ReviewInternational journal of molecular sciences2025
Roles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer's Disease.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Two-year follow-up assessment of a randomized controlled trial evaluating the durability of Tai Chi on cognitive function in older adults with type 2 diabetes and mild cognitive impairment.Aging clinical and experimental research · 2025Trial
- The Brown Algal Phlorotannin Dieckol Attenuates Amyloid-β Oligomer-Induced Oxidative DNA Damage and Senescence-like Stress in Human Neuron-like Cells.Marine drugs · 2026Article
- DomesticatedInternational journal of molecular sciences · 2026Article
- Salivary protein macromolecules as diagnostic and therapeutic biomarkers linking oral health and neurodegenerative diseases-emerging mechanisms and future perspectives.Inflammopharmacology · 2026Review
- Protein glycoxidation in neuropsychiatric disorders-from basic research to clinical practice.Redox biology · 2026Review
- Article
- SGLT2 Inhibitors in Alzheimer's Disease: Biochemical Insights and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Intranasal lipid nanocapsule administration of the new lipophenol quercetin-3-O-DHA-7-O-iPr reduces carbonyl stress and improves behavior in a mouse model of Alzheimer's disease.Drug delivery and translational research · 2026Article
- Network of interactions between the tumor necrosis factor superfamily members and small S100 proteins.PloS one · 2026Article
- Threshold effects of physical activity and cognitive function among older adults with diabetes mellitus in NHANES 2011-2014.Aging clinical and experimental research · 2025Article
- Algae-Derived C-Phycocyanin Mitigates AGE-RAGE-Induced ER Stress and Mitochondrial Apoptosis: Implications for Diabetes-Associated Neurodegeneration.International journal of molecular sciences · 2025Article
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- From metabolic dysregulation to neurodegenerative pathology: the role of hyperglycemia, oxidative stress, and blood-brain barrier breakdown in T2D-driven Alzheimer's disease.Metabolic brain disease · 2025Review
- Machine learning assisted CRCA multi-color fluorescent droplet imaging for high-sensitivity simultaneous detection of Maillard hazards.iScience · 2025Article
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- Oxidative Stress, Advanced Glycation End Products (AGEs), and Neurodegeneration in Alzheimer's Disease: A Metabolic Perspective.Antioxidants (Basel, Switzerland) · 2025Review
- Djulis (Molecules (Basel, Switzerland) · 2025Review
- Nanozymes in neuropathic pain: strategies bridging oxidative stress, mitochondrial repair, and neuroimmune modulation for targeted therapy.Journal of neuroinflammation · 2025Review
- Exploring new drug treatment targets for immune related bone diseases using a multi omics joint analysis strategy.Scientific reports · 2025Article
- Structure and function of the blood-brain barrier in perioperative neurocognitive disorders.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer's disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), including advanced glycation end products (AGEs), beta-amyloid peptide (Aβ), high mobility group box 1 (HMGB1), and S100 calcium-binding proteins. This interaction impairs the brain's ability to clear Aβ, resulting in increased Aβ accumulation, neuronal injury, and mitochondrial dysfunction. This further promotes inflammatory responses and oxidative stress, ultimately leading to a range of age-related diseases. Given RAGE's significant role in AD, inhibitors that target RAGE and its ligands hold promise as new strategies for treating AD, offering new possibilities for alleviating and treating this serious neurodegenerative disease. This article reviews the various pathogenic mechanisms of AD and summarizes the literature on the interaction between RAGE and its ligands in various AD-related pathological processes, with a particular focus on the evidence and mechanisms by which RAGE interactions with AGEs, HMGB1, Aβ, and S100 proteins induce cognitive impairment in AD. Furthermore, the article discusses the principles of action of RAGE inhibitors and inhibitors targeting RAGE-ligand interactions, along with relevant clinical trials.
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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.