Neurological Research最新文献

Background: Middle cerebral artery (MCA) territory infarction commonly induces a variety of motor function deficits because it involves multiple descending motor pathways, including the corticospinal tract (CST) and corticofugal tract (CFT). Despite the importance of the MCA territory for motor function, there is currently insufficient evidence regarding an injury of the CFT from the secondary motor area in MCA territory infarctions.

Objective: We investigated injury of the CFT from the secondary motor area and CST in patients with MCA using diffusion tensor tractography (DTT).

Methods: Thirty-five patients with MCA territory infarctions and 30 controls were recruited. DTT parameters, including fractional anisotropy (FA) and tract volume (TV), of the CST and CFTs from the dorsal premotor cortex (dPMC) and supplementary motor area (SMA), were analyzed.

Results: In the affected hemisphere, the FA values of the CFTs from the secondary motor areas and CST were significantly lower than those in the unaffected hemisphere and control groups. Additionally, the TV of the CFTs from the dPMC and SMA were significantly lower than those from the unaffected hemisphere.

Conclusion: We observed concurrent injury to the CFTs from the secondary motor area and CST after MCA territory infarction. Our findings contribute to the anatomical understanding of MCA infarction disruption of multiple descending motor pathways.

Background: Ventriculostomy is a common intervention to treat acute hydrocephalus in patients with primary intracerebral (PICH) and primary intraventricular hemorrhage (PIVH). A variety of risk-factors for external ventricular drain (EVD)-associated infections (EVDAI) have been identified, however, it remains unclear how blood extent in PICH and PIVH impacts EVDAI-rates.

Methods: Retrospective single-center cohort study of PICH and PIVH patients undergoing EVD-placement between 01/2009 and 02/2023. Uni- and multivariable logistic regression analysis was used to assess potential predictors of EVDAI.

Results: We included a total of 165 patients with PICH and PIVH who underwent ventriculostomy. EVDAI occurred in 13/165 patients (7.8%) with a median onset time of 8 days (IQR 7;10). Diabetes mellitus (OR 4.91, 95%-CI [1.53-15.71]), postoperative CSF-leakage (OR 4.06, 95%-CI [1.11-12.79]) and CSF-sampling frequency (OR 1.11, 95%-CI [1.00-1.24]) were positively associated with EVDAI. A higher IVH score (OR 1.27, 95%-CI [0.95-1.70]) and intracerebral blood volume (OR 0.76, 95%-CI [0.21-2.80]) showed no significant correlation with higher EVDAI-rates.

Conclusion: In the subpopulation of PICH and PIHV patients, the risk of EVDAI was not associated with a larger radiological blood clot extent. These findings contribute to narrowing down risk factors and targeting further research.

Objective: To evaluate the clinical outcomes and safety of venous sinus stenting in idiopathic intracranial hypertension (IIH) patients across multiple centers in the Middle East and North Africa (MENA) region through the Venous stEnt for idiopathic intraCranial hypertEnsion (VEHICLE) Registry.

Methods: We conducted a retrospective analysis of prospectively collected data from the VEHICLE Registry (NCT06692790) between August 2023 and August 2024. From an initial pool of 187 cases, 100 patients met all inclusion criteria: IIH diagnosis based on modified Dandy criteria, neuroimaging-confirmed venous sinus stenosis, refractory or intolerant to medical therapy, underwent venous pressure manometry, and had complete follow-up data. All patients underwent venous sinus stenting at nine collaborating centers.

Results: Of 100 patients, 73% were female. All presented with headaches, while 87% reported visual disturbances. Venous stenoses predominantly affected the right transverse sinus (56%). At six months, 83% achieved marked symptom resolution, 80% had normalized optic nerve heads, and stent patency was confirmed in 90%. Papilledema grades improved significantly from median Grade III at baseline to Grade I at 6 months (p < 0.001), correlating with increased QOL scores (p < 0.001). Sixteen percent required revision procedures. Complication rates were low, with no procedure-related mortality.

Discussion: Significant improvements in headache, papilledema, and quality of life were observed with a favorable safety profile with venous sinus stenting for medically refractory IIH. However, the retrospective design and lack of a control group limit definitive conclusions about efficacy.

Objectives: Cerebral ischemia-reperfusion (CI/R) injury is a significant hurdle in ischemic stroke treatment. Substantial evidence indicates that long non-coding RNAs (lncRNAs) are implicated in CI/R injury. Here, we explore the function of lncRNA MCM3AP-AS1 in CI/R injury.

Methods: Employed the middle cerebral artery occlusion/reperfusion (MCAO/R) mice model and oxygen-glucose deprivation/reoxygenation (OGD/R) HT22 cell model to mimic in vivo and in vitro CI/R injury. Morris water maze test assessed mice platform-finding latency and swimming distance. Real-time quantitative reverse transcription PCR were conducted to examine the levels of MCM3AP-AS1 and microRNA (miR)-27b-3p. Modified Neurological Severity Score (mNSS) assessed neurological deficits, and triphenyl tetrazolium chloride staining assessed cerebral infarct volume. Enzyme-linked immunosorbent assay quantified inflammatory factor levels. Cell count kit-8 and flow cytometry detected cell viability and apoptosis, respectively. Dual luciferase reporter and RNA immunoprecipitation assays verified targeting relationships.

Results: MAMC3AP-AS1 expression decreased in the brain tissue of MCAO/R mice and OGD/R-treated cells, while miR-27b-3p levels were rose. Upregulating MCM3AP-AS1 notably suppressed mNSS scores, reduced infarct volume, and alleviated cognitive dysfunction in MCAO/R mice; however, miR-27b-3p attenuated the function of MCM3AP-AS1. Furthermore, OGD/R treatment inhibited cell viability, increased apoptosis, and promoted inflammatory factors secretion, MCM3AP-AS1 reversed these effects, but miR-27b-3p significantly impaired this reversal. Mechanistically, MCM3AP-AS1 targeted miR-27b-3p.

Discussion: MCM3AP-AS1 exerts neuroprotection by attenuating miR-27b-3p levels, thereby mitigating CI/R injury.

Background: Biomarkers for disease activity are lacking in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We aimed to investigate whether motor nerve conduction studies (NCSs) and nerve ultrasound and their follow-up changes could predict steroid-dependency and treatment refractoriness.

Methods: Sixty-three CIDP patients were followed up with both nerve ultrasound and NCS. Cross-sectional areas (CSAs) were measured on the bilateral median, ulnar nerves and brachial plexus. NCSs were performed on the median and ulnar nerves.

Results: Patients with normal or mildly slow MCV at the first visit were less likely to be steroid-dependent and had lower INCAT at the last follow-up (median 0 [0,1]), whereas those with dramatically slow MCV were more likely to be steroid-dependent and had higher INCAT at the last follow-up (median 2[2,2]) (p = 0.009 for steroid dependent, p = 0.004 for INCAT). None of the patients whose MCV improved above the lower normal limit were steroid-dependent, whereas nearly half of those whose MCV decreased or remained unchanged were steroid-dependent (p = 0.005). A two-step method had a sensitivity of 85% and specificity of 80% for distinguishing patients with steroid dependency. First, we divided patients into three groups according to the MCV change. Second, we explored the trend of steroid-dependent and treatment-refractory based on the CSA at admission and change in CSA.

Conclusions: For patients whose MCV improved beyond the threshold, the risk of relapse was low, and we suggest more rapid tapering of steroid. For those with decreased MCV, the risk of relapse was greater and slower steroid tapering or immunosuppressant use is suggested.

Objective: This study aims to elucidate the mechanism by which astragaloside IV (AS-IV) mitigates cerebral ischemia-reperfusion injury (CIRI), with a focus on serotonin receptor 2B (HTR2B)-mediated microglial polarization and neuroinflammation.

Methods: In vivo, CIRI was induced in rats via middle cerebral artery occlusion-reperfusion (MCAO/R). Rats received AS-IV or HTR2B overexpression vector. In vitro, highly aggressive proliferating immortalized (HAPI) microglia were polarized to M1 with lipopolysaccharide (LPS), followed by AS-IV treatment and co-culture with neuron-like PC12 cells. Neurological function was scored using the Longa scale. Infarct volume and histopathology were assessed by TTC and HE staining, respectively. Levels of inflammatory cytokines in rat brain tissues and HAPI cells were quantified by enzyme-linked immunosorbent assay (ELISA). The viability of HAPI and PC12 cells was assessed using cell counting kit-8 (CCK-8). PC12 apoptosis was evaluated via terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining.

Results: CIRI rats exhibited significant neurological deficits, enlarged infarct area, and pronounced neuronal damage, which were markedly alleviated by AS-IV treatment. AS-IV also inhibited HTR2B expression and reduced pro-inflammatory cytokine release in both in vivo and in vitro models. In HAPI-PC12 co-culture system, AS-IV reversed LPS-induced microglial activation, restoring PC12 viability and reducing apoptosis. HTR2B overexpression abolished neuroprotective effects of AS-IV, promoting microglial M1 polarization and exacerbating neuroinflammation.

Conclusion: AS-IV protects against CIRI by downregulating HTR2B and inhibiting microglial M1 polarization. These findings identify the HTR2B-microglial axis as a promising therapeutic target for ischemic stroke.

Purpose: The study objectives were to construct lncRNA-miRNA-mRNA ceRNA regulation network of Alzheimer's disease (AD) and screen the key biomarkers related to AD.

Methods: The gene expression data GSE84422 and GSE101684 were downloaded from the NCBI-GEO databases. The differentially expressed RNAs (DElncRNAs, DEmiRNAs, and DEmRNAs) (DERs) were identified by the limma package in R. Then, the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway on the DEmRNAs were analyzed. Moreover, the lncRNA-miRNA-mRNA ceRNA network of AD was built, the key lncRNAs in the ceRNA network were obtained, and the GO and KEGG analysis of lncRNA target genes were performed.

Results: In total, we acquired 557 DEmRNAs, 36 DElncRNAs and 178 DEmiRNAs in AD. We found that the DEmRNAs were significantly associated with immune-related pathways, such as antigen processing and presentation and graft-versus-host disease. Moreover, the ceRNA regulation network of AD was construct. We identified two key up-regulated lncRNAs, including LINC01094 and LINC00092; and ten key down-regulated lncRNAs, such as CH17-264L24.1, LINC01140 and RP11-159D12.2, etc.

Conclusion: This research built a ceRNA regulation network of AD, which is of great significance for identifying the biomarkers related to AD.

Background: MicroRNAs (miRNAs) have attracted considerable attention as promising new tumor biomarkers.

Aims: This study primarily integrates computed tomography (CT) findings to investigate the expression and potential implications of miR-136-5p in glioma.

Methods: Human glioma samples were obtained from 122 glioma tissues and 80 adjacent tissues resected by surgery from confirmed patients. Reverse transcription quantitative PCR (RT-qPCR) was used to detect the expression of the genes. Receiver Operating Characteristic (ROC) curve was used to evaluate the diagnostic value of miR-136-5p combined with Computed Tomography (CT) in glioma. Correlation analysis was conducted employing Pearson's method. The target genes of miR-136-5p were identified using the TargetScan online database and validated through dual luciferase reporter assays.

Results: In glioma tissues, the expression of miR-136-5p was markedly downregulated. Its expression correlates with CT signs and clinicopathological features of glioma patients. Both CT detection and miR-136-5p expression showed significant potential in diagnosing glioma, and combining the two improved the diagnostic value of glioma. Furthermore, the overexpression of miR-136-5p has been shown to negatively regulate the expression of the BCL9L gene in U87 and U251 glioma cell lines, thereby inhibiting tumor cell proliferation and promoting apoptotic processes.

Conclusions: miR-136-5p is downregulated in glioma tissues and closely correlates with tumor CT signs. It may serve as a promising biomarker to assist in glioma diagnosis using CT scans.

Background: Multiple Sclerosis (MS) is a chronic neurological disorder affecting millions worldwide. Early detection is vital to prevent long-term disability. Magnetic Resonance Imaging (MRI) plays a crucial role in MS diagnosis, yet differentiating MS lesions from other brain anomalies remains a complex challenge.

Objective: To develop and evaluate a novel deep learning framework-2DRK-MSCAN-for the early and accurate detection of MS lesions using MRI data.

Methods: The proposed approach is validated using three publicly available MRI-based brain tumor datasets and comprises three main stages. First, Gradient Domain Guided Filtering (GDGF) is applied during pre-processing to enhance image quality. Next, an EfficientNetV2L backbone embedded within a U-shaped encoder-decoder architecture facilitates precise segmentation and rich feature extraction. Finally, classification of MS lesions is performed using the 2DRK-MSCAN model, which incorporates deep diffusion residual kernels and multiscale snake convolutional attention mechanisms to improve detection accuracy and robustness.

Results: The proposed framework achieved 99.9% accuracy in cross-validation experiments, demonstrating its capability to distinguish MS lesions from other anomalies with high precision.

Conclusion: The 2DRK-MSCAN framework offers a reliable and effective solution for early MS detection using MRI. While clinical validation is ongoing, the method shows promising potential for aiding timely intervention and improving patient care.

Objectives: PSMC3IP, a gene involved in proteasome function, has been linked to various cancers, though its role in low-grade glioma (LGG) remains underexplored. This study investigates its expression and mechanisms in LGG, offering insights into treatment and prognosis evaluation.

Methods: Integrate multi-omics data from TCGA, CGGA, and other sources to analyze the association between PSMC3IP expression and clinical features and survival prognosis, and combine methylation analysis, immune infiltration assessment, and GSEA-enriched pathways to elucidate its functional mechanisms.

Results: The overexpression of PSMC3IP in LGG was significantly correlated with malignant clinical features, including higher WHO grade, tumor recurrence, and 1p19q co-deletion (p < 0.05). Patients with high PSMC3IP expression exhibited significantly shortened overall survival (p < 0.001). Methylation analysis revealed that the cg12628062 locus negatively regulated PSMC3IP expression (r = -0.22, p < 0.001). Immune microenvironment profiling demonstrated that PSMC3IP overexpression promoted tumor associated macrophages to polarize towards M2 morphology, suppressed CD8+ T cell activity, and elevated expression of immune checkpoints (PDCD1/CTLA-4). Gene Set Enrichment Analysis (GSEA) further highlighted its enrichment in DNA replication and base excision repair pathways, suggesting its oncogenic role through genomic instability and immunomodulatory mechanisms.

Conclusion: PSMC3IP is overexpressed in LGG and serves as an independent prognostic factor for poor survival. Its involvement in immune regulation and key molecular pathways, including DNA replication, suggests it may be a target for therapeutic strategies in LGG.