Explores NAD+ restoration effects on vascular senescence and inflammation in Alzheimer's, suggesting it may be a therapeutic strategy.
Aβ-driven NAD⁺ deficiency initiates a VDAC1-mtDNA-cGAS/STING cascade that promotes endothelial senescence and neurovascular inflammation in AD pathology, and amplifies neuroinflammation through BEC-microglia crosstalk, highlighting NAD⁺ restoration as a promising AD therapeutic strategy.
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Luo et al. (2026) studied this question.
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