Mitochondrial dysfunction plays a crucial role in the development of Alzheimer's disease (AD), and boosting the mitochondrial stress response (MSR) may help slow neurodegeneration, although research in this area is limited.*
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The study investigates how nicotinamide mononucleotide (NMN), a NAD-boosting agent, enhances MSR in AD models by restoring NAD levels and activating the ATF4-dependent unfolded protein response (UPR). *
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NMN supplementation in mouse models of AD shows promising results, including reduced mitochondrial damage, improved hippocampal function, and enhanced overall healthspan, indicating that targeting MSR could be a viable therapeutic strategy for AD.*