Advanced Glycation End Products in Health and Disease
V Prakash Reddy1, Puspa Aryal1, Emmanuel K Darkwah1
1Department of Chemistry, Missouri University of Science and Technology, Rolla, MO 65409, USA.
Advanced glycation end products (AGEs) contribute to diseases like diabetes and Alzheimer's by forming harmful crosslinks. Developing AGE inhibitors and breakers offers potential new treatments for these AGE-mediated pathologies.
Area of Science:
- Biochemistry
- Pathology
- Microbiology
Background:
- Advanced glycation end products (AGEs) form via nonenzymatic reactions and oxidative stress.
- AGEs are implicated in diabetes, atherosclerosis, Alzheimer's disease (AD), and traumatic brain injury (TBI).
- AGEs crosslink proteins, deactivate enzymes, and interact with receptors for AGEs (RAGE), triggering inflammation.
Purpose of the Study:
- To explore the role of AGEs in disease pathogenesis.
- To investigate the therapeutic potential of AGE inhibitors and breakers.
- To examine the influence of AGEs on gut microbiota and their potential as AGE-breakers.
Main Methods:
- Literature review on AGE formation, disease association, and therapeutic strategies.
- Analysis of AGEs' role in neurodegenerative diseases and gut microbiota.
- Exploration of AGE inhibitor and breaker compounds and gut-microbiota-derived enzymes.
Main Results:
- AGEs contribute to various diseases by crosslinking proteins and activating inflammatory pathways via RAGE.
- Maillard reactions occur in gut bacteria, with AGEs affecting microbiota composition and promoting inflammation.
- AGE inhibitors extend bacterial lifespan, suggesting a role for gut microbiota in AGE metabolism.
Conclusions:
- AGEs play a significant role in the pathogenesis of multiple diseases.
- Targeting AGEs with inhibitors or breakers presents a promising therapeutic avenue.
- Gut microbiota and their enzymes may offer novel strategies for AGE-related disease treatment.
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