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[17] reported that methionine could activate nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) pathway to increase intracellular antioxidant (glutathione, GSH) synthesis and stimulate the methionine sulfoxide reductase antioxidant system, resulting in an endogenous antioxidant response to suppress oxidative stress

Furthermore, comparative analyses between AD and PD and across disease stages remain scarce

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Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes)