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Otherwise, Nfkb1 , as the central regulator of neuroinflammationassociated disease pathogenesis (Niranjan, 2013), induces reactive oxygen species and proinflammatory cytokines (such as IL1, interferon, and TNF) that cause secondary neurotoxicity (Block, Zecca, & Hong, 2007

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In the late 1970's and early 1980's there was some debate whether IDE or glutathione insulin transhydrogenase (GIT, now identified as protein disulfide isomerase, PDI) acted first on insulin [39]

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