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It has been shown that administration of -glutamylcysteine (GGC) increases cellular levels of GSH, circumventing the regulation of GSH biosynthesis by providing the limiting substrate (Nakamura et al., Whilst extracellular A plaques, NFT, inflammation in the form or reactive astrocytes and microglia, and neuronal loss are all consistent pathological features of AD, a mechanistic link between these factors is yet to be clarified
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