The convergence of Aβ42 and tau at the synapse has been proposed to underlie synaptic dysfunction in AD (McInnes et al., 2018; Ittner et al., 2010; Roberson et al., 2007; Spires-Jones and Hyman, 2014), and recent assessment of APP-CTF levels in synaptosome-enriched fractions from healthy control, SAD, and FAD brains (temporal cortices) has shown that APP fragments concentrate at higher levels in the synapse in AD-affected than in control individuals (Ferrer-Raventós, 2023). This evidence concerns the gene MAPT and Alzheimer disease.