In the AD model literature we noted that reports indicating that wild type forms of other proteins rendered amyloidogenic by autosomal dominant mutations, e.g. Bri2 [215], cystatin C [213,214], gelsolin [217,218,238], and perhaps neuroserpin [239] (mutations result in non-amyloid neuropathologic aggregation), seem to be over-represented as a class. This evidence concerns the gene GSN and Alzheimer disease.