Toxic Advanced Glycation End Products (TAGE) Theory in Alzheimer’s Disease

Several epidemiological studies have reported moderately increased risks of Alzheimer’s disease (AD) in diabetic patients compared with general population. In diabetes mellitus, the formation and accumulation of advanced glycation end products (AGEs) progress more rapidly. Recent understanding of th...

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Bibliographic Details
Published in:American journal of Alzheimer's disease and other dementias 2006-05, Vol.21 (3), p.197-208
Main Authors: Sato, Takashi, Shimogaito, Noriko, Wu, Xuegang, Kikuchi, Seiji, Yamagishi, Sho-ichi, Takeuchi, Masayoshi
Format: Article
Language:English
Subjects:
Alzheimer Disease - metabolism
Alzheimer Disease - physiopathology
Animals
Apoptosis
Brain - metabolism
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Glycation End Products, Advanced - metabolism
Humans
Neurons - metabolism
Receptor for Advanced Glycation End Products
Receptors, Immunologic
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Summary:Several epidemiological studies have reported moderately increased risks of Alzheimer’s disease (AD) in diabetic patients compared with general population. In diabetes mellitus, the formation and accumulation of advanced glycation end products (AGEs) progress more rapidly. Recent understanding of this process has confirmed that interactions between AGEs and their receptor (RAGE) may play a role in the pathogenesis of diabetic complications and AD. The authors have recently found that glyceraldehyde-derived AGEs (AGE- 2), which is predominantly the structure of toxic AGEs (TAGE), show significant toxicity on cortical neuronal cells and that the neurotoxic effect of diabetic serum is completely blocked by neutralizing antibody against the AGE-2 epitope. Moreover, in human AD brains, AGE-2 is distributed in the cytosol of neurons in the hippocampus and parahippocampal gyrus. These results suggest that TAGE is involved in the pathogenesis of AD as well as other age-related diseases. In this review, the authors discuss the molecular mechanisms of AD, especially focusing on TAGE-RAGE system.
ISSN:1533-3175
1938-2731
DOI:10.1177/1533317506289277