Overexpression of Pin1, a member of the parvulin family of immunophilins [9], reduces Aβ and knockout of Pin1 increases Aβ production in Alzheimer's disease brains, through the isomerization of the cytoplasmic domain of APP at a phosphorylated Thr668/Pro motif [10]. Here, PIN1 is linked to early-onset autosomal dominant Alzheimer disease.