The triple-transgenic model of AD, which contains the APPSWE, Presenilin-1 (PSENM146V) and tau mutations (tauP301L) offers the advantage that they develop Aβ plaques, tau tangles, synaptic dysfunction and LTP deficits which all manifest in an age-related manner (Oddo et al., 2003). This evidence concerns the gene PSEN1 and Alzheimer disease.