NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer’s disease via cGAS–STING

Cyclic GMP-AMP synthase promotes the inflammatory and autophagy responses in Huntington disease

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Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease

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NAD+ metabolism governs the proinflammatory senescence-associated secretome

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Senolytic therapy alleviates Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an Alzheimer’s disease model

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Accumulation of cytoplasmic DNA due to ATM deficiency activates the microglial viral response system with neurotoxic consequences

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Nicotinamide Riboside Augments the Aged Human Skeletal Muscle NAD+ Metabolome and Induces Transcriptomic and Anti-inflammatory Signatures

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CD38 Deficiency Alleviates D-Galactose-Induced Myocardial Cell Senescence Through NAD+/Sirt1 Signaling Pathway

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NAD+supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency

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Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline

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STING-mediated type-I interferons contribute to the neuroinflammatory process and detrimental effects following traumatic brain injury

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NAD + Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair

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NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

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NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation

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Phosphorylation of ULK1 (hATG1) by AMP-Activated Protein Kinase Connects Energy Sensing to Mitophagy

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