This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Sato, T. Articles by Takeuchi, M. Search for Related Content PubMed PubMed Citation Articles by Sato, T. Articles by Takeuchi, M. Pubmed/NCBI databases Substance via MeSH Medline Plus Health Information Alzheimer's Disease Diabetes Genetics Home Reference Genetics Home Reference - Alzheimer disease Social Bookmarking                         What's this?

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

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan

Noriko Shimogaito

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan

Xuegang Wu

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan

Seiji Kikuchi, MD, PhD

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan

Sho-ichi Yamagishi, MD, PhD

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan

Masayoshi Takeuchi, PhD

Department of Pathophysiological Science, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan; Department of Neurology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and the Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan, m-takeuchi{at}hokuriku-u.ac.jp

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.

Key Words: advanced glycation end product (AGEs) • glyceraldehyde-derived AGEs (AGE-2) • toxic AGE (TAGE) • receptor for AGEs (RAGE) • Alzheimer’s disease (AD) • diabetic complications

American Journal of Alzheimer's Disease and Other Dementias®, Vol. 21, No. 3, 197-208 (2006)
DOI: 10.1177/1533317506289277


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				H. J. Cho, S. M. Son, S. M. Jin, H. S. Hong, D. H. Shin, S. J. Kim, K. Huh, and I. Mook-Jung RAGE regulates BACE1 and A{beta} generation via NFAT1 activation in Alzheimer's disease animal model FASEB J, August 1, 2009; 23(8): 2639 - 2649. [Abstract] [Full Text] [PDF]