ReviewCellular and molecular neurobiology2015
Microglial Aβ receptors in Alzheimer's disease.
Review in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 2 of them syntheses that pooled it.
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
136 citing papers in PubMed, 2 syntheses or guidelines pooled it, 242 citations in OpenAlex.
- Identification of methylation-regulated genes modulating microglial phagocytosis in hyperhomocysteinemia-exacerbated Alzheimer's disease.Alzheimer's research & therapy · 2023Pooled it
- Neuroinflammation: A Common Pathway in Alzheimer's Disease and Epilepsy.Journal of Alzheimer's disease : JAD · 2023Pooled it
- Minocycline at 2 Different Dosages vs Placebo for Patients With Mild Alzheimer Disease: A Randomized Clinical Trial.JAMA neurology · 2020Trial
- A metabolic perspective on microglia in Alzheimer's disease.Neural regeneration research · 2026Article
- Deconvolution in Alzheimer's disease.Neural regeneration research · 2026Article
- β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026Review
- Article
- Modulating Th17/Treg Balance in Alzheimer's Disease: Therapeutic Insights from Natural Compounds and Immunometabolism.Brain sciences · 2026Review
- Multi-omics and mendelian randomization uncover microbial-metabolite-gene interactions in age-related hearing loss.AMB Express · 2026Article
- Immuno-Regulation of Brain Region-Specific Organoids Containing Isogenic Microglia-Like Cells.Advanced healthcare materials · 2026Article
- Targeting Adipocyte Enhancer-Binding Protein 1 to Induce Microglial Phenotype Shift for Immunotherapy in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Neuroprotective role of rice bran extract and its constituents in a neuroinflammatory mouse model.BMC complementary medicine and therapies · 2025Article
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- ALX/FPR2 Receptor Activation by Inflammatory (fMLFII) and Pro-resolving (LXAACS physical chemistry Au · 2025Article
- Pathological mechanisms and treatment progression of Alzheimer's disease.European journal of medical research · 2025Review
- Alzheimer model chip with microglia BV2 cells.Microsystems & nanoengineering · 2025Article
- Fructose induces inflammatory activation in macrophages and microglia through the nutrient-sensing ghrelin receptor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis.Neurochemical research · 2025Review
- Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer's disease.Cellular & molecular immunology · 2025Article
- Review
76 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid β (Aβ) plays a pivotal role in the progression of Alzheimer's disease (AD) through its neurotoxic and inflammatory effects. On one hand, Aβ binds to microglia and activates them to produce inflammatory mediators. On the other hand, Aβ is cleared by microglia through receptor-mediated phagocytosis and degradation. This review focuses on microglial membrane receptors that bind Aβ and contribute to microglial activation and/or Aβ phagocytosis and clearance. These receptors can be categorized into several groups. The scavenger receptors (SRs) include scavenger receptor A-1 (SCARA-1), MARCO, scavenger receptor B-1 (SCARB-1), CD36 and the receptor for advanced glycation end product (RAGE). The G protein-coupled receptors (GPCRs) are formyl peptide receptor 2 (FPR2) and chemokine-like receptor 1 (CMKLR1). There are also toll-like receptors (TLRs) including TLR2, TLR4, and the co-receptor CD14. Functionally, SCARA-1 and CMKLR1 are involved in the uptake of Aβ, and RAGE is responsible for the activation of microglia and production of proinflammatory mediators following Aβ binding. CD36, CD36/CD47/α6β1-intergrin, CD14/TLR2/TLR4, and FPR2 display both functions. Additionally, MARCO and SCARB-1 also exhibit the ability to bind Aβ and may be involved in the progression of AD. Here, we focus on the expression and distribution of these receptors in microglia and their roles in microglia interaction with Aβ. Finally, we discuss the potential therapeutic value of these receptors in AD.
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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.