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-ce...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.展开更多
基金Supported by the Grant from the National Bank of Austria,No.13402the Fund of the Major of the City of Vienna,No.08052
文摘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.
