Neuroscience Insights: Advances in Brain Studies
Research Article Volume: 1 & Issue:1
Abstract
Background and Objectives: Glial neoplasms account for approximately 50% of adult primary brain tumors. Seizures are a common manifestation, affecting nearly 90% of low-grade and 50% of high-grade glioma patients. Of these, around 30% remain drug-resistant despite surgical resection. The mechanisms underlying glioma-associated seizures are complex and not fully elucidated. Emerging evidence points toward multifactorial origins involving genomic, transcriptomic, proteomic, and metabolomic dysregulation. Notably, the glutamate signalling and immune modulation pathways have been implicated. This study aimed to investigate the mRNA expression of SLC17A7 (glutamate signalling) and CXCL8 (immune trafficking) genes in intraoperative tumor tissue of glioma patients with a particular focus on the potential differences between patients who experience seizures and those who do not.
Methods: In this prospective study, 50 glioma patients were enrolled, 25 with seizures and 25 without. Patients with recurrent tumors or non-tumor-related seizures were excluded. Following preoperative assessments and surgical intervention, intraoperative tumor tissue samples were collected. mRNA expression of SLC17A7 and CXCL8 was analysed using RT-PCR. All ethical standards were adhered to, and the genetic analysis team was blinded to clinical seizure status.
Results: CXCL8 downregulation was observed in 64% of glioma patients with seizures, compared to 44% without seizures. Although the difference was not statistically significant, this trend suggests a potential role for CXCL8 in the pathogenesis of seizures. SLC17A7 mRNA could not be reliably detected, despite repeated attempts. The likely cause is mRNA instability, possibly due to microRNA interference or alternative splicing.
Conclusions: CXCL8 downregulation appears more frequent in glioma patients with seizures, indicating a possible link to immune dysregulation in epileptogenesis. SLC17A7 mRNA was undetectable via RT-PCR, possibly due to its instability or alternative splicing in glioma tissue. Despite DNA-level amplification of SLC17A7 reported in other studies, this may not translate to increased mRNA or protein expression. Further mRNA expression studies in larger cohorts are needed to validate these findings.