SOD1 and amyotrophic lateral sclerosis: With familial ALS accounting for 5–10% of cases, neurodegeneration is a hallmark of ALS and results from the complex interaction between genetic and molecular pathways, encompassing glutamate excitoxicity, generation of free radicals, cytoplasmic protein aggregates, modifications of the superoxide dismutase (SOD1) enzymes activity, mitochondrial dysfunction, accumulation of intracellular calcium, all leading to disruption of axonal transport through accumulation of intracellular aggregates [225,226,227,228,229].