CAMK2A and Alzheimer disease: To dissect the specific role of neuronal FT in AD pathogenesis and to circumvent the impact of FT deletion during the embryonic development, we crossed FT-floxed (FTf/f) mice with the CaMKIIα promoter-driven Cre recombinase (Cre+) transgenic mice to generate conditional FT knockout mice (FTnKO) (Fig. 3A), in which FT is selectively deleted in the forebrain neurons postnatally [33, 34].