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Current Alzheimer Research

Author(s): Hayahide Ooi and Yoshiki Koriyama*

DOI: 10.2174/0115672050288723240213053342

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Toxic Advanced Glycation End-Products-Dependent Alzheimer’s Disease- Like Alternation in the Microtubule System

Page: [677 - 681] Pages: 5

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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.

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