This result is consistent with previous findings that the genetic knockdown of BDNF in 3 × Tg-AD mice with mutant human presenilin-1, APP and human tau did not alter tau phosphorylation levels.35 In contrast, in an in vitro model of differentiated neurons from embryonic carcinoma cells, BDNF was found to cause a rapid decline of phosphorylated tau levels,36 and in rat cerebellar granule cells, similarly, BDNF induces a rapid upregulation of dephosphorylated tau.37 This contradiction may be because of differences in the models used (in vivo versus in vitro). The gene discussed is BDNF; the disease is Alzheimer disease.