ArticleNeurochemical research2016
Effects of RAGE-Specific Inhibitor FPS-ZM1 on Amyloid-β Metabolism and AGEs-Induced Inflammation and Oxidative Stress in Rat Hippocampus.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 90 citations in OpenAlex.
- RAGE Signalling in Acute Inflammatory Disorders: Therapeutic Potential of Natural Products.Biomolecules · 2026Review
- Pharmaco-therapeutic modulation of the Glo1-Nrf2-RAGE functional network in chronic inflammation: polyphenols in the context of current anti-inflammatory therapy.Inflammopharmacology · 2026Review
- RAGE in Neutrophils: A Sensor for Pathogen-Associated Structures and Beyond.Biomedicines · 2026Article
- Genetic and pharmacologic modulation of RAGE rescues the diabetes-mediated impairments to bone at multiple length scales.bioRxiv : the preprint server for biology · 2026Article
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- Astrocyte-intrinsic signaling of chitinase-like protein CHI3L1 drives inflammation and amplifies demyelination in neuromyelitis optica.The Journal of clinical investigation · 2026Article
- Algae-Derived C-Phycocyanin Mitigates AGE-RAGE-Induced ER Stress and Mitochondrial Apoptosis: Implications for Diabetes-Associated Neurodegeneration.International journal of molecular sciences · 2025Article
- PTEN/PKM2/ERα-Driven Glyoxalase 1 Overexpression Sustains PC3 Prostate Cancer Cell Growth Through MG-H1/RAGE Pathway Desensitization Leading to HAntioxidants (Basel, Switzerland) · 2025Article
- The Inflammatory Nexus: Unraveling Shared Pathways and Promising Treatments in Alzheimer's Disease and Schizophrenia.International journal of molecular sciences · 2025Review
- Identifying RAGE inhibitors as potential therapeutics for Alzheimer's disease via integrated in-silico approaches.Scientific reports · 2025Article
- Xiahuo Pingwei San attenuated intestinal inflammation in dextran sulfate sodium-induced ulcerative colitis mice through inhibiting the receptor for advanced glycation end-products signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Article
- Roles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2025Review
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Cornuside ameliorates cognitive impairments via RAGE/TXNIP/NF-κB signaling in AβJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity.Cell reports. Medicine · 2023Article
- Advanced glycation end products: Key mediator and therapeutic target of cardiovascular complications in diabetes.World journal of diabetes · 2023Review
- Effect of β-amyloid on blood-brain barrier properties and function.Biophysical reviews · 2023Review
- Docking and Molecular Dynamics-Based Identification of Interaction between Various Beta-Amyloid Isoforms and RAGE Receptor.International journal of molecular sciences · 2022Article
- Advanced Glycation End Products in Health and Disease.Microorganisms · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increased level of advanced glycation end products (AGEs) is observed in brains of patients with Alzheimer's disease (AD). AGEs and receptor for AGEs (RAGE) play important roles in the pathogenesis of AD. FPS-ZM1 is a high-affinity RAGE-specific blocker that inhibits amyloid-β binding to RAGE, neurological damage and inflammation in the APP(sw/0) transgenic mouse model of AD. FPS-ZM1 is not toxic to mice and can easily cross the blood-brain barrier. In this study, an AGEs-RAGE-activated rat model were established by intrahippocampal injection of AGEs, then these rats were treated with intraperitoneal administration of FPS-ZM1 and the possible neuroprotective effects were investigated. We found that AGEs administration induced an-regulation of Abeta production, inflammation, and oxidative stress, and an increased escape latency of rats in the Morris water maze test, all of these are significantly reduced by FPS-ZM1 treatment. Our results suggest that the AGEs-RAGE pathway is responsible for cognitive deficits, and therefore may be a potential treatment target. FPS-ZM1 might be a novel therapeutic agent to treat AD patients.
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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.