THE STUDY OF ASSOCIATIONS BETWEEN IL1Β C3953T GENE POLYMORPHISM AND CLINICAL-NEUROLOGICAL, NEUROIMAGING, HEMODYNAMIC CHARACTERISTICS AND COGNITIVE DYSFUNCTION IN PATIENTS WITH POST-INFECTIOUS ENCEPHALOPATHY

The aim: To investigate potential associations between the C3953T polymorphic variant of the interleukin-one beta (IL1β) gene and clinical-neurological, neuroimaging, hemodynamic characteristics, as well as cognitive dysfunction in patients with post-infectious encephalopathy (PIE). Materials and methods: A total of 128 patients with post-infectious encephalopathy (PIE) who were receiving inpatient treatment in the neurological departments of the Communal Non-commercial Enterprise “Ternopil Regional Clinical Psychoneurological Hospital” of Ternopil Regional Council,” Ternopil, Ukraine, were examined and included in the retrospective analysis in 2021–2022. The molecular-genetic testing was performed for 26 patients in the molecular genetics laboratory of the State Institution “Reference Centre for Molecular Diagnostics of the Ministry of Health of Ukraine,” Kyiv. The control group consisted of 12 people, who were representative in age and gender. Statistical processing of the results was performed using the STATISTICA 10.0 software. Results: Analysis of the dependence of neuroimaging changes on the frequency of genotypes of the C3953T polymorphic variant of the IL1β gene in patients with PIE showed a significant relationship between their frequency distribution and the presence/absence of gliosis phenomena (p=0.009). Thus, gliosis was detected in all carriers of the T/T genotype C3953T polymorphic variant of the IL1β gene. Analyzing the dependence of changes obtained during the transcranial Doppler ultrasound scanning of cerebral vessels on the polymorphic variant C3953T of the IL1β gene in patients with PIE, all carriers of the T/T genotype were diagnosed with angiospasm (p=0.038) and vertebrobasilar insufficiency (p=0.010). Conclusions: Results suggest the reasonability of further researching the interaction between IL1β and glial cells and changes in the cognitive functioning of cytokine genotypes with larger sample sizes that may help explain the pathophysiological mechanisms leading to cognitive impairment in patients with PIE.