CD38 Deletion and Nicotinamide Riboside Supplementation Slow Axon Degeneration After Facial Nerve Injury: Preclinical Findings

Synopsis

After facial nerve injury (axotomy), nerve function often does not fully recover due to axon degeneration, neuron death, and ongoing inflammation. CD38, an enzyme that breaks down NAD+, may regulate these processes. Researchers studied mice lacking CD38 and tested NAD+ supplementation using nicotinamide riboside to see their effects on nerve damage and inflammation. Mice without CD38 showed less microglial activation in the brainstem’s facial nucleus, but no significant change in neuron death. However, these mice experienced slower axon degeneration, less demyelination, and reduced macrophage buildup in the injured nerve. NAD+ supplementation also slowed axon degeneration and demyelination but didn’t affect macrophage levels. These findings suggest that both CD38 deletion and NAD+ supplementation can protect injured axons directly after facial nerve injury.

Journal

Scientific Reports