ArticleJournal of neurochemistry2010
Microglial C5aR (CD88) expression correlates with amyloid-beta deposition in murine models of Alzheimer's disease.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- The Crosstalk Between Sepsis-Associated Encephalopathy and Alzheimer's Disease: Identifying Potential Biomarkers and Therapeutic Targets for Cognition.Molecular neurobiology · 2025Article
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Knowing the enemy: strategic targeting of complement to treat Alzheimer disease.Nature reviews. Neurology · 2025Review
- Hallmarks of aging in age-related macular degeneration and age-related neurological disorders: novel insights into common mechanisms and clinical relevance.Eye (London, England) · 2025Review
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- C5aR1 antagonism suppresses inflammatory glial responses and alters cellular signaling in an Alzheimer's disease mouse model.Nature communications · 2024Article
- Experimental colitis in young Tg2576 mice accelerates the onset of an Alzheimer's-like clinical phenotype.Alzheimer's research & therapy · 2024Article
- C5aR1 signaling promotes region- and age-dependent synaptic pruning in models of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Amyloid-βiScience · 2023Article
- Alzheimer's genes in microglia: a risk worth investigating.Molecular neurodegeneration · 2023Review
- C5aR1 signaling promotes region and age dependent synaptic pruning in models of Alzheimer's Disease.bioRxiv : the preprint server for biology · 2023Article
- Microglia in Alzheimer's disease: pathogenesis, mechanisms, and therapeutic potentials.Frontiers in aging neuroscience · 2023Review
- Mechanisms of abnormal adult hippocampal neurogenesis in Alzheimer's disease.Frontiers in neuroscience · 2023Review
- Complement System Inhibition Modulates the Inflammation Induced by the Venom ofInternational journal of molecular sciences · 2022Article
- C5aR1 antagonism alters microglial polarization and mitigates disease progression in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2022Article
- Modulation of C5a-C5aR1 signaling alters the dynamics of AD progression.Journal of neuroinflammation · 2022Article
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- Microglia in Alzheimer's Disease: A Favorable Cellular Target to Ameliorate Alzheimer's Pathogenesis.Mediators of inflammation · 2022Review
- Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.Biomedicines · 2021Review
- Dietary Protein Source Influences Brain Inflammation and Memory in a Male Senescence-Accelerated Mouse Model of Dementia.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by the accumulation of amyloid-beta protein and neuronal loss, is the leading cause of age-related dementia in the world today. The disease is also associated with neuroinflammation, robust activation of astrocytes and microglia, and evidence of activation of the complement system, localized with both fibrillar amyloid-beta (fAbeta) plaques and tangles. The observations are consistent with a complement-dependent component of AD progression. We have previously shown that inhibition of the major complement receptor for C5a (CD88) with the antagonist PMX205 results in a significant reduction in pathology in two mouse models of AD. To further characterize the role of complement in AD-related neuroinflammation, we examined the age- and disease-associated expression of CD88 in brain of transgenic mouse models of AD and the influence of PMX205 on the presence of various complement activation products using flow cytometry, western blot, and immunohistochemistry. CD88 was found to be up-regulated in microglia, in the immediate vicinity of amyloid plaques. While thioflavine plaque load and glial recruitment is significantly reduced after treatment with PMX205, C1q remains co-localized with fAbeta plaques and C3 is still expressed by the recruited astrocytes. Thus, with PMX205, potentially beneficial activities of these early complement components may remain intact, while detrimental activities resulting from C5a-CD88 interaction are inhibited. This further supports the targeted inhibition of specific complement mediated activities as an approach for AD therapy.
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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.