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.
World J Diabetes. 2011 Apr 15;2(4):49-53. doi: 10.4239/wjd.v2.i4.49.
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.
近年来，流行病学研究表明，2 型糖尿病（T2DM）和阿尔茨海默病（AD）经常同时出现。这可能是由于β细胞和神经元之间存在功能相似性，例如以严格控制的方式按需分泌高度特异性分子。另一个相似之处是 AD 患者中与年龄相关的过度磷酸化 tau 的改变。同样，在 T2DM 患者的β细胞中也发现了改变。胰岛淀粉样多肽与β细胞凋亡有关。随着年龄的增长，高度修饰的蛋白质积累，再生潜能下降，可能导致细胞凋亡率增加。此外，β细胞复制能力的降低导致哺乳动物β细胞数量减少，同时糖耐量受损。新的挑战是更多地了解与年龄相关的蛋白质修饰。这可以为减少 T2DM 和 AD 的发病率提供新的治疗策略。
