As in human, transgenic mice show an overexpression of Aβ and development of senile plaques; the main observation arising from mouse model was that an excess of Aβ is enough to induce cognitive impairment and synaptic dysfunction even in the absence of NTFs or neuronal loss (Gotz et al., 2004), confirming that Aβ overproduction must trigger AD, before tau deposition. Here, MAPT is linked to Cognitive impairment.