Physiological inhibitors for Tau fibrillization, such as molecular chaperones Hsp70 [6], [7] and PDI (this work), and molecular chaperones disaggregating Tau filaments, such as Hsp104 [68], hold promise for development of novel strategies for treatment and early diagnosis of Alzheimer disease. This evidence concerns the gene P4HB and early-onset autosomal dominant Alzheimer disease.