Atypical PKC, PKCλ/ι, activates β-secretase and increases Aβ<sub>1-40/42</sub> and phospho-tau in mouse brain and isolated neuronal cells, and may link hyperinsulinemia and other aPKC activators to development of pathological and memory abnormalities in Alzheimer's disease.

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作者： Mini P,Sajan ^[1] ; Barbara C,Hansen ^[2] ; Margaret G,Higgs ^[2] ; C Ron,Kahn ^[3] ; Ursula,Braun ^[4] ; Michael,Leitges ^[4] ; Collin R,Park ^[5] ; David M,Diamond ^[5] ; Robert V,Farese ^[6]

作者单位： Internal Medicine and Research Services, James A. Haley Veterans Medical Center, Tampa, Florida, USA; Department of Internal Medicine, University of South Florida College of Medicine, Tampa, Florida, USA. ^[1] Internal Medicine and Research Services, James A. Haley Veterans Medical Center, Tampa, Florida, USA. ^[2] Joslin Research Foundation, Harvard Medical School, Boston, MA, USA. ^[3] Biotechnology Centre of Oslo, Oslo, Norway. ^[4] Departments of Psychology, Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD, University of South Florida, Tampa, Florida, USA. ^[5] Internal Medicine and Research Services, James A. Haley Veterans Medical Center, Tampa, Florida, USA; Department of Internal Medicine, University of South Florida College of Medicine, Tampa, Florida, USA. Electronic address: rfarese@health.usf.edu. ^[6]

关键词 Akt Alzheimer's Atypical PKC Aβ Beta-secretase Insulin Metformin PKC-iota/lambda PKM-zeta Phospho-tau