Brain and Behavior最新文献

Background: Status epilepticus (SE) is a serious neuro-emergency that is often associated with unfavorable outcomes. It is known that inflammation is involved in the pathogenesis of SE, and various inflammatory markers have been suggested to be related to SE prognosis. Monocyte-to-albumin ratio (MAR), a novel biomarker of systemic inflammation, is derived from monocyte count and albumin levels. In this study, we sought to explore whether MAR could serve as a predictor of functional outcomes in SE.

Methods: This retrospective study collected the data of adult patients with SE. Functional outcomes of SE patients were evaluated by using the Modified Rankin Scale (mRS). Multivariable logistic regression analysis was performed to investigate the association of MAR with SE outcomes. Moreover, receiver operating characteristic (ROC) curve analysis was carried out to determine the optimal MAR threshold for predicting poor SE outcomes.

Results: This study included 163 SE patients. Poor outcome at discharge was observed in 39.3% (64/163). Multivariate analysis showed that higher MAR at admission was independently related to unfavorable outcomes of SE patients (odds ratio: 1.092; 95% confidence interval, 1.023-1.166; p = 0.008). ROC curve analysis demonstrated that MAR could predict poor SE outcomes, with an area under the curve of 0.717 (95% CI: 0.638-0.795, p < 0.001). The optimal predictive cutoff point of MAR for poor SE outcomes was 13.78 (sensitivity 59.38%, specificity 73.74%).

Conclusion: Higher MAR at admission is closely correlated with an elevated risk of poor functional outcomes at discharge of SE patients. Our data suggest that MAR may be a promising and easily measurable marker for predicting short-term SE outcomes.

Background: Acute stress has complex effects on executive function and social behavior; however, the direction of these effects is inconsistent across studies, and the underlying neural mechanisms remain poorly understood. This study investigated the behavioral and neural effects of acute stress on executive function and dyadic cooperation and their relationships.

Methods: Eighty-six healthy male undergraduates (18-25 years) were randomly assigned to stress (n = 44; Trier Social Stress Test for Groups [TSST-G]) or control groups (n = 42; placebo TSST-G). The participants completed executive function tasks (3-back, Go/Nogo, Stroop, and task-switching) and cooperative button-pressing tasks pre- and postintervention, with a counterbalanced order. Functional near-infrared spectroscopy (fNIRS) was performed simultaneously.

Results: Stress impaired the practice-induced improvement in 3-back accuracy observed in the control group, although it did not significantly affect other performance metrics. During the 3-back, Stroop, task-switching, and cooperative tasks, increased and decreased prefrontal cortex (PFC) activation from baseline to postintervention were observed in the stress and control groups, respectively. Furthermore, greater bilateral dorsolateral PFC (DLPFC) interbrain synchronization (IBS) changes during the cooperative task were observed in the stress group. Cognitive flexibility and cooperation were positively linked both behaviorally and neurally.

Conclusions: TSST-G-induced stress disrupted the learning-related enhancement of working memory; however, response inhibition, interference control, cognitive flexibility, and cooperative performance were preserved. The concurrent observation of trends toward increased neural activation and IBS under stress is compatible with, but does not prove, potential compensatory mechanisms. The identified neural and behavioral correlations point to a potential connection between executive and social processes under stress. We tentatively frame these exploratory observations within the "Executive-Social Function Coupling Hypothesis" as a heuristic model for future research. The implications of these preliminary findings are discussed.

Purpose: Sepsis-associated encephalopathy (SAE) is a common neurological complication of sepsis. UMI-77 has shown unique benefits in modulating inflammation to improve sepsis. However, the exact role of UMI-77 in the treatment of SAE and its mechanism are unknown.

Aim: This article analyzes UMI-77 based on metabolomics and explores its mechanism of action in treating SAE based on the brain-gut axis.

Method: In this study, hematoxylin and eosin (H&E) and immunofluorescence staining were used to evaluate the therapeutic effect of UMI-77 on SAE mice. Applying untargeted metabolomics analysis, the metabolic changes in the brain and intestines of septic mice treated with UMI-77 were examined. Furthermore, Receiver Operating Characteristic (ROC) analysis was used to select predictive biomarkers for exploring the mechanism of UMI-77 in treating SAE.

Findings: Sixty-six significant biomarkers in the brain were found and selected with the aid of untargeted the metabolomic method. Metabolic pathway analysis indicates that these differential metabolites are mainly involved in the metabolism of linoleic acid, biosynthesis of phenylalanine, tyrosine, and tryptophan, and phenylalanine metabolism. Seventy-eight important biomarkers were identified and selected in the intestine; metabolic pathway analysis revealed that these differential metabolites were mainly involved in phenylalanine, tyrosine, and tryptophan biosynthesis, and biotin metabolism. L-phenylalanine, L-tyrosine, and 5-hydroxy-tryptophan are the most important metabolites.

Conclusion: UMI-77 plays a positive regulatory role in disrupting the gut microbiota of mice through pathways such as the biosynthesis of phenylalanine, tyrosine, and tryptophan, and can significantly improve neurological function and reduce apoptosis of brain tissue cells.

Aim: The study utilized MRI-derived brain structure age (BSA) to compare global and regional subcortical BSA among healthy controls (HCs), Parkinson's disease (PD) patients with normal cognition (PD-NC), and mild cognitive impairment (PD-MCI), identifying regions with accelerated aging and linking altered BSA to native volumes.

Methods: We analyzed structural MRI data from 55 participants (22 HCs, 18 PD-NC, 15 PD-MCI) using the volBrain platform to estimate global and regional subcortical BSA. Group differences in age, global, and regional BSA were tested via Kruskal-Wallis. Follow-up analyses included Pearson correlations for significant regions and ANOVAs where assumptions were met.

Results: No significant group differences were found for chronological age (p = 0.111) or global BSA (p = 0.143). However, at the regional level, non-parametric analyses revealed significant group differences in the predicted age of the left amygdala (H = 6.42, p = 0.040) and the left basal forebrain (H = 6.01, p < 0.05), though effect sizes were small (ε² ≤ 0.07). The predicted ages of these two regions were highly collinear (r = 0.992). Subsequent parametric tests and Bonferroni-corrected pairwise comparisons on other subcortical regions did not yield any significant differences.

Conclusion: Accelerated aging appears to be a localized and asymmetric process confined to the limbic-cholinergic network, specifically involving the left amygdala and basal forebrain. Accelerated brain aging in PD is not global but a localized, asymmetric process in the left limbic-cholinergic network. Regional brain-age metrics offer a sensitive biomarker for detecting the specific neurodegeneration linked to cognitive decline.

Background: Vitamins, as a modifiable lifestyle factor, are increasingly recognized for their protective role in cognitive health. However, the synergy or interaction among vitamins remains unclear.

Objectives: This work aimed to analyze the association of serum vitamin D, folic acid (FA), and vitamin B12 with cognitive impairment in the elderly.

Methods: Data included 2582 elderly participants aged 60 and older from the NHANES, 2011-2014. Weighted logistic regression, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) models were used to analyze the association of serum vitamins and their mixture with cognitive disorder risk. Interaction effects among vitamins were investigated. Sensitivity analyses accounting for vitamin supplements, depression, and sleep disorders, and subgroup analyses focusing on high vitamin B12 levels were performed.

Results: After adjusting for confounding factors, serum Vitamin D (OR = 0.695, 95% CI: 0.534-0.905, p = 0.003) and FA (OR = 0.777, 95% CI: 0.604-0.999, p = 0.034) levels were inversely correlated with cognitive disorder risk. Both remained robust after considering vitamin supplements and comorbidities in the sensitivity analyses. The BKMR model indicated a significant increase in cognitive impairment risk when the overall vitamin mixture level fell below the 50th percentile. A U-shaped association was detected between vitamin B12 and cognitive disorder risk. Vitamin B12 and FA had potential interaction effects. The WQS model revealed the largest contribution by FA (56.0%) to the overall protective effect on the cognitive disorder risk. The association with high vitamin B12 was predominantly observed in individuals with specific metabolic conditions, including kidney stones and hypertension.

Conclusion: Optimizing vitamin D and FA levels remains the key to reducing cognitive impairment risk in FA-supplemented populations. Vitamin B12 management requires greater precision; its high level in specific metabolic patients may signal health risks. This study provides new evidence for precise nutritional intervention for the elderly.

Objectives: Electroencephalogram (EEG) microstates can precisely capture transient brain activity changes on sub-second time scales and are used to evaluate global dynamic functional alterations in the brains of Parkinson's disease (PD) patients. This study primarily investigates the differences in microstate features between PD patients and healthy subjects, while exploring their correlations with clinical symptoms.

Methods: We enrolled 75 PD patients and 44 healthy controls (HCs) who underwent simultaneous EEG microstate recording and Montreal Cognitive Assessment (MoCA) evaluation. All PD patients underwent comprehensive evaluation using the International Movement Disorder Society Unified Parkinson's Disease Rating Scale Parts I and III (MDS-UPDRS I & III).

Results: PD patients demonstrated significantly increased mean coverage and duration of microstate D compared with HCs, together with elevated transition probabilities from microstates A, B, and C to D. Importantly, both the mean coverage of microstate D and the transition probability from microstate B to D showed significant positive correlations with MDS-UPDRS III scores. Furthermore, receiver operating characteristic (ROC) curve analysis revealed that the mean coverage of microstate D (AUC = 0.674) and the transition probability from microstate B to D (AUC = 0.617) could distinguish between PD patients and HCs.

Conclusion: The observed abnormalities in microstate dynamics among PD patients may stem from an imbalance in neural network dynamics. These results indicate that EEG microstates may serve as potential biomarkers for assessing and monitoring motor function in PD.

Introduction: Insomnia and other sleep disorders are becoming increasingly prevalent worldwide, while current sedative medications such as benzodiazepines, though effective, are often limited by side effects and dependency risks. Therefore, identifying safe natural compounds with sedative potential is of growing scientific and clinical interest. L-quebrachitol (LQL), a naturally occurring cyclitol compound with antioxidant, antimicrobial, and antidiabetic properties, has not been previously evaluated for its sedative effects. The aim of this study is to evaluate the potential sedative effects of LQL through both in vivo and in silico methods.

Methods: In this experiment, 2-day-old broiler chicks (Gallus gallus domesticus) were given thiopental sodium (10 mg/kg, intraperitoneal [ip]) to induce sleep. LQL (1, 5, and 10 mg/kg, ip) and diazepam (2 mg/kg, ip) were administered alone or together to assess their synergistic or antagonistic effects on chicks. To assess its potential for interacting with the GABA_A receptor (α1 and β2 subunits), a molecular docking study was carried out.

Result: According to the in vivo investigation, the results indicate that LQL decreased the latency period while extending the animal's sleep duration time in a dose-dependent manner. Moreover, the combination of LQL-10 (10 mg/kg) and diazepam 2 (2 mg/kg) showed (p < 0.05) enhanced sedative effects significantly by decreasing latency time and prolonging sleeping duration. In addition, LQL has a moderate binding affinity of -5.3 kcal/mol against the GABA_A receptor (α1 and β2 subunits), but forms strong hydrogen bond interactions and similar amino acid residues with standard drug diazepam, suggesting potential therapeutic effects. Further, LQL also demonstrated promising pharmacokinetic properties and low toxicity.

Conclusion: These findings collectively enhance the potential of LQL as an effective sedative therapeutic agent. However, further research, including in vitro studies to confirm the molecular interactions and membrane permeability, followed by well-designed clinical trials, is necessary to fully establish LQL as a safe and effective sedative agent.

Objective: The purpose of this study is to assess the olfactory system of patients with T2DM using the cranial magnetic resonance imaging (MRI) method.

Method: This is a retrospective case-control study in which a group of T2DM patients and a control group were compared. The results of the examinations of the olfactory systems of the patients by cranial MRI were transferred to a data collection form. Descriptive statistical methods, chi-squared tests, the Mann-Whitney U test, and Spearman's correlation coefficient were used to analyze the data.

Results: It was determined that 66.7% of the case group were women, the mean age of the patients in the group was 52.50 ± 7.41, and their mean T2DM diagnosis duration was 6.48 ± 3.18 years. There were statistically significant differences between the case and control groups in terms of their olfactory bulb volume (OBV), olfactory tract length (OTL), and olfactory sulcus depth (OS) values. Longer T2DM durations and elevated HbA1c levels were significantly associated with structural disorders of the olfactory system (p < 0.01).

Conclusion: A longer duration of T2DM and elevated HbA1c levels trigger the structural disorders of the olfactory system. In comparison to healthy controls, we identified prominent changes in the olfactory bulb volumes, olfactory tract lengths, and olfactory sulcus depths of T2DM patients. This reveals the need for T2DM patients to pay more attention to their diet and insulin treatment. Similarly, olfactory dysfunction in T2DM patients should be carefully monitored by clinicians.

Background/objectives: Medicinal mushrooms have been gaining increasing attention as functional foods; however, scientific evidence from human studies remains limited.

Methods: In this study, 50 participants were randomly assigned to receive either Restake or a placebo. Psychological and physiological parameters were assessed at baseline, 6 weeks, and 12 weeks using validated tools, including the Pittsburgh Sleep Quality Index (PSQI), Visual Analog Scale for Fatigue (VAS-F), Multidimensional Fatigue Inventory (MFI), State-Trait Anxiety Inventory (STAI-S), Perceived Stress Scale (PSS), Hamilton Anxiety Scale (HAM-A), and Beck Depression Inventory (BDI). Serum biomarkers-cortisol, norepinephrine (NE), melatonin, adrenocorticotropic hormone (ACTH), and C-reactive protein (CRP)-were analyzed via ELISA.

Results: Anxiety, assessed by STAI-S and HAM-A, showed greater reductions in the Restake group at both 6 weeks (STAI-S: p = 0.025; HAM-A: p = 0.002) and 12 weeks (STAI-S: p = 0.011; HAM-A: p = 0.002). Depression (BDI) scores significantly decreased at 6 weeks (p < 0.001) and 12 weeks (p = 0.008). Fatigue levels showed significant reductions in general fatigue (p = 0.043), physical fatigue (p = 0.027), and mental fatigue (p = 0.043). Restake supplementation led to reductions in sleep quality scores (PSQI) at 6 weeks (p = 0.005) and 12 weeks (p < 0.001). Biomarker analysis revealed significant reductions (p < 0.001) in cortisol and ACTH levels and a decrease in CRP levels (p = 0.042). NE levels significantly (p = 0.033). Compared to the placebo group, Restake supplementation exhibited an increased morning melatonin trend after 12 weeks of intervention.

Conclusions: Restake supplementation was well tolerated and effectively reduced psychological stress, fatigue, and improved sleep quality without adverse effects.

Background: Acute psychotic symptoms like delusions and hallucinations are of major concern while treating patients with schizophrenia and alzheimer's psychosis, primarily impacting their daily life functioning and quality of life. The traditional antipsychotic medications, commonly prescribed to manage these symptoms, cause significant side effects with limited efficacy, requiring novel therapeutic agents that can overcome this challenge. While there is no definitive cure, symptomatic treatment can help relieve some of the symptoms and improve the quality of life of people with alzheimer's disease (AD).

Method: A comprehensive literature search of PubMed, scopus, google scholar, and ClinicalTrials.gov was conducted to identify studies on xanomeline-trospium chloride (KarXT) in schizophrenia and AD psychosis. After screening 802 unique records, 39 studies-including preclinical, clinical, and observational investigations-were included in this narrative review. Only English-language publications up to February 2025 were considered.

Result: KarXT, with its dual action on the M1 and M4 receptors and mAChR antagonism, greatly helps reduce the severity of the positive and negative symptoms, as it resulted in an 8.4-point greater reduction on the PANSS scale. Side effects were minimal and did not account for the discontinuation of treatment.

Conclusion: Psychosis is a common feature of schizophrenia and AD, most often caused by high concentrations of dopamine in the brain, characterized by hallucinations, delusions, and disorganized thinking, resulting in markedly reduced quality of life for the patient and associated caregiver. Conventional treatments targeting dopamine receptors produce extrapyramidal symptoms and metabolic side effects, leading to noncompliance with medication. KarXT, with its dual action on M1 and M4 receptors and mAChR antagonism, greatly helps reduce the severity of the positive and negative symptoms. The side effects experienced were minimal and did not account for the discontinuation of treatment.An overview of the mechanism of action, clinical trials, and classical findings of KarXT for the management of psychotic symptoms in patients with schizophrenia and alzheimer's disease.