These double transgenic animals express the human amyloid precursor protein (APP) with the Swedish mutation (K595N/M596L) and presenilin 1 with the deletion of exon 9 and show histopathological hallmarks of AD (e.g., Aβ deposition, amyloid plaques, astrogliosis, and tau pathology) and cognitive impairment by 7 months of age [27]. The gene discussed is APP; the disease is Cognitive impairment.