Toxic Advanced Glycation End Product-Dependent Alzheimer's Disease- Like Alternation in the Microtubule System

Curr Alzheimer Res. 2024 Feb 14. doi: 10.2174/0115672050288723240213053342. Online ahead of print.ABSTRACTType 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.PMID:38357957 | DOI:10.2174/0115672050288723240213053342
Source: Current Alzheimer Research - Category: Neurology Authors: Source Type: research