Open AccessAge related changes in pancreatic beta cells: A putative extra-cerebral site of Alzheimer’s pathology
Author(s) -
Magdalena Maj,
Ayşegül İlhan,
Dashurie Neziri,
Wolfgang Gärtner,
Tord Berggård,
Johannes Attems,
Wolfgang Base,
Ludwig Wagner
Publication year - 2011
Publication title -
world journal of diabetes
Language(s) - English
Resource type - Journals
ISSN - 1948-9358
DOI - 10.4239/wjd.v2.i4.49
Subject(s) - medicine , diabetes mellitus , disease , apoptosis , alzheimer's disease , amyloid (mycology) , amyloid beta , neuroscience , type 2 diabetes , pancreatic islets , endocrinology , bioinformatics , islet , pathology , biology , biochemistry
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.