We acknowledge that this minimal panel of biomarkers currently has insufficient sensitivity and specificity for clinical application, particularly because it has not been fully evaluated for its ability to discriminate AD from non-AD causes of dementia (although Aβ42, p-tau181, tau, and specific fragments of chromogranin A and cystatin C have shown some ability to distinguish AD from frontotemporal lobar degeneration [FTLD]) [22], [226], [227]. This evidence concerns the gene CST3 and frontotemporal dementia.