The possible therapeutic role of advanced glycation end-product inhibitors in ischemic stroke

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Nada H Aljarba1, Hayder M Al-Kuraishy2, Ali I Al-Gareeb3

  • 1Department of Biology, College of science, Princess Nourah bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.

Brain Research Bulletin
|February 1, 2025
PubMed

Insights

Advanced glycation end-products (AGEs) contribute to cellular aging and neurological disorders. This review explores how AGEs promote acute ischemic stroke (AIS) and the potential of AGEs inhibitors in managing this condition.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Pathology

Background:

  • Advanced glycation end-products (AGEs) are toxic molecules formed from sugar interactions.
  • AGEs induce oxidative stress, inflammation, and cellular aging, contributing to neurological disorders.
  • AGEs are linked to microvascular and macrovascular damage, increasing the risk of acute ischemic stroke (AIS).

Purpose of the Study:

  • To elucidate the role of AGEs in the development and progression of AIS.
  • To discuss the potential therapeutic benefits of AGEs inhibitors in AIS management.

Main Methods:

  • Literature review of studies on AGEs and neurological disorders.
  • Analysis of research linking AGEs to vascular damage and stroke pathogenesis.
  • Examination of evidence for AGEs inhibitors in preclinical and clinical settings.

Main Results:

  • AGEs promote reactive oxygen species generation and pro-inflammatory cytokine release.
  • AGEs-induced vascular damage triggers prothrombotic cascades, elevating AIS risk.
  • Elevated serum AGEs levels correlate with AIS incidence, severity, and pathogenicity.

Conclusions:

  • AGEs play a significant role in promoting AIS development and progression.
  • Targeting AGEs formation or action with inhibitors may offer a novel therapeutic strategy for AIS.
  • Further research is needed to fully understand the AGEs-AIS relationship and validate therapeutic interventions.
Keywords:
AGEs inhibitorsAdvanced glycation end-productsacute ischemic stroke

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