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This stress leads to suppression of forkhead box O1 (FoxO1) signaling and subsequent upregulation of thioredoxin interacting protein, inhibition of insulin and SOD-2 expression, re-expression of Neurog3, and -cell dedifferentiation and functional failure

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This comprehensive analysis aims to elucidate the multifaceted roles of HS in the CNS, emphasizing its potential as a therapeutic agent and guiding future research to exploit its neuroprotective properties fully.