ArticleNeurobiology of aging2012
Receptor for advanced glycation endproducts (RAGE) deficiency protects against MPTP toxicity.
Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
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Who cites it
38 citing papers in PubMed, 76 citations in OpenAlex.
- Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026Review
- High-mobility Group Protein 1/ Receptor for Advanced Glycation End Products/ Nuclear Factor-κB Signalling Pathway Contributes to the Pathogenic Process of Striatal Neuron Impairment in the Rat Model of Parkinson's Disease.Brain and behavior · 2026Article
- Brain-targeted drug delivery - nanovesicles directed to specific brain cells by brain-targeting ligands.Journal of nanobiotechnology · 2024Review
- Article
- HMGB1 Mediates Inflammation-Induced DMT1 Increase and Dopaminergic Neurodegeneration in the Early Stage of Parkinsonism.Molecular neurobiology · 2024Article
- Altered expression of Sialyl Lewis X in experimental models of Parkinson's disease.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Taming microglia: the promise of engineered microglia in treating neurological diseases.Journal of neuroinflammation · 2024Review
- The alteration and role of glycoconjugates in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- HMGB1 is a Potential and Challenging Therapeutic Target for Parkinson's Disease.Cellular and molecular neurobiology · 2023Review
- RAGE Against the Glycation Machine in Synucleinopathies: Time to Explore New Questions.Journal of Parkinson's disease · 2023Review
- Receptors for Advanced Glycation End Products (RAGE): Promising Targets Aiming at the Treatment of Neurodegenerative Conditions.Current neuropharmacology · 2023Review
- Biological Potential, Gastrointestinal Digestion, Absorption, and Bioavailability of Algae-Derived Compounds with Neuroprotective Activity: A Comprehensive Review.Marine drugs · 2022Review
- Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.Current drug targets · 2022Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- Influence of Dopamine on Fluorescent Advanced Glycation End Products Formation UsingBiomolecules · 2021Article
- Emerging role of S100B protein implication in Parkinson's disease pathogenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Absence of Receptor for Advanced Glycation End Product (RAGE) Reduces Inflammation and Extends Survival in the hSOD1Molecular neurobiology · 2020Article
- Metal-induced neurotoxicity in a RAGE-expressing C. elegans model.Neurotoxicology · 2020Article
- Effects of RAGE inhibition on the progression of the disease in hSOD1Pharmacology research & perspectives · 2020Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
Parkinson's disease (PD) is a common neurodegenerative disorder of unknown pathogenesis characterized by the loss of nigrostriatal dopaminergic neurons. Oxidative stress, microglial activation and inflammatory responses seem to contribute to the pathogenesis. The receptor for advanced glycation endproducts (RAGE) is a multiligand receptor of the immunoglobulin superfamily of cell surface molecules. The formation of advanced glycation end products (AGEs), the first ligand of RAGE identified, requires a complex series of reactions including nonenzymatic glycation and free radical reactions involving superoxide-radicals and hydrogen peroxide. Binding of RAGE ligands results in activation of nuclear factor-kappaB (NF-κB). We show that RAGE ablation protected nigral dopaminergic neurons against cell death induced by the neurotoxin MPTP that mimics most features of PD. In RAGE-deficient mice the translocation of the NF-κB subunit p65 to the nucleus, in dopaminergic neurons and glial cells was inhibited suggesting that RAGE involves the activation of NF-κB. The mRNA level of S100, one of the ligands of RAGE, was increased after MPTP treatment. The dopaminergic neurons treated with MPP(+) and S100 protein showed increased levels of apoptotic cell death, which was attenuated in RAGE-deficient mice. Our results suggest that activation of RAGE contributes to MPTP/MPP(+)-induced death of dopaminergic neurons that may be mediated by NF-κB activation.
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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.