位等方面的最新发现,主要进展有额叶皮层厚度的改变、左半球颞顶皮层及背外侧前额叶皮层的功能障碍与精神分裂症rTMS治疗的作用机制及疗效有关,基于MRI的神经导航定位有利于提高疗效.