Since the reduced activation of Akt in the PDK1K465E/K465E neurons protected cells against TNFα and ER stress, two proposed key mediators of Aβ-induced pathology, and the PDK1/Akt signaling pathway is hyperactivated in AD transgenic mice models, we reasoned that the PDK1K465E/K465E mutant neurons should be also protected from Aβ-induced neurotoxicity. Here, PDK1 is linked to Alzheimer disease.