The results presented here show that an expression of mutated human APP and PS-1 that produced β-amyloid1-42 and β-amyloid1-40 levels, plaque formation from 2–3 months onwards with the associated inflammatory response, and memory impairments from 8 months onwards [3] has distinct effects on synaptic plasticity in area CA1 of the hippocampus. Here, APP is linked to memory impairment.