Inflammation, or more specifically neuroinflammation, is one of the more heavily researched ALS contributors (Kim et al., 2015), which is frequently assessed in the familial or transgenic superoxide dismutase-1 guanine 93 to alanine (SOD1 G93A) murine model (Pfohl et al., 2015). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.