The presence of chaperones in extracellular insoluble protein aggregates has been reported in proteinopathies like amyloidotic cardiomyopathy [70], Alzheimer’s disease [71] and TTR amyloidosis [72], and related to failed attempts to keep misfolded proteins in a soluble state, under conditions of a large excess of aggregation-prone proteins [70, 72, 73]. This evidence concerns the gene TTR and early-onset autosomal dominant Alzheimer disease.