Neuropsychiatric Disease and Treatment最新文献

Purpose: Subthreshold depression (StD), depressive symptoms below the diagnostic threshold for major depressive disorder (MDD), is associated with functional impairment and increased risk of MDD onset, but its physiological and cognitive characteristics remain unclear. This study aimed to identify objective markers of StD and validate predictive factors for MDD onset.

Patients and methods: Among 168 university students, participants were classified into a StD group (n=87) and a healthy control group (n=81) using the Beck Depression Inventory-II (BDI-II). The StD group was further subdivided into "low depression" (BDI-II < 10, n = 21) and "maintained depression" (BDI-II ≥ 10, n = 66) based on their BDI-II scores at baseline. Assessments included voice characteristics, heart rate variability (HRV), peripheral body temperature, emotion recognition, and neurocognitive tasks. Between-group differences were tested using ANOVA and MANOVA, and participants were followed for MDD onset at 3-month intervals until March 2024.

Results: Compared to controls, the StD group showed increased vocal arousal (p = 0.007), elevated peripheral body temperature (p < 0.001), and reduced low-frequency HRV (p = 0.018). Sustained attention and executive function were impaired (p < 0.05). Accuracy in emotion recognition was lower for happy and surprised expressions (p = 0.030; p = 0.038). Subgroup analysis revealed more pronounced impairments in HRV, executive function, and emotion recognition in the maintained depression subgroup, which also had a higher MDD incidence (7 cases). In contrast, the low depression group showed selective attentional deficits and impaired emotion recognition, but no MDD onset.

Conclusion: StD correlates with physiological and cognitive abnormalities reflecting MDD, and persistent symptoms suggest increased progression risk. These findings present candidate markers (voice arousal, HRV, body temperature, emotion recognition) for early identification and risk stratification; however, conclusions should be interpreted cautiously given the exploratory design.

Objective: This study evaluated the antidepressant-like effects of Mongolian medical warm acupuncture (MMWA) in a chronic unpredictable mild stress (CUMS) model and examined its mechanistic involvement in the gut microbiota-metabolite-barrier axis, representing a novel multi-omics investigation of this traditional therapy.

Methods: Control, CUMS, and MMWA rats (n = 9/group) were assessed using sucrose preference, open-field activity, and Morris water maze tasks. Gut microbiota, fecal metabolites, and intestinal barrier markers were measured by 16S rRNA sequencing, UPLC-MS/MS metabolomics, qRT-PCR, and Western blotting.

Results: MMWA improved CUMS-induced deficits, increasing sucrose preference (p < 0.01), enhancing locomotor activity (p < 0.01), and reducing escape latency (p < 0.05). Treatment restored microbial diversity and increased beneficial short-chain fatty acid (SCFA)-producing genera, including Lactobacillus and Prevotella (p < 0.05). Metabolomic analysis showed recovery of key neuroactive metabolites such as taurine and arginine (adjusted p < 0.05). MMWA also enhanced intestinal barrier integrity by upregulating Occludin, TJP1/ZO-1, and Claudin-4 (p < 0.001). Associations across microbiota-metabolite pathways reflected coordinated restoration.

Conclusion: MMWA alleviates depressive-like behaviors by reshaping gut microbiota, normalizing metabolic profiles, and strengthening the intestinal barrier. These findings support its potential as a complementary approach for depressive-like conditions and highlight a mechanistic link involving the microbiota-metabolite-barrier axis.

Purpose: Post-stroke depression (PSD) is the most common psychiatric complication after stroke, and its persistent form carries greater symptom burden and poorer long-term outcomes. The mechanisms of persistent PSD remain unclear. We investigated genetic variants associated with persistent PSD and evaluated prespecified gene-environment (G×E) interactions with modifiable stroke risk factors (lifestyle, diet, and common biomarkers) to test whether genotype modifies susceptibility across different environmental exposures.

Patients and methods: Patients with first-onset acute ischemic stroke who met the inclusion criteria were recruited from three hospitals in Central China between May 2018 and October 2023. A nested case-control study from May 2018 to December 2020 was conducted for initial screening of PSD-associated single nucleotide polymorphisms (SNPs) via whole-exome sequencing (WES). Validation of risk SNPs was performed in a subsequent cohort enrolled between December 2020 and October 2023. Further, risk SNPs for persistent PSD were identified, and a G×E interaction model was applied to explore how environmental exposures modulate genetic risk in persistent PSD pathogenesis. Sensitivity analyses confirmed the robustness of the results.

Results: Through WES association analysis and validation, nine SNPs potentially related to PSD onset were identified: rs1055851, rs12647814, rs11108643, rs2481880, rs9965081, rs846791, rs4434123, rs1390318, and rs824695. Among these, rs9965081 showed a significant correlation with persistent PSD. This variant interacts with serum low-density lipoprotein cholesterol (LDL-C) levels in the development of persistent PSD and was validated by subgroup analysis.

Conclusion: rs9965081 may be a persistent PSD-associated SNP that interacts with serum LDL-C levels. Carriers of the rs9965081 risk allele are more sensitive to LDL-C fluctuations and therefore have greater susceptibility to persistent PSD.

Background: Hip fractures in the elderly often lead to high morbidity, prolonged hospitalization, and postoperative delirium-a prevalence noted to affect up to 50% of such patients. This study evaluates whether electroencephalogram (EEG)-guided general anesthesia can reduce postoperative delirium and enhance recovery in elderly hip fracture cases.

Methods: This retrospective cohort study analyzed patients aged ≥60 years who underwent hip fracture surgery under general anesthesia from November 2022 to May 2024. After propensity score matching, patients were divided into two groups: routine anesthesia (n=118) and EEG-guided anesthesia (n=105). Outcomes measured included the incidence of delirium (Confusion Assessment Method), cognitive recovery (SLUMS, Saint Louis University Mental Status Examination), hospital stay duration, post-anesthesia care unit (PACU) stay duration, and patient satisfaction.

Results: The EEG-guided group showed significant reductions in the incidence of postoperative delirium on the first and third days (8.57% vs 20.34%, P=0.014, and 8.57% vs 22.88%, P=0.004, respectively). However, this difference was no longer significant on the fifth day and thereafter. The EEG-guided group also demonstrated better early cognitive recovery with higher SLUMS scores on postoperative days 1 and 3 (both P=0.008). Hospitalization outcomes favored the EEG-guided group, with shorter PACU retention and hospital stays (P < 0.001 and P=0.008, respectively). Patient satisfaction was significantly higher in the EEG-guided group (P=0.007). Logistic regression identified EEG-guided anesthesia as a protective factor against delirium (OR 0.316; 95% CI, 0.134-0.685; P=0.005), reduced burst suppression duration, and reduced propofol dosage.

Conclusion: EEG-guided general anesthesia seems to be associated with lower rates of early postoperative delirium and improved cognitive recovery in elderly patients with hip fractures.

Objective: Acute ischemic stroke (AIS) may lead to varying degrees of cognitive impairment, while the inflammatory response plays a significant role in this process. This study aims to examine the relationship between residual inflammation risk (RIR) and the development of post-stroke cognitive impairment (PSCI) in patients with acute ischemic stroke.

Methods: This prospective cohort study enrolled a total of 172 patients diagnosed with AIS over the study period from January 2024 to December 2024. They were divided into four groups: RIR only [low-density lipoprotein cholesterol (LDL-C) < 2.6 mmol/L and high-sensitivity CRP (hsCRP) ≥ 2 mg/L], residual cholesterol risk (RCR) only (LDL-C ≥ 2.6 mmol/L and hsCRP < 2 mg/L), both risk or residual cholesterol and inflammatory risk (RCIR) (LDL-C ≥ 2.6 mmol/L and hsCRP ≥ 2 mg/L), and neither risk (LDL-C < 2.6mmol/L and hsCRP < 2 mg/L). PSCI is defined as a Montreal Cognitive Assessment (MoCA) score below 22 at 6 months after stroke. The final analysis included 172 patients who completed the follow-up. The association between RIR and PSCI was analyzed by multivariable logistic regression analyses.

Results: Among the 172 enrolled patients, 58 (33.7%) developed PSCI. The proportion of patients with neither risk, RIR, RCR, and RCIR was 23.8% (n=41),18.6% (n=32), 32.0% (n=55) and 25.6% (n=44), respectively. Compared to those without PSCI, patients with PSCI had a higher prevalence of hyperlipidemia (P = 0.026), a greater proportion of RIR (P = 0.015), and higher white blood cell count (P = 0.042) and neutrophil count (P = 0.016). Logistic regression analysis, adjusting for major confounding factors, identified RIR as an independent factor associated with PSCI occurrence (OR 4.496, 95% CI 1.571-17.477, P = 0.030; RCIR: OR 7.357, 95% CI 2.081-26.006, P = 0.002).

Conclusion: This study presents what is, to our knowledge, the first evidence that RIR is associated with PSCI among acute ischemic stroke patients.

[This corrects the article DOI: 10.2147/NDT.S543628.].

Purpose: To investigate the effects of short-chain fatty acids (SCFAs) on depression-like behaviors and the oral gut microbiota in rats subjected to chronic unpredictable mild stress (CUMS) using behavioral tests and high-throughput sequencing of 16SrRNA.

Methods: Sprague-Dawley rats were randomly divided into Control, CUMS, and SCFAs groups. Except for the Control group, all rats underwent CUMS modeling and drug administration for 28 days. Behavioral tests assessed depression-like behaviors, while 16SrRNA sequencing analyzed oral and gut microbiota changes. Histopathological examination of the colon tissues and immunohistochemical analysis of the tight junction protein ZO-1 were performed.

Results: Interventions using SCFAs can alleviate symptoms in rats with CUMS-induced depression. Analysis of microbial diversity revealed significant differences in both Alpha and Beta diversities of the gut microbiota among all three groups. The composition of the microbiota showed that, at the phylum level, in the intestinal microbiota, the Firmicutes/Bacteroidetes (F/B) ratio in the SCFAs group was significantly lower than that in the CUMS group. At the genus level, Lactobacillus was the dominant bacterium in the gut. Rothia was predominant among the oral bacteria. Linear discriminant effect size (LEfSe) analysis revealed that, in the gut, the relative abundances of Bifidobacterium, Collinsella, and Sphingobium increased in the SCFAs group. In the oral cavity, the relative abundance of Prevotella increased in the CUMS group but decreased in the SCFAs group. The histopathological examination of the colon revealed that, compared with the CUMS group, in the SCFAs group, the inflammatory cells in the lamina propria decreased, and the tight junction protein ZO-1 in colonic epithelium cells increased.

Conclusion: SCFAs intervention ameliorated depression-like behaviors, modulated gut microbiota composition, enhanced ZO-1 expression, reduced gut inflammation, and promoted immune function, thereby restoring oral gut microbiota homeostasis. This study elucidated SCFAs' therapeutic potential of SCFAs in depression and provided a theoretical foundation for their clinical application in antidepressant treatments.

Patients with post-stroke depression typically present with psychosocial impairments, including depressed mood and pessimism, accompanied by behavioral manifestations such as social withdrawal. These symptoms significantly impede rehabilitation compliance while elevating risks of self-harm and suicidal ideation. Recent advances in microbiota-gut-brain axis research have elucidated bidirectional communication pathways between the gut microbiota-mediated neuroendocrine-immune network and the central nervous system. Dysregulation of microbiota-gut-brain axis homeostasis may precipitate neuroinflammatory cascades and NE metabolic disturbances, potentially driving post-stroke depression pathogenesis. This paper attempts to propose a multimodal precision diagnosis and treatment framework for post-stroke depression based on the microbiota-gut-brain axis mechanism, representing the first effort to integrate perspectives from neurobiology, gut microbiota, and Traditional Chinese Medicine with modern scientific interpretation to construct such a framework. The paper encompasses four levels: mechanism, integration, evidence, and application. At the mechanism level, it explores the bidirectional regulatory mechanisms of the microbiota-gut-brain axis in post-stroke depression to identify potential therapeutic targets. At the integration level, it refines core principles for constructing a multimodal system applicable to post-stroke depression and builds an microbiota-gut-brain axis based multimodal research framework for post-stroke depression. At the evidence level, by integrating neuroimaging, metabolomics, and microbiomics technologies, it discusses the potential of a multimodal identification system, which is expected to aid in identifying molecular-cellular-circuit mechanisms associated with post-stroke depression. At the application level, it reviews research progress in treating post-stroke depression using the central nervous system interventions, gut microbiota modulation, pharmaceuticals, complementary medicine, and lifestyle interventions, summarizing them into multimodal interventional strategies to inform clinical practice for comprehensive treatment. By incorporating the roles of gut microbiota and oxidative stress in stroke-related complications and neuroimmune pathologies, this review offers a more comprehensive theoretical basis for the precise treatment of post-stroke depression. Future research should rely on large-scale cohorts and artificial intelligence to clarify the dynamic interactive networks of multiple biomarkers within critical time windows, ultimately facilitating the translation of this multimodal framework from theory to clinical practice.

Background: Postpartum depression (PPD), a prevalent perinatal mood disorder characterized by persistent depressive and anxiety symptoms, significantly impacts maternal-infant health. The COVID-19 pandemic has further increased the global burden of PPD, emphasizing the need for effective and accessible interventions. Although non-pharmacological interventions are widely used, their comparative efficacy remains uncertain.

Methods: We searched the Cochrane Library, Web of Science, EMBASE, PubMed, Scopus, CNKI, VIP Database, and Wanfang Database (inception to September 1, 2024) for randomized controlled trials (RCTs). Interventions included acupuncture (ACU), exercise (EXE), psychotherapy (PSY), exercise combined with psychotherapy (ECP), and music therapy (MT). Primary (depression) and secondary (anxiety) outcomes were pooled using mean differences (MD) with 95% credible intervals (CrI). Risk of bias was assessed via Cochrane RoB2. (PROSPERO: CRD42020166801).

Results: Thirty-five RCTs were included (n=4047). Meta-analyses for depressive symptoms (5 interventions, n=4047) showed a statistically significant improvement in the non-pharmacological intervention group compared with the control group (standard care, no intervention, or placebo et al), particularly for the ECP (95% CrI -2.3 to -0.85), followed by ACU (95% CrI -1.8 to -0.44) and EXE (95% CrI -1.7 to -0.48). Similarly, for anxiety symptoms (5 interventions, n=863), the overall effect of the non-pharmacological interventions was superior to that of the control group, with ECP again being the most effective modality (95% CrI -2.3 to -0.18), followed by EXE (95% CrI -2.0 to -0.0021) and ACU (95% CrI -0.96 to -0.052).

Conclusion: This study demonstrates the promise of non-pharmacological interventions, particularly exercise, acupuncture, and ECP, for alleviating PPD symptoms, positioning ECP as a potential first-line intervention for mild to moderate cases.

Background: Currently, the evidence regarding the relationship between family history of psychiatric disorders and post-stroke depression (PSD) is inconsistent. Some observational studies did not consider a positive family history of psychiatric disorders as a definite risk factor. Furthermore, the bulk of research on the association between family history of psychiatric disorders and PSD comes from earlier studies that were frequently constrained by modest sample sizes. Therefore, we plan to use a meta-analysis approach to study this correlation.

Methods: We systematically reviewed the studies related to PSD and family history of psychiatric disorders from PubMed, Embase and EBSCO. The studies eligible for inclusion were peer-reviewed observational studies that reported an odds ratio or contained sufficient data to enable its calculation. We conducted a random-effects meta-analysis of the proportion of PSD patients with a reported positive family history of psychiatric disorders.

Results: Eleven studies published between 1990 and 2020 were included, comprising data on stroke patients. The meta-analysis revealed an elevated odds ratio of 1.73 (95% CI: 1.29-2.33; I ² = 6.1%) for the development of PSD among stroke patients with a familial predisposition to psychiatric disorders. The findings of subgroup, sensitivity, and meta-regression analyses concurred with the primary analysis. According to GRADE, the overall certainty of the evidence was judged as moderate.

Conclusion: This study revealed moderate certainty of evidence, indicating that stroke patients with family history of psychiatric disorders have approximately a 1.73-fold risk of developing PSD compared to those without such a family history.