Article: Nicotinamide Riboside Counteracts Alcohol-Induced Neurotoxicity: Preclinical Findings

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Inflammation Neuroinflammation Neurological Health Preclinical

Nicotinamide Riboside Counteracts Alcohol-Induced Neurotoxicity: Preclinical Findings

Synopsis

Excessive alcohol intake causes cognitive impairment and neuronal injury driven by oxidative stress, inflammation, and profound mitochondrial dysfunction. This study shows that NRC, an NAD+ precursor, significantly improves alcohol-induced behavioral deficits and reduces neuroinflammation. Proteomic data and GEO analyses identified disrupted mitophagy and a suppressed mitochondrial unfolded protein response (UPRmt) as central mechanisms of alcohol-related neurotoxicity. NRC restored mitochondrial homeostasis by activating UPRmt and enhancing Fundc1-dependent mitophagy. Blocking UPRmt eliminated NRC’s benefits by reducing Fundc1 expression and mitophagy, while mitophagy inhibition did not suppress UPRmt—indicating that UPRmt acts upstream of Fundc1 signaling. Overall, NRC counteracts alcohol-induced neuronal damage by repairing mitochondrial quality control pathways, highlighting UPRmt-driven mitophagy restoration as a promising therapeutic strategy for alcohol-related neurodegeneration.

Journal

Genes & Diseases

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