In contrast to the basic synaptic transmission (input–output relationship and paired-pulse facilitation), the ‘classical’ n-methyl-d-aspartate (NMDA) receptor-dependent LTP paradigm at Schaffer collaterals/CA1 synapses—a long-lasting enhancement of the strength/efficacy of excitatory synaptic transmission which is widely used in investigations on numerous APP/Aβ models of Alzheimer’s disease (Rowan et al., 2003; Shankar et al., 2008)—turned out to be significantly compromised in 6-month-old Tg2576 mice in comparison to age-matched WTs (Fig. 7D). The gene discussed is APP; the disease is Alzheimer disease.