ReviewMicroorganisms2022
Advanced Glycation End Products in Health and Disease.
Review in Microorganisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 120 citations in OpenAlex.
- Antiglycation approach in selected autoimmune diseases: Where do we stand?Redox biology · 2026Review
- Metabolic regulation of the carbonyl stress pathway and methylglyoxal in Lyme disease and relapsing fever spirochetes.PLoS pathogens · 2026Article
- Advanced glycation end products and PTSD: molecular insights and dietary approaches for neuropsychiatric health.Metabolic brain disease · 2026Review
- Plant-Based Approaches for Inhibition of Advanced Glycation End Products Formation: Dietary Polyphenols.Molecules (Basel, Switzerland) · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Identification of senescence-related genes in Parkinson's disease reveals candidate therapeutic targets and pathological processes.Animal models and experimental medicine · 2026Article
- Growth Month-Associated Variation in Volatile Profiles, Anti-Glycation Capacity, and Antioxidant Activity ofFoods (Basel, Switzerland) · 2026Article
- Targeting the AGE-RAGE/NF-κB Pathway: An Integrative Study Decoding the Anti-Colitis Effect of Five-Flavor Sophora Flavescens Enteric-Coated Capsule.Biomedicines · 2026Article
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- The Effect of Metabolic Syndrome on Alzheimer's Disease: Physical Activity as a Preventive and Therapeutic Measure.Brain sciences · 2026Review
- Potential Cosmetic Applications of Dihydroartemisinin.Molecules (Basel, Switzerland) · 2026Article
- Is Insulin Resistance the Driver or the Outcome of Diabetes Mellitus? A Critical Review.Journal of nutrition and metabolism · 2026Review
- Bridging pathologies: Mechanistic insights into the diabetes-Alzheimer's nexus.EXCLI journal · 2026Review
- Heat-processed rodent chow alters nutritive content and improves metabolic outcomes in insulin-resistant female mice.Frontiers in nutrition · 2026Article
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- Unlocking the Sugar Code: Implications and Consequences of Glycosylation in Alzheimer's Disease and Other Tauopathies.Biomedicines · 2025Review
- Current Developments in Analytical Methods for Advanced Glycation End Products in Foods.Molecules (Basel, Switzerland) · 2025Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs), formed through the nonenzymatic reaction of reducing sugars with the side-chain amino groups of lysine or arginine of proteins, followed by further glycoxidation reactions under oxidative stress conditions, are involved in the onset and exacerbation of a variety of diseases, including diabetes, atherosclerosis, and Alzheimer's disease (AD) as well as in the secondary stages of traumatic brain injury (TBI). AGEs, in the form of intra- and interprotein crosslinks, deactivate various enzymes, exacerbating disease progression. The interactions of AGEs with the receptors for the AGEs (RAGE) also result in further downstream inflammatory cascade events. The overexpression of RAGE and the AGE-RAGE interactions are especially involved in cases of Alzheimer's disease and other neurodegenerative diseases, including TBI and amyotrophic lateral sclerosis (ALS). Maillard reactions are also observed in the gut bacterial species. The protein aggregates found in the bacterial species resemble those of AD and Parkinson's disease (PD), and AGE inhibitors increase the life span of the bacteria. Dietary AGEs alter the gut microbiota composition and elevate plasma glycosylation, thereby leading to systemic proinflammatory effects and endothelial dysfunction. There is emerging interest in developing AGE inhibitor and AGE breaker compounds to treat AGE-mediated pathologies, including diabetes and neurodegenerative diseases. Gut-microbiota-derived enzymes may also function as AGE-breaker biocatalysts. Thus, AGEs have a prominent role in the pathogenesis of various diseases, and the AGE inhibitor and AGE breaker approach may lead to novel therapeutic candidates.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.