An array of diverse processes has also been mooted as the primary drivers of ALS symptomatology, including the truncated version of the brain-derived neurotrophic factor (BDNF) receptor, TrkB-TI [22] acid sphingomyelinase [23], ceramide [24], aryl hydrocarbon receptor (AhR) [25], kynurenine [26], tryptophan metabolism [27], melatonin [28], and circadian rhythm disruption [29]. This evidence concerns the gene BDNF and amyotrophic lateral sclerosis.