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Significance Alzheimer’s disease (AD) is the leading cause of dementia in the elderly. Although dysregulated hydrogen sulfide (H 2 S) metabolism has been reported in AD, and H 2 S donors are beneficial, molecular mechanisms underlying neuroprotective effects of H 2 S are largely unknown. We now show that H 2 S confers neuroprotection by sulfhydrating GSK3β to inhibit its activity, thereby preventing hyperphosphorylation of Tau, a key pathogenic event in AD. Administering H 2 S donors improves motor and cognitive functions in a mouse model of AD.
Giovinazzo et al. (Mon,) studied this question.