Abnormally folded protein aggregates responsible for the neurodegeneration were either directly generated by inflammasome components, as in the case of the cleavage of α-synuclein by caspase-1 in Parkinson’s disease, or constituted a trigger for NLRP3 activation such as β-amyloid in Alzheimer’s disease. This evidence concerns the gene CASP1 and early-onset autosomal dominant Alzheimer disease.