ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Microglial phagocytosis induced by fibrillar beta-amyloid and IgGs are differentially regulated by proinflammatory cytokines.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 273 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
273 citing papers in PubMed, 1 synthesis or guideline pooled it, 471 citations in OpenAlex.
- Predictors of cognitive decline in older individuals without dementia: An updated meta-analysis.Annals of clinical and translational neurology · 2023Pooled it
- Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Review
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- The bidirectional mechanistic links between Alzheimer's disease and cardiovascular disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Annexin A1 in Alzheimer's disease: A new therapeutic strategy focusing on neuroinflammation.Neural regeneration research · 2026Article
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- Impact of Klotho genotype on lactylation in Alzheimer's disease and mechanistic insights.Immunity & ageing : I & A · 2026Article
- Exploration of borneol essential oil function in the treatment of Alzheimer's disease based on network pharmacology and experimental validation.BMC complementary medicine and therapies · 2026Article
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
- Microglial Deletion of Hrh4 Alleviates Alzheimer's Disease Pathologies by Enhancing Microglial Phagocytosis of Amyloid-β and Tau.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bornyl Acetate and Menthol Provide Neuroprotection Against Lipopolysaccharide-Induced Alzheimer's Disease-Like Condition in C57BL/6 Mice by Downregulating NARC-1 Lipid Antagonist.Molecular neurobiology · 2025Article
- Transcriptional Activation of theGenes · 2025Article
- P2RX7 modulates the function of human microglia-like cells and mediates the association of IL18 with Alzheimer's disease traits.Neurobiology of disease · 2025Article
- Factors Driving Amyloid Beta Fibril Recognition by Cell Surface Receptors: A Computational Study.Molecules (Basel, Switzerland) · 2025Article
- Elucidating the specific mechanisms of the gut-brain axis: the short-chain fatty acids-microglia pathway.Journal of neuroinflammation · 2025Review
- A 3D human iPSC-derived multi-cell type neurosphere system to model cellular responses to chronic amyloidosis.Journal of neuroinflammation · 2025Article
- The Complementary Role of Morphology in Understanding Microglial Functional Heterogeneity.International journal of molecular sciences · 2025Review
- Photobiomodulation modulates mitochondrial energy metabolism and ameliorates neurological damage in an APP/PS1 mousmodel of Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- How the gut microbiota impacts neurodegenerative diseases by modulating CNS immune cells.Journal of neuroinflammation · 2025Review
213 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 1 institution in 1 country.
Funding
Abstract
Microglia undergo a phenotypic activation in response to fibrillar beta-amyloid (fAbeta) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAbeta deposits. However, they can be induced to do so during Abeta vaccination therapy attributable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abeta plaques. We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAbeta-containing plaques within the AD brain. The proinflammatory suppression of fAbeta-elicited phagocytosis is dependent on nuclear factor kappaB activation. Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Abeta vaccination-based therapy. Importantly, the proinflammatory suppression of fAbeta phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. These findings support anti-inflammatory therapies for the treatment of 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.