mouse tissue sequencing

This study investigates the intricate role of nicotinamide adenine dinucleotide (NAD+) in mammalian aging and addresses the challenge of regulating NAD+ synthesis for anti-aging purposes. By overexpressing nicotinamidase (PncA) in mice, responsible for converting nicotinamide to nicotinic acid, the research reveals organ-specific preferences for NAD+ synthesis pathways and precursors. The novel approach of modulating conversion in situ, bypassing systemic variables, highlights pronounced heterogeneity in precursor utilization efficiency among different organs. Furthermore, the study explores the impact of PncA on aging in various mouse organs, demonstrating delayed aging markers in the liver and kidney of older mice, while paradoxically accelerating cardiac aging and cognitive decline in younger mice. These findings underscore the importance of organ-specific strategies in NAD+ precursor supplementation, offering a nuanced perspective on NAD+ metabolism and emphasizing the need for tailored interventions in the aging process.