The same can be speculated to all the others extracellular chaperones observed to be overrepresented, as clusterin, that was previously implicated in fibrillogenesis and extracellular misfolded protein clearance in Alzheimer disease [63] and its overexpression was described to have possible protective role in transthyretin deposition in ATTR [57], although significantly lower levels of circulating clusterin were associated with amyloid deposition in the heart in ATTR, is what appears to reflect a unique difference in amyloidosis pathology, dependent on organ involvement [64]. This evidence concerns the gene CLU and early-onset autosomal dominant Alzheimer disease.