These experiments were performed in a different amyloid precursor protein/presenilin-1 (APP/PS1) AD mouse model (Radde et al. 2006) than that used in previous studies (Aytan et al. 2016; Carreras et al. 2019), and completely rescued synaptic deficits (i.e., reduced number of synaptic spines and reduced long-term potentiation in hippocampal CA1 pyramidal neurons) that were present in sham-treated APP/PS1 animals (Kartalou et al. 2020). This evidence concerns the gene PSEN1 and Alzheimer disease.