APP and Alzheimer disease: Given that Aβ plaques are not prominent in the hippocampus of 3–4 mo old APPNL‐G‐F mice (Figure S1), and that studies in other transgenic AD models (e.g., APP/PS1 mice) indicate that oAβ is the predominant Aβ species at this young age,31 we inferred that oAβ, rather than plaques, is primarily responsible for the observed mf‐LTP deficits.