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This research investigates how NAD+ depletion affects vascular aging and inflammation in Alzheimer's disease.

April 27, 2026Alzheimer s & Dementia0 citationsOpen Access

Endothelial NAD + depletion drives vascular senescence and neuroinflammation via mtDNA‐cGAS/STING‐CD38 signaling in Alzheimer's disease

QLQinghua LuoNanchang University FLF LiJiangnan University LYLi YangNanchang University

Key Points

This research investigates how NAD+ depletion affects vascular aging and inflammation in Alzheimer's disease.
Examined the role of Aβ in inducing NAD+ deficiency and its effects on endothelial cells.
Analyzed the VDAC1-mtDNA-cGAS/STING signaling pathway and its implications for neuroinflammation.
Focused on the crosstalk between brain endothelial cells and microglia.
NAD+ deficiency significantly correlates with increased endothelial senescence and neurovascular inflammation.
Restoration of NAD+ levels decreased neuroinflammation and improved endothelial function in experimental models.

Abstract

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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