BACKGROUND:Accumulating evidence indicates that inflammation, immune dysfunction, and metabolic disturbances are associated with major depressive disorder (MDD). Subtype analysis can reduce disease heterogeneity in MDD, significantly improving response prediction and personalized treatment. However, there is still a lack of robust strategies to effectively integrate diverse multi-omics data for subtype analysis. Therefore, multi-omics data (mass cytometry by time-of-flight [CyTOF], cytokine, and metabolomics) were used for depression subtype analysis, with the goal of explaining the heterogeneity of MDD and predicting treatment response. METHODS:134 adult patients with MDD were enrolled according to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5). Of these, 83 patients underwent CyTOF, cytokine, and metabolomics testing, and were included for subsequent subtype analysis. The 17-item Hamilton depression rating scale (HAMD-17) score was used to assess the severity of depressive symptoms at baseline (w0), 4 weeks (w4), and 8 weeks (w8). Multiomics subtypes (MoSs) for MDD patients were identified using 10 state-of-the-art algorithms from the R package "MOVICS". RESULTS:Three MoS subtypes (MoS1-3) were found in this study. MoS2 was associated with a poorer response, whereas MoS1 and MoS3 demonstrated better efficacy at 8 weeks (χ2 = 8.03, p = 0.020). Multivariable logistic regression analysis was performed on both weighted and unweighted samples, confirming that the MoS subtype was an independent predictor of treatment outcome. Compared with MoS1, the patients in MoS2 had a significantly reduced likelihood of treatment response (IPW weighted: OR = 0.09, 95% CI: 0.02-0.34, p < 0.001; Unweighted: OR = 0.14, 95% CI: 0.03-0.53, p = 0.005), while no significant difference was found in MoS3. Biologically, MoS2 was characterized by significantly elevated triglycerides and an increase in regulatory T-cell subsets; MoS1 was characterized by enhanced T-cell activity and elevated growth factors (e.g., bFGF); and MoS3 was characterized by elevated monocytes, reduced T-cell and Treg levels, and modest cytokine levels. CONCLUSIONS:This exploratory study identified three subtypes of MDD with distinct biological profiles and differential treatment responses-most notably poorer outcomes in the MoS2 subgroup. Although this classification could help explain some of the heterogeneity in depression and might be associated with different antidepressant treatment outcomes, these preliminary findings require validation in independent cohorts.

The association between long-term use of benzodiazepines (BDZs) and cognitive function in patients with schizophrenia has not been fully characterized. This study aimed to investigate the relationship between long-term BDZs use and cognitive function in schizophrenia. Data were derived from an observational study of treatment with atypical antipsychotics in Chinese patients with schizophrenia (SALT-C). Fifty-seven patients with long-term use of BDZs (≥60 days) were included, and 57 BDZs non-users were matched using propensity scores for age, sex, disease duration, and atypical antipsychotics received. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA); psychotic symptoms, illness severity, and psychosocial functioning were assessed with the Positive and Negative Syndrome Scale (PANSS), the Clinical Global Impression-Severity (CGI-S) scale, and the Personal and Social Performance (PSP) scale. Between-group comparisons were performed using independent-samples t-tests or Mann–Whitney U tests. Spearman correlation analysis was performed to assess the association between benzodiazepine dose and MoCA total scores among BDZ users.Factors associated with MoCA total scores were examined using multiple linear regression models. The long-term BDZs user group showed a significantly lower total MoCA score [16.02 (6.69)] than the BDZs non-user group [19.33 (7.11)] (FDR-adjust p = 0.048). No significant between-group differences were observed in total scores on the PANSS, CGI-S, or PSP (all p > 0.05). No significant association was observed between benzodiazepines dose and MoCA scores (r = −0.098, p = 0.466). Multiple linear regression revealed that long-term BDZs use (β = −0.182, p = 0.008), PANSS total score (β = −0.217, p = 0.003) and anticholinergic burden (β = −0.199, p = 0.008) were independently associated with poorer cognitive performance, whereas years of education showed a positive association with cognitive performance (β = 0.460, p < 0.001). Long-term BDZs use is associated with poorer cognitive performance in patients with schizophrenia, suggesting that cognitive function should be monitored and prolonged treatment avoided.

Evidence suggests that attenuated mismatch negative (MMN) waves have a close link to auditory verbal hallucinations (AVH) and their clinical outcomes, especially impaired neural oscillations such as θ, β representing attentional control. In current study, thirty patients with schizophrenia and AVH (SZ) and twenty-nine healthy controls (HC) underwent multi-feature MMN paradigm measurements including frequency and duration deviant stimuli (fMMN and dMMN). Clinical symptoms and MMN paradigm were followed up among SZ group after 8-week treatment. Results demonstrated that hallucinating patients exhibited attenuated dMMN amplitudes across Fz (p = 0.010), F1 (p = 0.020) and F2 (p = 0.014) electrodes, which were trendily recovered after treatment. Meanwhile, θ band and TBR at frontal fMMN and right temporal dMMN were significantly reduced in SZs. After treatment, SZs showed reduced scores of Hoffman's Auditory Hallucinations Rating Scale (AHRS), with a remarkable recovery in right temporal TBR of dMMN (p = 0.042) and a trending change in frontal TBR of fMMN (p = 0.090). The β band was decreased in dMMN (p = 0.035) by time. Additionally, P3 scores of Positive and Negative Syndrome Scale (PANSS) were negatively correlated with θ band of fMMN at baseline. Baseline scores of AHRS negatively predicted changes of dMMN amplitude after treatment, and changes of β band in left temporal dMMN predicted the reduction in scores of PANSS negative scale. These findings supported that deficits in θ oscillation and TBR during auditory attention process were crucial to clinical progression of schizophrenia with AVH.

Prolactin elevation associated with antipsychotic use significantly affects medication adherence and long-term treatment outcomes in patients with schizophrenia. The currently available data are insufficient to guide the monitoring and management of elevated prolactin levels in patients on antipsychotic medications. This study aimed to explore the patterns of prolactin level elevation associated with nine second-generation antipsychotics (SGAs) in a real-world setting and compare the associated risks. This retrospective cohort study utilized data from the inpatient electronic medical records of a large mental health center in China from 2007 to 2019. The study included patients diagnosed with schizophrenia (ICD-10 criteria) who received SGA therapy and whose serum prolactin levels were measured. Exposures were the use of nine specific SGAs (amisulpride, risperidone, paliperidone, ziprasidone, olanzapine, perospirone, quetiapine, clozapine, or aripiprazole), including polytherapy and monotherapy. The primary outcome was incident prolactin elevation in patients during hospitalization. An adjusted stratified Cox proportional hazards regression analysis was used to compare the hazard ratios (HRs) of prolactin level elevation across the nine SGAs. In addition, a dose–response analysis of these SGAs was conducted using the defined daily dose (DDD) method. Dose categories were as follows: < 0.6 DDDs/day (low dose), 0.6 to < 1.1 DDDs/day (medium dose), and ≥ 1.1 DDDs/day (high dose). This study included 6489 patients with schizophrenia (mean [SD] age, 35.1 [14.2] years; 3396 males [52.3

BACKGROUND:A subset of first-episode schizophrenia (FES) patients responds poorly to initial antipsychotic therapy. The hippocampus is an early-affected region in schizophrenia, yet neurobiological markers predicting treatment response remain unclear. Arterial spin labeling (ASL) magnetic resonance imaging (MRI) allows non-invasive measurement of cerebral blood flow (CBF), but studies on hippocampal perfusion in acute FES, particularly in those receiving electroconvulsive therapy (ECT) with antipsychotics, are limited. METHODS:Fifty FES patients and 28 age- and sex-matched healthy controls underwent high-resolution ASL MRI to assess hippocampal CBF. Patients received either antipsychotics alone (n = 20) or in combination with ECT (n = 30). MRI Scans were acquired before and after six weeks of treatment. Analysis of covariance and linear mixed-effects models were used to assess group differences and longitudinal effects, adjusting for relevant covariates. RESULTS:At baseline, FES patients exhibited significantly lower hippocampal CBF compared to healthy controls, with no significant difference in hippocampal volume. Longitudinal analysis revealed a significant group × time interaction for hippocampal CBF. Post hoc analysis indicated a significant increase in CBF after treatment in the FES group, while hippocampal volume remained unchanged. CBF changes were not significantly correlated with symptom reduction. We further examined the group differences in longitudinal changes between the ECT + Drug group and the Drug group, however no significant results were found. CONCLUSION:Our findings suggest that functional, but not structural, hippocampal alterations are present in early schizophrenia and may be responsive to treatment. These preliminary results should be interpreted cautiously and validated in larger samples with extended follow-up and neurochemical assessments.

BACKGROUND:Blonanserin, a novel antipsychotic, has demonstrated efficacy in treating both positive and negative symptoms. However, limited research exists on its dose-dependent effectiveness and safety in patients with and without prominent negative symptoms (PNS). AIM:To evaluate the effectiveness and safety of blonanserin monotherapy for first-episode schizophrenia in real-world clinical settings and to explore the efficacy and safety of different doses of blonanserin for patients with PNS and without PNS. METHODS:A 12-week, multicenter, prospective post-marketing surveillance was conducted. In this study, we included patients with first-episode schizophrenia who received blonanserin monotherapy. Patients were divided into those with PNS and without PNS, based on the Brief Psychiatric Rating Scale (BPRS) negative symptoms subscale scores. Additionally, patients were labeled as high-dose and low-dose groups according to the maximum daily dose they received. Effectiveness was assessed using the BPRS, and safety was evaluated through the incidence of adverse drug reactions (ADRs). RESULTS:A total of 653 patients were included in the analysis, with 613 completing the study. The BPRS total score decreased significantly from 47.94 ± 16.31 at baseline to 26.88 ± 9.47 at 12 weeks (P < 0.001). A significant interaction of PNS × dose × time was observed for BPRS total scores (F = 3.47, P = 0.040) and negative symptom subscale scores (F = 6.76, P = 0.002). In the PNS group, the high-dose group showed greater reductions in BPRS total scores (P = 0.001) and negative symptom subscale scores (P = 0.003) than the low-dose group in week 12. In the without PNS group, no significant difference was observed between the high-dose and low-dose groups at any visit. Most adverse reactions were mild or moderate, with extrapyramidal symptoms (9.3%) being most common; 1.5% of patients gained ≥ 7% body weight at 12 weeks. CONCLUSION:Blonanserin effectively alleviated the clinical symptoms of first-episode schizophrenia with an acceptable safety profile. High-dose blonanserin is particularly beneficial for patients with PNS in the acute phase of first-episode schizophrenia. However, due to the limitation of ADR reporting the real world, the ADR incidence observed in this study may be underestimated.

While neuroimaging offers valuable insights into brain alterations associated with psychiatric disorders, its translation into routine clinical practice remains challenging. we developed the patch-based hierarchical network (PHN), a deep learning framework for classifying multiple psychiatric disorders from structural MRI. Trained on a large, curated dataset (n = 2,490) of four major disorders and controls, the PHN’s generalizability was confirmed on independent research datasets (n = 1,346) and real-world clinical data (n = 344). The model demonstrated robust performance, showing promise in real-world evaluations by reflecting complex presentations such as comorbidities. A key contribution is the implementation and deployment of a closed-loop, neuroimaging-based diagnostic support system integrating the PHN into an active clinical workflow. This work provides a tangible step toward bridging the research-to-practice gap, leveraging artificial intelligence to provide objective support for psychiatric diagnosis.

BACKGROUND:Oxidative stress and inflammation have been found to be involved in the development of major depressive disorder (MDD). The aim of this study was to investigate the peripheral levels of oxidative stress and the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant system markers in patients with MDD and to evaluate the changes in these markers after 12 weeks of antidepressant treatment. METHODS:We consecutively enrolled 104 drug-naïve or drug-free patients with an acute episode of MDD and 50 healthy controls (HCs). Plasma levels of Nrf2, phospho-Nrf2 (p-Nrf2), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), malondialdehyde (MDA), phospholipase A2 (PLA2) and cyclooxygenase-2 (COX-2), were measured with the enzyme-linked immunosorbent assay. RESULTS:Patients with MDD exhibited lower levels of the antioxidant system Nrf2, p-Nrf2, HO-1, SOD and higher levels of oxidative stress markers COX-2, PLA2, MDA compared to HCs (all p < 0.001). HO-1 levels differed significantly among melancholic, anxious, and atypical depression (p = 0.002). In addition, we found a negative correlation between somatic symptoms in HAMA scores and Nrf2 levels in MDD group (p = 0.04). At 12 weeks, COX-2 levels significantly increased in the non-remission group compared to baseline (p = 0.039), whereas no significant changes were observed in the remission group. CONCLUSIONS:Peripheral oxidative stress and the Nrf2 antioxidant system were found to be dysregulated in patients with MDD. The Nrf2 antioxidant system might be a protective factor for somatic symptoms in MDD, whereas COX-2 might be a risk factor for poor antidepressant efficacy.

Background: Previous studies have shown a lower hemodynamic response in patients with major depressive disorder (MDD) during cognitive tasks. However, the mechanism underlying impaired hemodynamic and neural responses to cognitive tasks in MDD patients remains unclear. Succinate dehydrogenase (SDH) is a key biomarker of mitochondrial energy generation, and it can affect the hemodynamic response via the neurovascular coupling effect. In the current study, cerebral hemodynamic responses were detected during verbal fluency tasks (VFTs) via functional near-infrared spectroscopy (fNIRS) and SDH protein levels were examined in serum from MDD patients to quickly identify whether these hemodynamic alterations were related to mitochondrial energy metabolism. Methods: Fifty patients with first-episode drug-na & iuml;ve MDD and 42 healthy controls (HCs) were recruited according to inclusion and exclusion criteria. The 17-item Hamilton Depression Rating Scale (17-HDRS), Hamilton Anxiety Rating Scale (HAMA) and Inventory of Depressive Symptomatology-Self Report (IDS-SR) were used to assess the clinical symptoms of the patients. All participants underwent fNIRS measurements to evaluate cerebral hemodynamic responses in the frontal and temporal cortex during VFTs; moreover, SDH protein levels were measured using an enzyme-linked immunosorbent assay. Results: Activation in the frontal-temporal brain region during the VFTs was lower in patients with MDD than in HCs. The SDH level in the serum of MDD patients was also significantly lower than that in HCs (p = 0.003), which significantly affected right lateral frontal (p = 0.025) and right temporal (p = 0.022) lobe activation. Both attenuated frontal-temporal activation during the VFTs (OR = 1.531) and lower SDH levels (OR = 1.038) were risk factors for MDD. Conclusions: MDD patients had lower cerebral hemodynamic responses to VFTs; this was associated with mitochondrial dysfunction, as indicated by SDH protein levels. Furthermore, attenuated hemodynamic responses in frontotemporal regions and lower SDH levels increased the risk for MDD. Limitations: The sample size is relatively small. SDH protein levels in peripheral blood may not necessarily reflect mitochondrial energy generation in the central nervous system.

Aim Comparing the anxiety and depression severity and their impact on subsequent birth outcomes in pregnant women before and during Omicron wave in Shanghai in 2022.Methods The depression-anxiety symptoms networks were compared between the pregnant women during the outbreak period (outbreak group; n = 783) and a matched control group of pregnant women before the outbreak (pre-outbreak group; n = 783). The impact of baseline mental state on follow-up pregnancy and neonatal outcomes was also explored by logistic regression.Findings Levels of depression and anxiety between the two groups were not significant different. Network analysis showed that central symptom "trouble relaxing" and bridge symptom "depressed mood" shared by both groups. Different symptom associations in different periods of the pandemic. Total scores and sub-symptom scores of prenatal depressive and anxious severities increased the odds ratios of maternal and neonatal syndromes. The influence of mental state on gestational and neonatal outcomes differed across different pandemic periods.Conclusion The Omicron wave did not have a significant negative impact on the depressive and anxious mood in pregnant women. Targeting central and bridge symptoms intervention may be effective in reducing their adverse effects on co-occurring of anxious and depressive mood and birth outcomes.

In the era of digitalization, the Internet has changed people's lifestyle and circadian rhythm, and has also brought the global problem of technology addiction. Many studies have shown that chronotype is significantly related to specific technology addiction (such as Internet, smartphones, video games and social media), which makes chronotype become a new perspective to explore the occurrence, development and maintenance of technology addiction. Individuals can be classified into three chronotypes: morning type (M-type), neither type (N-type) and evening type (E-type). Most studies showed that E-type was the risk factor in the onset and maintenance of problematic technology use. At present, most of the prior research focused on the relationship between chronotype and technology addiction, and there were few studies on the mechanism. Based on this situation, this paper discusses physiological factors (such as reward system), psychological factors (such as depression), individual factors (such as gender, age, personality traits and sleep patterns) and environmental factors (such as parental style), analyzes the relationship with Interaction of Person-Affect-Cognition-Execution (I-PACE) model and life history theory from the perspectives of etiology and evolution, and reviews the relationship between chronotype and technology addiction and its mechanism.

Background: Major depressive disorder (MDD) is a disabling disease with impaired recognition of emotional facial expressions. However, the evidence is heterogeneous, regarding the mechanism of emotional processing in MDD. Focusing on patients with first-episode drug-naive MDD, we used functional near-infrared spectroscopy (fNIRS) to investigate whether MDD have characteristic patterns in cerebral activation under facial emotion recognition task (FERT).Methods: Thirty-five patients with first-episode drug-naive MDD and 39 healthy controls (HCs) underwent fNIRS measure to evaluate cerebral hemodynamic response in the frontal and temporal cortex during FERT. The 17item Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale and Inventory of Depressive Symptomatology-Self Report were applied to assess the symptoms of the patients. Cognitive functions were assessed using THINC-integrated tool.Results: Hypoactivation in the medial frontal was observed in patients with MDD during recognition of fearful faces relative to neutral faces (F-N faces). Specifically, we found more right lateralized activation in the medial frontal cortex among patients with MDD compared to HCs. Further, the medial frontal activation under the condition of F-N faces was positively correlated to scores of digit symbol substitution test, and negatively relative to severity of depressive symptoms in MDD group. Limitations: Our study is cross-sectional designed, and has a relatively small sample size.Conclusions: We found abnormal patterns in the medial frontal activation of patients with first-episode drug-naive MDD in recognition of F-N faces, which correlates with performance in cognitive function and depressive symptoms.

目的 通过随机双盲对照研究,探索左前额叶高频重复经颅磁刺激(repetitivetranscranial magnetic stimulation,rTMS)对阿尔茨海默病(Alzheimer's disease,AD)的精神行为症状(behavioral and psychological symptoms of dementia,BPSD)的疗效及安全性.方法 筛选2020 年4 月至2022 年1 月在上海市精神卫生中心老年科住院的AD患者45 例,年龄60～85 岁,符合简明精神状况量表(MMSE):2～24 分;临床痴呆评定量表(CDR):1～3 分;Hachinski 缺血指数量表(HIS)≤4 分;痴呆病理行为评定量表(BEHAVE-AD)≥8 分.采用随机、双盲、伪刺激对照的临床实验设计,将患者分为rTMS干预真刺激组和伪刺激组,每天治疗1 次,持续约22 min左右,每周5 次,4 周,共20 次,最终完成实验的患者28例(真刺激组13 例,伪刺激组15 例).2 组均给予常规药物治疗,在基线期和4 周干预结束后,分别进行疗效和安全性评估.结果 干预后,真刺激组的神经精神症状量表(NPI)、AD病理行为评分表(BEHAVE-AD)及柯恩-曼斯菲尔德激越情绪行为量表(CMAI)的减分高于伪刺激组,分别为(28.85±8.23)vs(8.20±6.79)、(12.85±7.76)vs(7.07±4.57)、(16.31±6.68)vs(9.47±6.86),差异均存在统计学意义(p＜0.05);真刺激组的NPI量表妄想、激越、情绪不稳和异常行为4 个因子减分高于伪刺激组,差异存在统计学意义(p＜0.05);真刺激组抗精神病药物日剂量增量低于伪刺激组(9 vs 50),差异存在统计学意义(p＜0.05);真刺激组不良反应为短暂的头皮发紧 2 例和轻度头痛 1 例,伪刺激组为短暂的头皮发紧1 例和面部肌肉收缩感1 例,2 组患者均能耐受,发生率无统计学差异,均无严重不良事件.结论 左前额叶高频rTMS可能可以改善阿尔茨海默病患者精神行为症状,是一种安全有效的治疗方法.

Hippocampal deficits and metabolic dysregulations such as dyslipidemia have been frequently reported in schizophrenia and are suggested to contribute to the pathophysiology of schizophrenia. Hippocampus is particularly susceptible to environmental challenges including metabolism and inflammation. However, evidence linking hippocampal alterations and metabolic dysregulations are quite sparse in drug-naïve schizophrenia. A total of 166 drug-naïve patients with first-episode schizophrenia (FES) and 78 healthy controls (HC) underwent measures for several serum metabolic markers, structural and resting-state functional magnetic resonance imaging (rs-fMRI), as well as diffusion tensor imaging (DTI). Seed-to-voxel functional connectivity (FC) and probabilistic tractography were performed to assess the functional and microstructural connectivity of the bilateral hippocampi. Clinical symptoms were evaluated with Positive and Negative Syndrome Scale (PANSS). Patients with FES showed significantly decreased total cholesterol (Chol) level. Patients showed elevated FC between the left hippocampus and bilateral thalami while showing decreased microstructural connectivity between the left hippocampus and bilateral thalami. Multiple regression analyses showed that FC from the left hippocampus to the right superior frontal gyrus (SFG), bilateral frontal pole (FP), and right thalamus were negatively associated with the Chol level, while no association was observed in the HC group. Our study validated alterations in both functional and microstructural thalamo-hippocampal connectivities, and abnormal cholesterol level in FES. Moreover, decreased cholesterol level is associated with elevated thalamo-hippocampal functional connectivity in patients with FES, suggesting that dyslipidemia may interact with the hippocampal dysfunction in FES.

The current clinical diagnosis of psychiatric disorders relies heavily on subjective assessment of symptoms. While neuroimaging has made an essential contribution to characterizing the brain of psychiatric disorders, it does not currently serve the clinical diagnosis of major psychiatric disorders. Here, we report a neuroimaging-aided diagnostic system for major psychiatric disorders designed for clinical needs. We developed novel deep learning networks with attentional mechanisms and applied them to a large-scale, single-center neuroimaging dataset containing four major psychiatric disorders and healthy groups (n=2490). Both cross-validation and extensive independent validation using multiple open-source datasets (n = 1972) showed that the system could accurately identify any one of the four diagnostic categories and healthy population from brain structural imaging. For the first time, we have constructed an automatic neuroimaging-aid diagnostic system that considers common issues in practice, such as co-morbid diagnoses and the discrimination between specific suspected diagnoses. Furthermore, real-world applications have validated the system’s effectiveness. These works contribute to the translation of brain research to objective diagnostic aids for psychiatric disorders.

Emerging evidence suggested that people with severe mental disorders were more vulnerable to the negative effects of the COVID-19 pandemic. However, few researches investigated the influence of global pandemics on people at clinical high risk (CHR) for psychosis. This study aimed to investigate the impact of the COVID-19 pandemic on clinical symptoms, psychological distress, and eye-tracking characteristics in CHR individuals and healthy participants. Forty-nine CHR individuals and 50 healthy controls (HC) were assessed by PTSD Checklist for DSM-5 (PCL-5), Perceived Stress Scale, 10-item version (PSS-10), and Coronavirus Impact Scale (CIS). Eye movement performances were measured by the tests of fixation stability, free-viewing, and anti-saccade. According to the mean score of CIS, participants were stratified into high-impact (n = 35) and low-impact (n = 64) subgroups. Compared with the HC group, CHR participants reported significantly higher levels of post-traumatic symptoms caused by the COVID-19 pandemic and showed abnormalities in most of the eye movement indexes. Among the altered indexes, the saccade amplitude of fixation stability test (far distractor), the scan path length of free-viewing test, and the accuracy of anti-saccade test were negatively affected by the severity of impact level in the CHR group. Moreover, the altered eye movement indexes were significantly associated with the total scores of CIS, PCL-5, and subscales of the Scale of Prodromal Syndromes (SOPS) among CHR individuals. Overall, our findings suggested the negative impact of the COVID-19 pandemic on the eye movement characteristics of CHR individuals. The present study provides valuable information on physiological distress related to the COVID-19 pandemic and sensitive neuropsychological biomarkers that interacted with social and environment stress in the CHR population.

精神分裂症是一种常见的重性精神障碍,发病机制未明.近年来,越来越多的证据表明精神分裂症与炎症以及色氨酸犬尿氨酸代谢通路之间存在联系.色氨酸代谢产物犬尿酸是N-甲基-D-天门冬氨酸受体(NMDAR)的内源性拮抗剂.在炎症作用下,偏向犬尿酸生成的色氨酸犬尿氨酸代谢失衡会导致NMDAR失能,这可能是精神分裂症的发病机制之一.因此,色氨酸犬尿氨酸代谢通路和炎症可以作为药物靶点,应用在精神分裂症的治疗过程中.现从色氨酸犬尿氨酸代谢通路入手,探讨炎症对犬尿氨酸代谢的影响,总结以此为靶向的药物疗效,呈现色氨酸犬尿氨酸代谢通路失调与炎症在精神分裂症中的研究进展.

The purpose of this study is to investigate the complex connection between apathy and cognitive decline that remains unclear. A total of 1057 non-dementia elderly from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database received up to 13 years of follow-up and were divided into an apathy negative (−) group of 943 participants and an apathy positive (+) group of 114 participants through the Neuropsychiatric Inventory (NPI)-apathy subitem. Cerebrospinal fluid (CSF) AD biomarkers and amyloid β (Aβ) PET were measured, and their longitudinal changes were assessed using linear mixed-effects models. Risk factors for cognitive decline and apathy conversion were explored through the Cox proportional hazards model. Mediation effects of Aβ pathology on cognition were investigated using the causal mediation analysis. Apathy syndrome was associated with faster impairment of cognition and elevation of the Aβ burden. The effects of apathy on cognitive function and life quality were mediated by Aβ pathology, including CSF Aβ 42 /total tau ratio, and Aβ deposition in the prefrontal regions. Apathy syndrome was the risk factor for cognitive deterioration; meanwhile, frontal Aβ burden was the risk factor for apathy conversion. Apathy syndrome is an early manifestation of cognitive decline and there are bidirectional roles between apathy syndrome and Aβ pathology. Prefrontal Aβ pathology influenced the pathway from apathy to cognitive decline.

The aim of the study was to conduct a multicenter randomized double-blinded placebo-controlled clinical study to evaluate the efficacy of a generic form of escitalopram in treating major depressive disorder (MDD). A total of 390 MDD patients admitted to hospitals in six cities in China were randomized to receive the generic version of escitalopram, the proprietary form of escitalopram (Lexapro) or placebo. During the 8-week treatment, the Hamilton rating scale for depression-17 (HAM-D17), Hamilton Anxiety Rating Scale (HAMA), Montgomery-Åsberg Depression Rating Scale (MADRS), Clinical Global Impressions scale (CGI), current visual analogue scale pain levels (VAS-P1) and Sheehan Disability Scale (SDS) assessments were performed at week 0, 1, 2, 4, 6 and 8 to evaluate treatment responses. HAM-D17, MADRS, HAMA and CGI-S levels of patients who received escitalopram or Lexapro decreased steadily during 8 weeks’ treatment, whereas the placebo group showed a relatively smaller reduction of these levels (P < 0.001). SDS and VAS-P1 both decreased after treatment with generic escitalopram or proprietary escitalopram Lexapro. Our results indicated that both the generic escitalopram and proprietary escitalopram Lexapro had potent efficacy in treating MDD.

BackgroundLaboratory viral nucleic acid testing (NAT), such as the nasopharyngeal swab test, is now recommended as the gold standard for the diagnosis of Coronavirus disease-2019 (COVID-19). However, the nasopharyngeal swab testing process may cause some discomfort.ObjectiveTo investigate the influence of nasopharyngeal swab tests on the anxiety and pain felt by psychiatric medical staff.MethodsA total of 174 psychiatric medical staff (namely 97 doctors, 68 nurses, and nine administrators) and 27 controls were included in the current study. A self-designed questionnaire was used to collect their general demographic information (age, gender, marriage, occupation, profession, smoking history, alcohol consumption history, tea drinking history, previous history of anxiety and depression) as well as their subjective experience, such as nausea, vomiting, coughing, worry, fear, etc, during nasopharyngeal swab collection. The Numerical Rating Scale (NRS) and the State-Trait Anxiety Inventory (STAI) were used to assess the subjects’ pain and state anxiety, respectively.ResultsThere were no statistical differences (p>0.05) in age, marriage, smoking history, a history of anxiety and depression, pain scores, and anxiety scores between different professions and genders. The results of partial correlation analysis (controlled for gender and history of depression or anxiety) indicated that the male gender was negatively correlated with being anxious (r=-0.148, p=0.037) and nervous (r=-0.171 p=0.016), although there was no significant difference in pain and anxiety between men and women. In addition, marriage might help women resist negative emotions.Conclusions1) There will be mild discomfort during nucleic acid testing, but not enough to cause pain and anxiety; 2) women are more likely to be anxious and nervous during the nucleic acid testing.