PIN1 and dementia: If Aß were a major neuro-toxic peptide in dementia, FDDKI/APPTA/TA mice should either have deficits comparable to FDDKI mice based on the evidence that the Thr668Ala mutation does not change Aß levels [28], [29], or should present with a worsened phenotype based on the hypothesis that binding of Pin1 to APPpThr668 reduces Aß levels [27].