In addition to the loss of MNs, canine models affected by CDM share some other pathological features with SOD1-ALS rodent models and patients, such as oligodendrocyte damage leading to demyelination [192], an increase of arginase 1-expressing microglia in the vicinity of motor neurons [193], and upregulation of CB2 receptors in glia cells that serve as a marker of major cellular and biological responses to disease [194]. Here, SOD1 is linked to amyotrophic lateral sclerosis.