Beta amyloid and hyperphosphorylated tau deposits in the pancreas in type 2 diabetes
Authors
Judith Miklossy, University of British Columbia
Hong Qing, University of British Columbia
Aleksandra Radenovic, Swiss Federal Institute of Technology
Andras Kis, Swiss Federal Institute of Technology
Bertrand Vileno, Swiss Federal Institute of Technology
Forro Laszlo, Swiss Federal Institute of Technology
Lisa Miller, National Synchrotron Light Source, Upton, NY. USA
Ralph Martins, Edith Cowan University
Gerard Waeber, National Synchrotron Light Source, Upton, NY. USA
Vincent Mooser, GlaxoSmithKline
Fred Bosman, CHUV, Switzerland
Kamel Khalili, Temple University, Philadelphia, PA. USA
Nune Darbinian, Temple University, Philadelphia, PA. USA
Patrick McGeer, University of British Columbia
Document Type
Journal Article
Publisher
Elsevier Inc.
Faculty
Faculty of Computing, Health and Science
School
School of Exercise, Biomedical and Health Science / Centre of Excellence for Alzheimer's Disease Research and Care
RAS ID
10677
Abstract
Strong epidemiologic evidence suggests an association between Alzheimer disease (AD) and type 2 diabetes, To determine if amyloid beta (AP) and hyperphosphorylated tau occurs in type 2 diabetes, pancreas tissues from 21 autopsy cases (IO type 2 diabetes and 11 controls) were analyzed. APP and tau mRNAs were identified in human pancreas and in cultured insulinoma beta cells (INS~ I) by RT-PCR. Prominent APP and tau bands were detected by Western blotting in pancreatic extracts. Aggregated AB. hyperphosphorylated rau, ubiquilin, apolipoprotein E. apolipoprotein(a), IBI/JlP-1 and JNKI were detected in Langerhans islets in type 2 diabetic patients. AB 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 AP deposits und hyperphosphorylated tau are also associated with type 2 diabetes, highlighting common pathogenetic features in neurodegenerative disorders, including AD and type 2 diabetes und suggesting that AB deposits and hyperphosphorylated tau may also occur in other organs than the brain.
DOI
10.1016/j.neurobiolaging.2008.08.019
Comments
Miklossy, J., Qing, H., Radenovic, A., Kis, A., Vileno, B., Laszlo, F., Miller, L., Martins, R. N., Waeber, G., Mooser, V., Bosman, F., Khalili, K., Darbinian, N., & McGeer, P. (2010). Beta amyloid and hyperphosphorylated tau deposits in the pancreas in type 2 diabetes. Neurobiology of Aging, 31(9), 1503-1515. Available here