This mouse model that overexpresses a human βAPPSwe and tau P301L in PS1M146v knock-in background, although a genetic mixture of AD and fronto-temporal dementia mutations, shows synaptic compensation associated with cognitive impairment at the age of 12–16 weeks, and Aβ plaque and tau pathologies several months later [14, 15]. The gene discussed is MAPT; the disease is frontotemporal dementia.