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Age related changes in pancreatic beta cells: A putativeextra-cerebral site of Alzheimer's pathology

Age related changes in pancreatic beta cells: A putativeextra-cerebral site of Alzheimer’s pathology
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摘要 Frequent concomitant manifestation of type 2 diabetesmellitus (T2DM) and Alzheimer's disease (AD) hasbeen recently demonstrated by epidemiological studies.This might be due to functional similarities between β-cells and neurons, such as secretion on demand ofhighly specific molecules in a tightly controlled fashion.An additional similarity represents the age-relatedalteration of hyperphosphorylated tau in AD patients.Similarly, alterations have been identified in β-cells of T2DM patients. The islet amyloid polypeptide has beenassociated with β-cell apoptosis. As a consequence ofincreasing age, the accumulation of highly modified proteins together with decreased regenerative potentialmight lead to increasing rates of apoptosis. Moreover, reduction of β-cell replication capabilities results in reduction of β-cell mass in mammals, simultaneously withimpaired glucose tolerance. The new challenge is tolearn much more about age-related protein modifications. This can lead to new treatment strategies forreducing the incidence of T2DM and AD. Frequent concomitant manifestation of type 2 diabetesmellitus (T2DM) and Alzheimer’s disease (AD) hasbeen recently demonstrated by epidemiological studies.This might be due to functional similarities between β-cells and neurons, such as secretion on demand ofhighly specific molecules in a tightly controlled fashion.An additional similarity represents the age-relatedalteration of hyperphosphorylated tau in AD patients.Similarly, alterations have been identified in β-cells of T2DM patients. The islet amyloid polypeptide has beenassociated with β-cell apoptosis. As a consequence ofincreasing age, the accumulation of highly modified proteins together with decreased regenerative potentialmight lead to increasing rates of apoptosis. Moreover, reduction of β-cell replication capabilities results in reduction of β-cell mass in mammals, simultaneously withimpaired glucose tolerance. The new challenge is tolearn much more about age-related protein modifications. This can lead to new treatment strategies forreducing the incidence of T2DM and AD.
出处 《World Journal of Diabetes》 SCIE CAS 2011年第4期49-53,共5页 世界糖尿病杂志(英文版)(电子版)
基金 Supported by the Grant from the National Bank of Austria,No.13402 the Fund of the Major of the City of Vienna,No.08052
关键词 Type 2 diabetes MELLITUS Pancreatic betacells Age Alzheimer’s disease Hyperphosphorylatedtau ISLET AMYLOID POLYPEPTIDE Type 2 diabetes mellitus Pancreatic betacells Age Alzheimer’s disease Hyperphosphorylatedtau Islet amyloid polypeptide
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