Publication Details
Abstract
Background; Epilepsy is caused by hyper excitability and an imbalance between excitation and inhibition, which results in seizures. Epilepsy is a highly common neurological disorder on a global scale, impacting approximately 50 million individuals as stated by the World Health Organization (WHO). It is identified as a neurological condition marked by repetitive seizures triggered by sudden surges in electrical activity within the brain. These seizures arise from abnormal discharges of neurons or the synchronized hyper excitability of neurons. However, various people experience these seizures at different rates. Based on the etiology, epilepsy is categorized into three categories: acquired, idiopathic, and epilepsy of genetic or developmental origin. The onset of idiopathic epilepsy starts in childhood, and it lacks any neurological symptoms. Idiopathic epilepsies include juvenile myoclonic epilepsy and childhood absence epilepsy, among others. Acquired epilepsy is linked to observable structural abnormalities in the brain. The causes of acquired epilepsy encompass various factors that occur during prenatal and infantile stages, cerebral trauma, tumors, infections, hippocampal sclerosis, cerebrovascular disorders, and disorders of the cerebral immune system. For instance, specific examples include viral meningitis, meningioma, cavernous hemangioma, cerebral infarction, and epilepsy triggered by open head surgery. The cause of cryptogenic epilepsy is uncertain. It can be challenging to determine the etiology among acute and distant factors. The 7.5 kb IL-1 gene has a distinct TATA box in its proximal promoter region 1, seven exons, and six introns. It is controlled by distal and proximal promoter elements. IL-1 is expressed as a 31-kDa inactive precursor, as is the case with the majority of the cytokines within the IL-1 family, mostly in response to inflammatory stimuli. A microbial product may serve as the stimulus, although cytokines including tumor necrosis factor (TNF), IL-18, IL-1, and even IL-1 itself can trigger IL-1 transcription. Contrary to IL-1, which is present constitutively in healthy cells, IL-1 must first undergo a sequence of intracellular events before it may cause inflammation. Only a small subset of cell types, including tissue macrophages, blood monocytes, and dendritic cells.
Methodology: The study comprised 90 patients (51 male, 39 female) 50 epilepsy patient and 40 control, the patient and control who attended in Basra Teaching Hospital between November-2022 to March-2023 in Basrah, Southern Iraq. Apparently healthy people age range 2 to 62 years were considered as control groups in this study. IL-1b is examination by molecular processes (Nested PCR). This work was carried out at the College of Health and Medical Techniques' molecular biology laboratory.
Results: From the data provided, we can see that there is a difference in the AA, GG and GA genotypes between the patient group and the control group, this difference is represented by the p-value calculated as 0.0001. Also there is a statistically significant difference in genotype frequencies between the focal and generalized epilepsy.
Conclusions: In conclusion, interleukin-1 beta (IL-1β) appears to be involved in the pathogenesis of epilepsy, particularly in the context of genetic susceptibility.