After injection of the vector, CYP46A1 and 24-OH content were increased to control levels, and cognitive deficits were remedied, whereas tau hyperphosphorylation and associated gliosis were unaffected, indicating that CYP46A1 may be a relevant therapeutic target for tauopathies, and especially for AD [17]. This evidence concerns the gene CYP46A1 and Cognitive impairment.