Finally, through the use of pharmacological inhibitors the authors showed that the injury-induced synaptic deficits due to tau hyperphosphorylation were mediated likely by GSK3β and CDK5, kinases that phosphorylate tau and whose expression has been observed to be upregulated in AD brains (Yamaguchi et al., 1996; Blalock et al., 2004). This evidence concerns the gene MAPT and Alzheimer disease.