SOD1 and amyotrophic lateral sclerosis: The development of disease-associated aggregates has been attributed to abnormal cleavage of amyloidogenic peptides (e.g. β-amyloid (1–42) in Alzheimer’s disease); over-expression of intrinsically disordered proteins (e.g. amylin in type 2 diabetes); and the introduction of amyloidogenic mutations into wild-type amino acid sequences (e.g. SOD1 in amyotrophic lateral sclerosis: ALS)13–16.