Maj M, Ilhan A, Neziri D, Gartner W, Berggard T, Attems J, Base W, Wagner L. Age related changes in pancreatic beta cells: A putative extra-cerebral site of Alzheimer’s pathology. World J Diabetes 2011; 2(4): 49-53 [PMID: 21537460 DOI: 10.4239/wjd.v2.i4.49]
Corresponding Author of This Article
Ludwig Wagner, MD, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. ludwig.wagner@meduniwien.ac.at
Article-Type of This Article
Editorial
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World J Diabetes. Apr 15, 2011; 2(4): 49-53 Published online Apr 15, 2011. doi: 10.4239/wjd.v2.i4.49
Age related changes in pancreatic beta cells: A putative extra-cerebral site of Alzheimer’s pathology
Magdalena Maj, Aysegul Ilhan, Dashurie Neziri, Wolfgang Gartner, Tord Berggard, Johannes Attems, Wolfgang Base, Ludwig Wagner
Magdalena Maj, Aysegul Ilhan, Dashurie Neziri, Wolfgang Gartner, Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, 1090 Vienna, Austria
Johannes Attems, Newcastle University, Institute for Ageing and Health, Newcastle upon Tyne, NE4 5PL, United Kingdom
Author contributions: Maj M, Berggard T, and Wagner L wrote this manuscript; Ilhan A and Neziri D were responsible for manuscript correction and discussion; Gartner W and Base W participated in manuscript correction and critical review; and Attems J was responsible for consultation and discussion.
Supported by the Grant from the National Bank of Austria, No. 13402, and the Fund of the Major of the City of Vienna, No. 08052
Correspondence to: Ludwig Wagner, MD, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. ludwig.wagner@meduniwien.ac.at
Telephone: +43-1-40400-4319 Fax: +43-1-40400-7790
Received: May 28, 2010 Revised: March 29, 2011 Accepted: April 5, 2011 Published online: April 15, 2011
Abstract
Frequent concomitant manifestation of type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) has been recently demonstrated by epidemiological studies. This might be due to functional similarities between β-cells and neurons, such as secretion on demand of highly specific molecules in a tightly controlled fashion. An additional similarity represents the age-related alteration of hyperphosphorylated tau in AD patients. Similarly, alterations have been identified in β-cells of T2DM patients. The islet amyloid polypeptide has been associated with β-cell apoptosis. As a consequence of increasing age, the accumulation of highly modified proteins together with decreased regenerative potential might lead to increasing rates of apoptosis. Moreover, reduction of β-cell replication capabilities results in reduction of β-cell mass in mammals, simultaneously with impaired glucose tolerance. The new challenge is to learn much more about age-related protein modifications. This can lead to new treatment strategies for reducing the incidence of T2DM and AD.
