Specifically, increases in CYP46A1 activity were beneficial in mouse models of Alzheimer's disease (AD), Huntington's, Niemann-Pick type C, and Machado-Joseph (spinocerebellar ataxia type 3) diseases, amyotrophic lateral sclerosis, glioblastoma, depression, epileptic seizures, and prion infection (17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 29, 30, 31), whereas CYP46A1 inhibition reduced seizures in mice with Dravet syndrome and animals infected with the Theiler's encephalomyelitis virus (27, 28). This evidence concerns the gene CYP46A1 and major depressive disorder.