This alteration leads to PSEN1 over-expression, enhanced amyloidogenesis and increased senile plaque burden, which lead to worse behavioral scores in three-month-old TgCRND8 AD transgenic mice, which bear a doubly mutated human APP transgene and produce amyloid plaques starting at 2 months of age [15,16]. The gene discussed is PSEN1; the disease is Alzheimer disease.