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4,11,15 Inflammatory responses mediated by proinflammatory cytokines and pathways, such as nuclear factor kappa B (NF-B) and Toll-like receptor 4 (TLR4), worsen the condition by amplifying oxidative stress and hindering neuronal repair

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This has implications for signaling, ion transport, or endocytosis/exocytosis, all of which are impaired at AD (Wood et al., 2002, 2014)