Introduction
Hypercholesterolemia (Hch) is a metabolic disorder classi fied among civilization diseases. It is also a known risk fac tor for several cardiovascular and neurodegenerative diseases (Lowe 2001; Taghizadeh et al. 2019; Leszek et al. 2021; Tucker et al. 2023). The role of Hch in the pathogenesis of these diseases stems from its ability to trigger numerous pathophysiological processes across various organs and tis sues (Ferroni et al. 2003a). Compared to other organs, cho lesterol metabolism in the central nervous system (CNS) is highly autonomous (Bahrami et al. 2020; Zhou et al. 2022). The unique aspect of cholesterol transformation in the brain is due to high level of energy metabolism (Ahmad et al. 2019; Ho et al. 2022), its involvement in myelin metabo lism (Berghoff et al. 2022; Barnes-Vélez et al. 2023), and its role in maintaining the integrity and function of the neuronal membranes and axodendritic system (Orth and Bellosta 2012; Martín et al. 2014). Physiological barriers, such as the blood–brain barrier (BBB), effectively prevent cholesterol transfer between the brain tissue and blood ves sels (Loura et al. 2001; Petrov et al. 2016). Given these con siderations, it can be assumed that Hch affects the function of each component of brain tissue, potentially leading to impaired myelin metabolism, BBB leakage, activation of neuroglia, induction of an inflammatory response, and cell death (Orth and Bellosta 2012; Gamba et al. 2015; Loera Valencia et al. 2019; Barnes-Vélez et al. 2023; de Dios et al. 2023). These processes are also involved in the development of neurodegenerative diseases (Petrov et al. 2016). Among the key mediators of inflammatory response are interleukin IL-1β, IL-4, and IL-6 (Black et al. 2011; Khan et al. 2023),
