With respect to hepatotoxicity, animal studies have demonstrated that high doses of quercetin can markedly elevate serum transaminase levels and induce lipid peroxidation as well as glutathione depletion in hepatic tissues (Singh et al., 2021), indicating that excessive quercetin intake may contribute to hepatocellular injury by activating oxidative stress pathways
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The adoption of a pro-inflammatory phenotype in microglia can be driven by various factors, including the presence of pro-inflammatory mediators, infiltration of peripheral immune cells, pathological deposits (such as tau aggregates), and viral proteins [e.g., proteins trans-activator of transcription (Tat)] [26, 27]
