Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Given the conflicting evidence regarding the impact of adherence to the Mediterranean diet (MedDiet) on MS development and the lack of a systematic review on this topic, this study aimed to examine this association.
Following the PRISMA and JBI methods, a search of electronic databases was conducted through PubMed, Embase, Web of Science, and Scopus up to March 2024. Clinical original studies assessing the association between the MedDiet adherence and MS development were included. Risk of bias was evaluated using JBI critical appraisal tools. Meta-analyses were performed using CMA4 software.
Out of 202 screened records, eight studies, including five case-control and three cohort studies, met the inclusion criteria. Retrospective evidence from three case-control studies suggested that MedDiet adherence is associated with decreased odds of MS, whereas cohort studies showed no significant relationship. Based on the meta-analysis, there was a significant association between high adherence to the MedDiet and reduced odds of MS (fixed-effect OR: 0.275, 95% CI: 0.11-0.72, p-value <0.01, least MedDiet adherence as the reference).
Although the meta-analysis showed a significant inverse association between higher adherence to the MedDiet and the odds of MS, the overall body of evidence does not provide strong support for a preventive role of the MedDiet. Considering the limited number of included studies, the predominantly retrospective design, the high risk of bias in several studies, and the substantial observed heterogeneity, further well-designed prospective studies are needed.
Progressive balance exercises may change corticomotor excitability during the learning process of postural stability control. The primary purpose of the present study was to assess corticomotor excitability corresponding to the peroneus longus muscle under transcranial magnetic stimulation following 6 weeks of progressive balance exercises in individuals with chronic ankle instability.
Eligible volunteers diagnosed with chronic ankle instability were randomly assigned to either the intervention group or the control group. The intervention group practiced progressive balance exercises every other day for 6 weeks, while the control group continued their daily activities. The corticomotor excitability outcome measures included the active and resting corticomotor thresholds, the motor evoked potential, and the cortical silent period of the peroneus longus muscle, which were measured using an electromyography device under a transcranial magnetic stimulator. The outcome measures were measured in the intervention group before and after progressive balance exercises, and in the control group at baseline and again after a 6-week interval.
The corticomotor thresholds and cortical silent period of the peroneus longus muscle were significantly decreased within groups (p-values < 0.001; η2p > 0.580). In addition, the normalized motor evoked potential of the peroneus longus muscle exhibited a significant increase within groups (p-value < 0.001; η2p = 0.265). Interestingly, a significant interaction effect was revealed between the within-group and between-group effects for the corticomotor excitability outcome measures related to the peroneus longus muscle (p-values < 0.001; η2p > 0.311).
Six weeks of progressive balance exercises significantly increased corticomotor excitability corresponding to the peroneus longus muscle in individuals with chronic ankle instability.
Secondary hemophagocytic lymphohistiocytosis (sHLH) with central nervous system (CNS) involvement poses significant diagnostic and therapeutic challenges. This study aimed to characterize the clinical features, laboratory profiles, and prognostic impact of neurological involvement in adult-onset sHLH.
We analyzed 130 adult sHLH patients, comparing 28 with CNS involvement to 102 without neurological manifestations. Clinical parameters, neuroimaging, cerebrospinal fluid (CSF) profiles, cytokine levels, treatment responses, and survival outcomes were evaluated.
Patients with CNS involvement were older (median age, 54 vs. 46 years; p = 0.013) and had higher disease severity (median HScore, 250 vs. 210; p < 0.001). Malignancy-associated sHLH was more prevalent in the CNS-positive group (42.9% vs. 29.4%; p = 0.038). Neurological manifestations included altered mental status, impaired consciousness, and seizures. Neuroimaging revealed abnormalities in 71.4% of the cases, primarily T2-weighted fluid-attenuated inversion recovery hyperintensities and leptomeningeal enhancement. CNS-positive patients exhibited markedly elevated inflammatory markers, most notably CSF Interleukin-6 (p < 0.001). In multivariable analysis adjusted for malignancy, age, ferritin, and HScore, CNS involvement independently predicted mortality (adjusted HR = 2.0, 95% CI: 1.1–3.7, p = 0.023), with a significantly shorter median overall survival (6.5 vs. 11.5 months, p < 0.0001). Malignancy-associated etiology and HScore ≥ 250 were also independent prognostic factors. The DEP (dexamethasone, etoposide, and polyethylene glycol-asparaginase) regimen achieved a faster median time to initial response than the HLH-94 protocol (9 vs. 14 days, p = 0.02).
CNS involvement defines a severe phenotype of adult-onset sHLH, characterized by malignancy-prone etiology, intense neuroinflammation, and poor prognosis. We establish CNS involvement as an independent predictor of mortality, underscoring the critical need for early recognition and CNS-directed therapies.
High-mobility group protein 1 (HMGB1) is a ligand known to bind to the receptor for advanced glycation end products (RAGE), and it can activate nuclear factor-κB (NF-κB) to mediate cellular damage. RAGE and Parkinson's disease (PD) are closely associated, but it remains unclear whether the HMGB1/RAGE/NF-κB signaling pathway contributes to the pathophysiology of PD.
PD was induced by administration of 6-hydroxydopamine (6-OHDA), while RAGE was inhibited using an inhibitor, FPS-ZM1. The grip strength test and Morris water maze were used to evaluate sensorimotor and memory skills. Then detect the expression levels of RAGE, HMGB1, and NF-κB in the striatal sample using immunohistochemistry, western blotting, and RT-qPCR.
(1) In PD rats, treatment with FPS-ZM1 improved learning and memory ability and alleviated sensorimotor deficits. (2) The striatum of PD rats exhibited a significant increase in the number of HMGB1-, RAGE-, and NF-κB-positive cells, which could be reduced through the administration of FPS-ZM1. Immunofluorescence double-labeling results indicated that NeuN-positive neurons were the primary sites of HMGB1-, RAGE-, and NF-κB-positive responses. Furthermore, these double-labeled neurons demonstrated a significant increase following 6-OHDA-induced depletion of striatal dopamine (DA). However, the FPS-ZM1 administration considerably attenuated these changes. (3) The treatment of FPS-ZM1 significantly reduced the increase in protein expression of HMGB1, RAGE, and NF-κB that followed striatal DA depletion. Similarly, NF-κB and RAGE mRNA expression were increased by striatal DA deprivation; however, injection of FPS-ZM1 significantly reduced these changes.
The HMGB1/RAGE/NF-κB signaling pathway plays a critical role in the pathogenesis of striatal neuronal damage in PD, highlighting its potential as a therapeutic target.
Postoperative delirium (POD) is a common acute cognitive disorder among older adults following elective surgery. It prolongs hospitalization, increases the risk of complications and readmission, and may contribute to long-term cognitive decline, thereby reducing patients' quality of life. Although various preventive strategies have been developed, single interventions often yield limited efficacy. This study systematically evaluates, through meta-analysis, the effectiveness of multicomponent interventions in preventing POD among older adults undergoing elective surgery.
A systematic search was conducted in PubMed, Embase, Web of Science, and the Cochrane Library for randomized controlled trials (RCTs) published through July 2025. Risk ratios (RRs) with 95% confidence intervals (CIs) were calculated to assess intervention effects, and pooled analyses were performed using a random-effects model.
Eleven RCTs comprising 3857 patients undergoing elective surgery were included in the final analysis. Multicomponent interventions significantly reduced POD incidence in older adults (RR: 0.71; 95% CI: 0.59–0.85; p < 0.001), representing a 29% risk reduction. Between-study heterogeneity was low (I2 = 18.0%, p = 0.272). Sensitivity analyses supported the robustness of results. Subgroup analyses indicated a greater effect in Eastern populations compared to Western populations (interaction p = 0.045).
Multicomponent interventions are effective in reducing POD incidence in older adults undergoing elective surgery, with geographical variation influencing effect size. These findings support broader clinical adoption of such interventions for POD prevention.
To compare the clinical outcomes among various infarct patterns and to investigate the associations between the morphological parameters of contralateral middle cerebral artery (cMCA) M1 segment and infarct patterns in ischemic stroke attributed to large vessel occlusion (LVO) in M1 segment caused by intracranial atherosclerotic disease (ICAD).
Patients with stroke attributed to M1-ICAD-LVO were enrolled. The infarct patterns were categorized into artery-to-artery embolism (AAE), large infarct, borderzone infarct (BZI), and perforating artery infarction (PAI). The morphological parameters of cMCA-M1 segment included proximal and distal diameter, arc, and chord length. The tortuosity index of cMCA-M1 segment was calculated by (arc length/chord length − 1) × 100%.
A total of 171 participants were enrolled. Compared to AAE, the risk of poor outcome increased in BZI (odds ratio [OR] = 5.51, 95% confidence interval [CI] = 1.71–17.78, p = 0.004) and large infarct (OR = 10.92, 95% CI = 2.01–59.27, p = 0.006) and was comparable in PAI. The tortuosity index (OR = 2.85, 95% CI = 1.13–7.18, p = 0.026) and arc length (OR = 2.47, 95% CI = 1.02–5.97, p = 0.045) significantly increased in BZI than other three patterns. Participants other than BZI were categorized into large infarct (n = 32) and non-large-infarct (n = 46) groups, and the proximal diameter (OR = 0.22, 95% CI = 0.07–0.72, p = 0.012), arc length (OR = 0.88, 95% CI = 0.78–0.98, p = 0.018), and chord length (OR = 0.87, 95% CI = 0.77–0.995, p = 0.042) were associated with large infarct.
For patients with M1-ICAD-LVO, large infarct and BZI had poorer outcomes than PAI and AAE. The cMCA-M1 segment with elevated tortuosity and arc length was associated with BZI, whereas a thin and short M1 segment was correlated with large infarct in patients with a less tortuous cMCA trunk.
Trigeminal neuralgia (TN) patients are at risk for glymphatic dysfunction due to their prolonged headaches and sleep disturbances.
The aim of this study is to compare the glymphatic function changes in TN patients with healthy controls, to investigate whether there are differences in glymphatic function after decompression surgery, and to examine their relationship with clinical parameters.
The data for this hybrid design study were obtained from the OpenNeuro dataset titled “A large-scale dataset of pre- and post-surgical MRI data in patients with chronic trigeminal neuralgia.” The DTI-ALPS index values were calculated for 62 TN patients with normal brain MRIs and 35 age- and sex-matched healthy controls, as well as for 53 TN patients who had both preoperative and postoperative diffusion tensor imaging. Statistical analyses involved nonparametric tests and Spearman correlation to assess differences between groups and relationships with clinical variables such as age, disease duration, and Sindou grading.
There were no significant differences in DTI-ALPS indices between TN patients and controls. Additionally, preoperative and postoperative comparisons in the TN cohort revealed no significant changes in glymphatic function following surgery. Furthermore, no correlations were observed between DTI-ALPS indices and clinical parameters, including patient age, disease duration, or the severity of neurovascular compression.
The findings of this preliminary study suggest that glymphatic dysfunction is not a contributing factor in the pathogenesis of TN and that microvascular decompression surgery does not alter glymphatic clearance. These results indicate that the underlying mechanisms of TN may be independent of glymphatic impairment, despite the presence of sleep disturbances in this population.
Despite observational studies suggesting a link between asthma and delirium, establishing a definitive causal relationship has been challenging. This study aims to investigate the genetic causality between these conditions, with a particular focus on age-related genetic associations using data from large-scale genome-wide association studies (GWASs).
Bidirectional two-sample Mendelian Randomization (MR) analyses were performed using GWAS summary statistics to evaluate the genetic association between asthma (overall, adult-onset, childhood-onset, and age at asthma diagnosis) and delirium. The inverse variance-weighted (IVW) method was the primary analytic approach, supplemented by weighted median, weighted mode, and MR-Egger methods. Multivariable Mendelian Randomization (MVMR) analyses were conducted to adjust for major confounders, including smoking, body mass index (BMI), alcohol intake, and education. Sensitivity analyses included MR-Egger regression, MR-PRESSO outlier tests, Cochran's Q for heterogeneity, and leave-one-out analyses.
The primary MR analyses found no evidence of a significant genetic causal relationship between asthma and delirium in either direction (asthma to delirium: IVW OR = 1.02, 95% CI: 0.79–1.32, p = 0.86; delirium to asthma: IVW OR = 1.05, 95% CI: 0.99–1.11, p = 0.13). Age-stratified MR analyses for adult-onset and childhood-onset asthma, as well as age at asthma diagnosis, also showed no significant associations with delirium risk. In MVMR analyses adjusting for smoking, BMI, alcohol intake, and education, the direct effects of asthma and its subtypes on delirium, and of delirium on asthma phenotypes, remained non-significant (all p > 0.05). Sensitivity analyses confirmed the robustness of these results, with no evidence of pleiotropy or heterogeneity.
These comprehensive bidirectional MR and MVMR analyses do not support a genetic causal association between asthma and delirium, even after adjusting for key confounders and across age-related asthma subtypes. These findings suggest that previously observed associations may be attributable to non-genetic factors. Future studies integrating clinical and biomarker data are warranted to further explore these relationships.
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