In a model of AD, the APP/PS1 double transgenic mouse expressing a chimeric mouse/human amyloid precursor protein and a mutant human presenilin 1, and development of relevant behavioral and histopathological features observed in AD patients (e.g., Aβ peptide deposition and cognitive impairment), is accompanied by a decrease in the levels of PPARα in the hippocampus [144]. The gene discussed is APP; the disease is Cognitive impairment.