Aβ activates GSK3β in APP-V7171x Tau-P301L bigenic mice (with combined Aβ and τ pathology), which accelerates τ pathology because of tyrosine phosphorylation of GSK3β itself— thereby implicating GSK3β in the Aβ cascade hypothesis of AD pathology.10 This evidence concerns the gene GSK3B and Alzheimer disease.