Affiliation:
1. Institute of Engineering in Medicine University of California San Diego La Jolla California USA
2. Department of Neurosciences University of California San Diego La Jolla California USA
Abstract
AbstractAxonal degeneration is a key component of neurodegenerative diseases such as Huntington's disease (HD), Alzheimer's disease, and amyotrophic lateral sclerosis. Nicotinamide, an NAD+ precursor, has long since been implicated in axonal protection and reduction of degeneration. However, studies on nicotinamide (NAm) supplementation in humans indicate that NAm has no protective effect. Sterile alpha and toll/interleukin receptor motif‐containing protein 1 (SARM1) regulates several cell responses to axonal damage and has been implicated in promoting neuronal degeneration. SARM1 inhibition seems to result in protection from neuronal degeneration while hydrogen peroxide has been implicated in oxidative stress and axonal degeneration. The effects of laser‐induced axonal damage in wild‐type and HD dorsal root ganglion cells treated with NAm, hydrogen peroxide (H2O2), and SARM1 inhibitor DSRM‐3716 were investigated and the cell body width, axon width, axonal strength, and axon shrinkage post laser‐induced injury were measured.