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Cockayne Syndrome Proteins Maintain Mitochondrial Health Through NAD+ Signaling: Preclinical Findings
Synopsis
Cockayne syndrome (CS) is a rare premature aging disorder involving DNA repair defects and mitochondrial dysfunction. Across human, mouse, and nematode models, mitochondrial dysfunction was a consistent feature. NAD+ supplementation improved lifespan and healthspan in nematode models, and NAD+ precursors, such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) corrected mitochondrial issues in CS patient cells. The findings link DNA damage, mitochondrial dysfunction, and poor cellular cleanup processes (mitophagy/autophagy) as drivers of accelerated aging in CS—issues that can be partly reversed by restoring NAD+.
Journal
Aging Cell