In the ALS model of SOD1-G93A mice, MEMRI (nasal administration of MnCl2) was used to estimate the axonal transport rate, and anterograde axonal transport was significantly reduced in the rhinencephalon of ALS mice but returned to normal after acute treatment with davunetide (a neuroprotective compound that facilitates microtubule stabilization and repair). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.