In addition, VO-OH(pic) treatment of APP/Psen transgenic mice, a mouse model of AD, rescued synaptic function and mouse cognitive deficits, in parallel with protecting from Aβ (49)-induced NMDAR-dependent long term depression and synaptic toxicity events, a phenomena which was dependent on PTEN recruitment to synaptic spines through PTEN-PDZ interactions [94,164]. This evidence concerns the gene APP and Alzheimer disease.