In transgenic murine models of advanced stages of AD-like pathology with highly expressed Aβ plaques (Zumkehr et al., 2015; Hefendehl et al., 2016), CEF neuroprotective effects were attributed to the attenuation of glutamatergic excitotoxicity induced by Aβ deposits, while no pronounced effect on APP processing, overall Aβ species levels (except for the increase in Aβ40 levels in the CEF-treated mice), or plaque pathology was observed (Zumkehr et al., 2015). This evidence concerns the gene APP and Alzheimer disease.