Our results were consistent with similar published fibrilisation experiments [15], [23], [24], [25], [26], [27] and we have gone on to demonstrate the relevance of the seeding phenomenon to in vivo disease by seeding fibrillization reactions with spinal cord homogenates from an ALS transgenic mouse model (tgSOD1G93A[28]) that overexpresses a human fALS mutant SOD1. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.