Nicotinamide Riboside Protects Against High-Altitude Hypoxia Brain Injury: Preclinical Findings

Synopsis

Exposure to low oxygen at high altitudes can harm learning and memory by affecting neuron function and connections in the hippocampal CA1 region of the brain. Research shows that mitochondrial reactive oxygen species (mtROS) can over-activate microglia, causing brain inflammation and damage. Nicotinamide riboside (NR), which the body converts into NAD+ to help mitochondria produce energy, may protect these neurons. In mice exposed to simulated high-altitude hypoxia and in low-oxygen cell models, hypoxia reduced memory performance, dendritic spine density, and synaptic connections, while increasing mtROS and inflammatory markers. Treatment with NR improved memory, increased dendritic spines and synaptic density, boosted mitochondrial ATP, partially restored mitochondrial health, and reduced microglial activation and inflammation. These findings suggest that NR can protect the hippocampal CA1 region from hypoxia-induced damage mainly by reducing harmful mtROS and calming overactive microglia.

Journal

Biomolecules