Miklossy, J.Qing, H.Radenovic, A.Kis, A.Villeno, B.Forro, L.Miller, L.Martins, R.Waeberf, G.Mooser, V.Bosman, F.Khalili, K.Darbinian-Sarkissian, N.McGeer, P. L.2010-07-222010-07-222010-07-22201010.1016/j.neurobiolaging.2008.08.019https://infoscience.epfl.ch/handle/20.500.14299/51835WOS:000280454700002Strong epidemiologic evidence suggests an association between Alzheimer disease (AD) and type 2 diabetes. To determine if amyloid beta (A$\beta$) and hyperphosphorylated tau occurs in type 2 diabetes, pancreas tissues from 21 autopsy cases (10 type 2 diabetes and 11 controls) were analyzed. APP and tau mRNAs were identified in human pancreas and in cultured insulinoma beta cells (INS-1) by RT-PCR. Prominent APP and tau bands were detected by Western blotting in pancreatic extracts. Aggregated A$\beta$, hyperphosphorylated tau, ubiquitin, apolipoprotein E, apolipoprotein(a), IB1/JIP-1 and JNK1 were detected in Langerhans islets in type 2 diabetic patients. A$\beta$ was co-localized with amylin in islet amyloid deposits. In situ beta sheet formation of islet amyloid deposits was shown by infrared microspectroscopy (SIRMS). LPS increased APP in non-neuronal cells as well. We conclude that A$\beta$ deposits and hyperphosphorylated tau are also associated with type 2 diabetes, highlighting common pathogenetic features in neurodegenerative disorders, including AD and type 2 diabetes and suggesting that A deposits and hyperphosphorylated tau may also occur in other organs than the brain.Alzheimer's diseaseAmylinBeta amyloidApolipoprotein-EApolipoprotein-aAPPLPSType 2 diabetesIB1/JIP-1JNK-1TauUbiquitintext::journal::journal article::research article