Studies using transgenic mouse models expressing the Swedish familial AD mutant (APP/TTBK1) demonstrated that the induced upregulation of tau tubulin kinase-1 (TTBK1) can promote axonal degeneration via phosphorylation of CRMP-2 and tau within the entorhinal cortex and hippocampus, implicating TTBK1 as a potential therapeutic target for AD [120]. The gene discussed is APP; the disease is Alzheimer disease.