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A growing body of evidence emphasizes the pivotal role of inflammation in the progression of HACE ( HH triggers the activation of the NF-B signaling pathway and facilitates the release of proinflammatory cytokines, such as IL-6, IL-1, and TNF-, leading to detrimental inflammatory responses within the central nervous system ( Hypoxia also promotes an inflammatory environment and triggers an inflammatory cascade in CNS tissue, which is further exacerbated by glial cells releasing proinflammatory cytokines ( The activation of glial cells and the release of cytokines have been demonstrated to initiate and contribute to cognitive impairments in individuals with HH ( Figure 4 illustrates the proposed inflammation mechanisms hypothesized to underlie HACE

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As a potent antioxidant, hydroxytyrosol reduces the risk of atherosclerosis and heart disease