Immunization with antibody directed against the N-terminal end of full-length tau protein (Dai et al., 2017) significantly reduced the level of amyloid precursor protein (APP), amyloid-β peptides (Aβ40) and Aβ42 in CA1 region of Alzheimer’s disease animal models, indicating that tau-based immunotherapy is actually able to restore the Aβ-dependent and/or independent synaptic dysfunction(s) which occur at early stages in Alzheimer’s disease and other related dementias (Pedersen and Sigurdsson, 2015; Panza et al., 2016). This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.