We investigated whether the N-Aβcore could rescue LTP and LTD dysfunction resulting from prolonged, elevated levels of Aβ in an APP/PS1 transgenic mouse model harboring mutations found in familial Alzheimer’s disease (FAD), while assessing the impact on AMPA-type glutamate receptor expression in reference to the neuroprotective action of the N-Aβcore in Aβ-synaptotoxicity (Forest et al., 2020). The gene discussed is APP; the disease is familial Alzheimer disease.