Other studies also suggest that the endocytosis of assemblies with an ordered β-sheet structure may be an important factor in amyloid disease, for example in the cytotoxicity of Ure2p amyloid-like protofibrils and Aβ1–42 oligomers (59, –, 61); synaptic disruption induced by Aβ1–42 oligomers (62); intracellular aggregate formation by Aβ1–40, α-synuclein, polyglutamine sequences, and superoxide dismutase-1 (63, –, 66); and for the activation of the inflammasome by Aβ1–42 fibrils (67). This evidence concerns the gene SOD1 and amyloidosis.