Brain and Behavior最新文献

Background: This study explores the relationship between neurofilament light (NfL) levels, a biomarker of neuronal injury, and cardiovascular health and vascular injury among US Mexican American (MA) and non-Latino White (NLW) adults.

Methods: Data from 1317 participants in the Health and Aging Brain Study: Health Disparities (HABS-HD) were analyzed, including phenotypic, neuroimaging, and plasma NfL data. Cardiovascular health factors included hypertension, diabetes, and cardiovascular disease (CVD), while vascular injury markers were white matter hyperintensities (WMH).

Results: We found that NfL levels differed between MA and NLW participants based on diabetes and CVD diagnosis, with more pronounced differences in the MA group. In addition, the association between WMH volume and NfL was steeper in the MA group.

Conclusion: These findings suggest NfL's potential as a prognostic biomarker for CVD and neurodegeneration, especially in MA adults. Further research is needed to understand these associations and develop targeted prevention strategies for brain aging disparities.

Introduction: Daytime dysfunction is a significant manifestation of sleep problems in adolescents, which increases individuals' negative emotional experiences by weakening their cognitive regulation and social adaptation. Meanwhile, emotional distress, such as depressive and anxiety symptoms, may further exacerbate daytime dysfunction, creating a negative cycle. Therefore, the present study employed a longitudinal follow-up design to explore the bidirectional relationship between daytime dysfunction and depressive and anxiety symptoms in adolescents.

Methods: This three-wave longitudinal study used stratified random sampling to recruit 936 adolescents (50.96% girls; mean age = 14.37 ± 1.32 years) from four secondary schools in Bengbu, Anhui Province, China. Data were collected between September 2023 and September 2024 at 4-month intervals. Standardized questionnaires measured daytime dysfunction, social ostracism, depressive symptoms, and anxiety symptoms. Random intercept cross-lagged panel models (RI-CLPM) were used to examine within- and between-person associations and to test the longitudinal mediating roles of two distinct forms of social ostracism.

Results: At the between-individual level, the results indicated a significant positive association between daytime dysfunction and depressive and anxiety symptoms (r = 0.319-0.495, p < 0.001), and a significant positive association between social ostracism and depressive and anxiety symptoms (r = 0.120-0.504, p < 0.05). The link between social ostracism and daytime dysfunction was weaker, mainly involving social rejection. At the within-individual level, social neglect at T2 significantly mediated the longitudinal relationship between daytime dysfunction at T1 and anxiety symptoms at T3.

Conclusions: These findings suggest the negative impact of daytime dysfunction on adolescents' depressive and anxiety symptoms and highlight the role of social neglect in social ostracism on this influence.

Objectives: To verify the abnormal brain electrical activity of idiopathic tinnitus through auditory event-related potentials and elucidate the impact of mild hearing loss.

Design: Auditory event-related potentials were collected from 74 patients with idiopathic tinnitus as the primary complaint (divided into a normal hearing group of 39 and a mild hearing loss group of 35 based on hearing level) and 37 healthy volunteers. Various auditory event-related potential indicators were compared among the groups, and the correlation between these indicators and the clinical characteristics of idiopathic tinnitus patients was analyzed.

Results: Idiopathic tinnitus patients with normal hearing have increased P1 amplitude, delayed P300 latency, decreased P300 amplitude, and decreased mismatch negativity (MMN) amplitude. Idiopathic tinnitus patients with mild hearing loss have further reduced P300 amplitude and delayed MMN latency. In addition, the P300 latency of idiopathic tinnitus patients is significantly correlated with the duration of tinnitus and Tinnitus Handicap Inventory (THI) score, the P300 amplitude is significantly correlated with the Pittsburgh Sleep Quality Index (PSQI) score, and the MMN latency is significantly correlated with the duration of tinnitus.

Conclusion: Patients with idiopathic tinnitus exhibit abnormalities in multiple auditory event-related potentials, with mild hearing loss exacerbating some of these abnormalities. Idiopathic tinnitus and mild hearing loss may lead to selective attention and preprocessing dysfunction.

Background: Stroke has always been a huge medical challenge faced by China. Previous studies have found a negative correlation between high-density lipoprotein cholesterol (HDL-C) and stroke, but in recent years, with unsatisfactory drug experiments, researchers have begun to re-examine this relationship. Our research is based on the large population of middle-aged and elderly people in China, exploring the relationship between HDL-C and stroke and all-cause mortality.

Methods: The participants of this study were from the China Health and Retirement Longitudinal Study (CHARLS) database. We utilized univariate/multivariate logistic regression to screen the influencing factors of stroke. Using Cox regression, we calculated the hazard ratio (HR) for stroke and mortality, presenting our findings through Kaplan-Meier (KM) curves. We also presented the relationship between HDL-C and stroke and mortality by restricted cubic spline (RCS) regression analysis. A time-varying Cox analysis was conducted to evaluate the impact of changes in HDL-C on various outcomes. To strengthen the robustness and causal interpretation, we performed subgroup analysis, sensitivity analysis, and mediation pathway, and established a competing-risk model.

Results: HDL-C was negatively correlated with stroke. After adjusting for confounders, HDL-C remained a protective factor for stroke (HR 0.99, 95% CI 0.99-1.00, P < 0.05), especially in the male group, the normal BMI group, the group without dyslipidemia, and the group with hypertension in the subgroup analysis. However, no significant association was observed between HDL-C and all-cause mortality after adjustment (HR 1.00, 95% CI 1.00-1.01, p = 0.482). The results remained robust in sensitivity analysis and competitive risk models. The impact of HDL-C on the risk of stroke (HR 1.00, 95% CI 0.999-1.001, p = 0.887) and all-cause mortality (HR 1.00, 95% CI 0.9995-1.001, p = 0.539) did not show a significant trend over time. Mediation analysis revealed that BMI mediated 25% of the effect of HDL-C on stroke.

Conclusions: In Chinese people over 45 years old, HDL-C was a protective factor for stroke, while it had no significant association with all-cause mortality. BMI mediated the effect of HDL-C on stroke. This research highlights the critical role of HDL-C in stroke risk assessment.

Purpose: Traumatic brain injury (TBI) remains a major global public health challenge with high morbidity and mortality, and secondary injury characterized by neuroinflammation, brain edema, and neuronal cell death is a critical determinant of patient prognosis. Neutrophil extracellular traps (NETs) and necroptosis are involved in TBI pathology, but their crosstalk remains unclear. Here, we used NETs inhibitors (Cl-amidine and DNase I) and the necroptosis inhibitor Necrostatin-1 (Nec-1) to investigate the roles of NETs and necroptosis in neuronal injury following TBI.

Method: Male C57BL/6J mice were used to establish a TBI model via controlled cortical impact (CCI). Cl-amidine, DNase I, and Necrostatin-1 were administered to explore the mechanism by which NETs regulate necroptosis and exacerbate TBI-induced secondary injury. The modified neurological severity score (mNSS) assessment, brain edema measurement, enzyme-linked immunosorbent assay (ELISA), Western blotting, immunofluorescence staining, and TUNEL staining were performed in this study. Mice were sacrificed at 1, 3, 5, and 7 days post-TBI, with Day 3 post-TBI designated as the key time point for primary analyses due to the peak expression of NETs markers: myeloperoxidase (MPO) and peptidyl arginine deiminase 4 (PAD4).

Finding: Our results showed that TBI induced a time-dependent upregulation of MPO and PAD4 in the ipsilateral cortex. Inhibition of NETs or blockade of necroptosis significantly reduced neuronal apoptosis, alleviated brain edema, improved mNSS scores, preserved blood-brain barrier integrity, and decreased levels of pro-inflammatory cytokines (TNF-α, IL-1β). Western blot analysis revealed that TBI markedly upregulated the expression of RIP1, RIP3, MLKL, and their phosphorylated forms, while NETs inhibition downregulated these necroptosis-related proteins. Notably, combined inhibition of NETs and necroptosis did not exert synergistic protective effects on TBI-induced brain injury.

Conclusion: NETs exacerbate TBI-induced secondary brain injury partially by activating the necroptosis pathway. Inhibition of NETs exerts neuroprotective effects. Targeting NETs may serve as a promising therapeutic strategy to improve prognosis in TBI patients.

Background: Multiple sclerosis (MS) is a chronic autoimmune disease that leads to significant disability, with its precise etiology still not fully understood. Recent studies indicate the crucial role of immune cells in MS pathogenesis. However, traditional research often focuses on major immune cell populations, potentially neglecting the roles of newly identified immune cell subsets with distinct receptors and functions. Moreover, conventional observational studies are prone to biases, hindering the establishment of definitive causal relationships. This study aims to investigate the causal relationships between 731 immune cell traits and MS susceptibility using Mendelian randomization (MR) analysis to provide more robust insights into the underlying mechanisms of MS.

Methods: We performed MR analyses to assess associations between various immune cell traits and MS risk. Following this, we explored the molecular mechanisms of the significant associations, focusing particularly on B-cell antigen presentation and the involvement of human leukocyte antigen (HLA) pathways.

Results: Our analysis revealed specific causal links between B cells and dendritic cells with MS susceptibility. We identified 61 pleiotropic genes associated with MS. Notably, B-cell antigen presentation and HLA-related pathways play pivotal roles in MS pathogenesis. Additionally, alterations in immune cell populations post-MS onset were observed, suggesting potential biomarkers for early diagnosis.

Conclusion: This study offers a comprehensive examination of immune cell contributions to MS pathogenesis, identifying potential therapeutic targets and diagnostic markers. Given the side effects of anti-B cell monoclonal antibodies in MS treatment, our findings propose avenues for more precise therapeutic strategies aimed at minimizing adverse effects.

Objective: In 2021, Rossi et al. developed a cortical mapping algorithm that enabled a reliable mapping of an anatomical subdivision of the precentral gyrus. This approach allowed for the differentiation between an anterior subregion, characterized by lower excitability and slower motor responses, and a posterior subregion (named "M1 proper"), exhibiting higher excitability and faster motor responses. Based on these findings, we conducted a navigated transcranial magnetic stimulation (nTMS) study to investigate whether this anatomical subdivision can also be identified using a non-invasive mapping technique.

Methods: Fifteen healthy volunteers were examined. Using nTMS, the motor cortex at the hand knob area was subdivided into four distinct strips aligned parallel to the central sulcus: s, precentral non-proper, precentral proper, and postcentral. After determining the resting motor threshold (RMT), 10 stimulation points in each strip were stimulated with 150% RMT. Electromyographic (EMG) amplitudes and latencies were recorded and compared across the four stimulation strips to detect potential differences.

Results: Although descriptively higher mean EMG amplitudes were observed in the precentral proper strip, generalized linear mixed-effects modeling revealed no statistically significant differences in EMG amplitude between the precentral proper and non-proper regions, nor across any of the four stimulation strips.

Conclusions: Using the applied protocol, a clear delineation between a functionally separated ventral and dorsal subdivision of the precentral gyrus could not be observed. However, it is noteworthy that the application of relatively high stimulation intensity may have masked subtle differences. Further examinations at the lower end of the stimulation spectrum (e.g., 90% or 100% RMT) or a specific paired pulse protocol may allow for a more precise differentiation between these two anatomical areas.

Background: Mutations in the telomerase reverse transcriptase promoter (pTERT) are important molecular markers in glioblastoma (GBM). Although several imaging-based approaches have attempted to predict pTERT mutation status preoperatively, the value of quantitative metrics extracted from lesion subregions remains unclear. This study investigated whether quantitative FLAIR metrics derived from contrast-enhanced T1-weighted imaging (CE T1WI)-FLAIR fused images contribute to the differentiation of pTERT subtypes in GBM.

Methods: MRI and clinical data from 135 GBM patients, 94 with pTERT-mutant (pTERTm) and 41 with pTERT-wild-type (pTERTw) tumors, were retrospectively analyzed. Patients were randomly assigned to training and validation cohorts in a 7:3 ratio. Clinical characteristics and conventional MRI variables were compared between pTERTm and pTERTw groups. FLAIR signal intensity (SI) metrics were measured in three subregions on CE T1WI-FLAIR fused images: the enhancement region, the edema region (non-enhancing), and the whole lesion (enhancement + edema). Significant variables identified by logistic regression were incorporated into clinical, MRI, and combined predictive models. Model performance was internally evaluated using leave-one-out cross-validation (LOOCV) in the training cohort and externally assessed in the validation cohort.

Results: Significant differences between pTERTm and pTERTw groups were observed in age, FLAIR SI standard deviation (FLAIR_SD) and relative FLAIR SI (rFLAIR) of the edema region, and FLAIR_SD of the enhancement region (all p < 0.05). Logistic regression identified older age (> 42.5 years; OR = 1.09; p = 0.002), higher FLAIR_SD in the enhancement region (> 62.45; OR = 1.01; p = 0.027), and higher rFLAIR in the edema region (> 1.706; OR = 7.49; p = 0.025) as independent predictors of pTERTm. In the training cohort, the combined model achieved an area under the ROC curve (AUC) of 0.833, outperforming the clinical model (0.675) and MRI-based model (enhancement-region FLAIR_SD: 0.737; edema-region rFLAIR: 0.699). The combined model achieved the highest predictive performance, with LOOCV in the training cohort yielding a mean AUC of 0.784 (95% CI: 0.672-0.895) and external validation showing an AUC of 0.667 (95% CI: 0.466-0.867).

Conclusions: Quantitative FLAIR metrics extracted from subregions on CE T1WI-FLAIR fused images differ significantly between pTERTm and pTERTw GBM. Subregional quantitative analysis may therefore contribute to noninvasive preoperative prediction of pTERT mutation status.

Background: Given that a significant proportion of the growing number of individuals in prisons may have antisocial personality traits (ASPT), it is important to test and report on the results of pilot psycho-educational intervention programmes developed for this purpose.

Aim: The primary aim of this study is to examine the effect of the psychoeducation programme on ASPT among prisoners. The secondary aim is to investigate whether there is any interaction between ASPT after intervention.

Methods: Twenty-six participants were randomly assigned to the experimental group (n = 13) and the control group (n = 13). The ASPT Scale was administered as a pre-test and post-test at 8-week intervals. Findings were examined using independent samples t-tests and repeated measures analysis of variance (ANOVA) via SPSS 27. PROCESS macro was used to examine whether reductions in the aggression subscale were moderated by rule-breaking.

Results: Group-based psychoeducational intervention did not lead to effective results in overall ASPT scores in the experimental group. However, intervention led to significant decreases in aggression scores both within groups (p < 0.01) and between groups (p < 0.05). Furthermore, it was found that a decrease in aggression scores was moderated by rule-breaking scores of the prisoners (β = 0.60, p < 0.05, [0.88; 1.12]).

Conclusions: Group-based psychoeducational interventions are associated with a reduction in aggressive behavior among prisoners. In experimental interventions aimed at reducing aggressive behavior, it is important to prioritize individuals with low levels of rule-breaking tendencies.

Background: Cerebrovascular disease (CVD) remains a leading cause of death, with obesity exacerbating stroke risk through multiple metabolic pathways. However, long-term trends in CVD-related mortality among obese adults in the United States remain inadequately defined.

Methods: We analyzed national mortality data from 1999 to 2020 using the CDC WONDER database. Deaths were included if CVD (ICD-10 I60-I69) was the underlying cause and obesity (E66) a contributing cause. Age-adjusted mortality rates (AAMRs) were calculated, and temporal trends were evaluated using Joinpoint regression to estimate annual percent change (APC) and average annual percent change (AAPC).

Results: From 1999 to 2020, 26,410 CVD-related deaths occurred among obese adults. The overall AAMR was 0.53 per 100,000, with an AAPC of 4.59% (95% CI: 3.94 to 5.24). A statistically significant change in trend slope was observed after 2008, with accelerated mortality increases. Females had higher AAMRs (0.56) than males (0.49), though males experienced steeper increases (AAPC 5.98% vs. 3.64%). American Indian/Alaska Native and Black adults had the highest AAMRs (1.11 and 1.01, respectively). Mortality increased in all racial/ethnic groups, most rapidly among White individuals (AAPC 4.66%). Non-metropolitan areas showed higher mortality than metropolitan areas (0.71 vs. 0.50), with a widening urban-rural gap. Regionally, the West and Midwest had the highest AAMRs (0.59 and 0.57, respectively). Mortality rose across all age groups, with the steepest increases in younger adults aged 25-54 years. Most deaths occurred in hospitals (56%), followed by home (22.8%) and nursing facilities (15.7%).

Conclusions: CVD-related mortality among obese adults has increased significantly since 1999, with substantial disparities across sex, race, geography, and age, highlighting the need for focused public health strategies.