Although almost all of the proteins encoded by the human genome can be efficiently removed from the cell when misfolded, a number of polypeptides produced from post-translational conjugation, such as hyperphosphorylated tau in Alzheimer’s disease (AD), or due to endoproteolytic cleavage, such as amyloid β peptides, tend to be rapidly aggregated into oligomers enriched in β-sheet and escape the regular degradation process [70,71,72,73]. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.