ArticleACS chemical neuroscience2017
Identification of Inhibitors of CD36-Amyloid Beta Binding as Potential Agents for Alzheimer's Disease.
Article in ACS chemical neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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
18 citing papers in PubMed, 45 citations in OpenAlex.
- CD36 is associated with myocardial ischemia-reperfusion-induced renal injury in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway.Journal of anesthesia and translational medicine · 2026Article
- Astragaloside IV Improves Diabetic Kidney Disease by Regulating NLRP3 Inflammasome.Journal of diabetes research · 2025Review
- Role of CD36 in central nervous system diseases.Neural regeneration research · 2024Review
- Nanotechnology for microglial targeting and inhibition of neuroinflammation underlying Alzheimer's pathology.Translational neurodegeneration · 2024Article
- Research progress of microglial surface receptors in perioperative neurocognitive disorders.Ibrain · 2024Review
- [3+3]-Annulation of Cyclic Nitronates with Vinyl Diazoacetates: Diastereoselective Synthesis of Partially Saturated [1,2]Oxazino[2,3-Molecules (Basel, Switzerland) · 2023Article
- Six genetically linked mutations in the CD36 gene significantly delay the onset of Alzheimer's disease.Scientific reports · 2022Article
- CD36-Binding Amphiphilic Nanoparticles for Attenuation of Alpha Synuclein-Induced Microglial Activation.Advanced nanobiomed research · 2022Article
- Low-Concentrations of Fatty Acids Induce an Early Increase in IL-8 Levels in Normal Human Astrocytes.Metabolites · 2022Article
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- Enhanced Uptake of Processed Bovine β-Lactoglobulin by Antigen Presenting Cells: Identification of Receptors and Implications for Allergenicity.Molecular nutrition & food research · 2021Article
- Synthesis of Chromeno[3,4-Molecules (Basel, Switzerland) · 2021Article
- Effects of α-Lipoic Acid on Phagocytosis of Oligomeric Beta-AmyloidFrontiers in aging neuroscience · 2021Article
- Microglia in Alzheimer's Disease: A Target for Therapeutic Intervention.Frontiers in cellular neuroscience · 2021Review
- CD36 and CD97 in Pancreatic Cancer versus Other Malignancies.International journal of molecular sciences · 2020Review
- Involvement of Lipids in Alzheimer's Disease Pathology and Potential Therapies.Frontiers in physiology · 2020Review
- Hexahydropyrrolo[2,3-ACS chemical neuroscience · 2019Article
- CD36 tango in cancer: signaling pathways and functions.Theranostics · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
Neuroinflammation is one of the hallmarks of Alzheimer's disease pathology. Amyloid β has a central role in microglia activation and the subsequent secretion of inflammatory mediators that are associated with neuronal toxicity. The recognition of amyloid β by microglia depends on the expression of several receptors implicated in the clearance of amyloid and in cell activation. CD36 receptor expressed on microglia interacts with fibrils of amyloid inducing the release of proinflammatory cytokines and amyloid internalization. The interruption of the interaction CD36-amyloid β compromises the activation of microglia cells. We have developed and validated a new colorimetric assay to identify potential inhibitors of the binding of amyloid β to CD36. We have found seven molecules, structural analogues of the Trichodermamide family of natural products that interfere with the interaction CD36-amyloid β. By combining molecular docking and dynamics simulations, we suggested the second fatty acids binding site within the large luminal hydrophobic tunnel, present in the extracellular domain of CD36, as the binding pocket of these compounds. Free energy calculations predicted the nonpolar component as the driving force for the binding of these inhibitors. These molecules also inhibited the production of TNF-α, IL-6, and IL-1β by peritoneal macrophages stimulated with fibrils of amyloid β. This work serves as a platform for the identification of new potential anti-inflammatory agents for the treatment of Alzheimer's disease.
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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.