Abstract：
Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer\'s Disease (AD). However, the detailed mechanism underlying T2DM-related AD remains unknown. In DM, many types of advanced glycation end-products (AGEs) are formed and accumulated. In our previous study, we demonstrated that Glyceraldehyde (GA)-derived Toxic Advanced Glycation End-products (Toxic AGEs, TAGE) strongly showed cytotoxicity against neurons and induced similar alterations to those observed in AD. Further, GA induced dysfunctional neurite outgrowth via TAGE-β-- tubulin aggregation, which resulted in the TAGE-dependent abnormal aggregation of β-tubulin and tau phosphorylation. Herein, we provide a perspective on the possibility that T2DM increases the probability of AD onset and accelerates its progression.
摘要：
2型糖尿病(T2DM)是阿尔茨海默病(AD)的危险因素。然而,T2DM相关AD的详细机制尚不清楚.在DM中,许多类型的糖基化终产物(AGEs)形成和积累。在我们之前的研究中,我们证明了甘油醛(GA)衍生的有毒晚期糖基化终产物(有毒AGEs，TAGE）强烈显示出对神经元的细胞毒性，并诱导了与AD中观察到的相似的改变。Further,GA通过TAGE-β-微管蛋白聚集诱导功能失调的神经突生长，这导致β-微管蛋白的TAGE依赖性异常聚集和tau磷酸化。在这里，我们对T2DM增加AD发病概率并加速其进展的可能性提供了一个观点.
