This allowed us to use Cyp46a1−/− (6) and EFV-treated 5XFAD mice (an Alzheimer’s disease model) (53) as animal models with lacking and increased, respectively, CYP46A1 activity, and hence altered brain cholesterol turnover and sterol flux (6, 19, 23). This evidence concerns the gene CYP46A1 and Alzheimer disease.