The amyloid-β42 peptide is more hydrophobic and the most common isoform of amyloid-β plaques.55–58 These insoluble peptides aggregate in the brain, forming amyloid-β plaques, and are associated with neurotoxicity.55,57,59 Neurofibrillary tangles caused by breakdown of the stabilizing protein Tau follow amyloid-β plaque onset.29,60 In AD, Tau is hyperphosphorylated, leading these proteins to dissociate from the neuron and tangle on other tau proteins.29,54,60 This causes neurons to collapse and prevents communication between synapses. Here, PPIB is linked to Alzheimer disease.