An important contribution of GluA1 to memory decline in AD is also supported by the fact that non-amyloidogenic cleavage of amyloid precursor protein (APP) by γ-secretase promotes LTP and counteracts memory decline by increasing the exocytic delivery and, thereby, the synaptic levels of CP-AMPARs (73), akin to the effects observed upon decreased expression of CALM in our functional electrophysiological experiments (see Fig. 2). The gene discussed is CP; the disease is Alzheimer disease.