Toxic advanced glycation end products (TAGE) theory in Alzheimer's disease

Takashi Sato, Noriko Shimogaito, Xuegang Wu, Seiji Kikuchi, Sho Ichi Yamagishi, Masayoshi Takeuchi

Research output: Contribution to journalReview articlepeer-review

117 Scopus citations


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.

Original languageEnglish
Pages (from-to)197-208
Number of pages12
JournalAmerican Journal of Alzheimer's Disease and other Dementias
Issue number3
StatePublished - 2006
Externally publishedYes


  • Advanced glycation end product (AGEs)
  • Alzheimer's disease (AD)
  • Diabetic complications
  • Glyceraldehyde-derived AGEs (AGE-2)
  • Receptor for AGEs (RAGE)
  • Toxic AGE (TAGE)


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