ArticleASN neuro2017
C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta.
Article in ASN neuro, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Complement dysregulation during the early phases of synucleinopathy.Acta neuropathologica · 2026Article
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- Circulatory extracellular vesicles transport complement C1q for promoting neuronal amyloid-β production in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Review
- Beneficial versus Detrimental Effects of Complement-Microglial Interactions in Alzheimer's Disease.Brain sciences · 2024Review
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 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
- Correlation of serum complement factor 5a level with inflammatory response and cognitive function in patients with Alzheimer's disease of different severity.BMC neurology · 2023Article
- Modulation of C5a-C5aR1 signaling alters the dynamics of AD progression.Journal of neuroinflammation · 2022Article
- A Set of Dysregulated Target Genes to Reduce Neuroinflammation at Molecular Level.International journal of molecular sciences · 2022Article
- Complement C4 Is Reduced in iPSC-Derived Astrocytes of Autism Spectrum Disorder Subjects.International journal of molecular sciences · 2021Article
- Systemic and cerebrospinal fluid immune and complement activation in Ugandan children and adolescents with long-standing nodding syndrome: A case-control study.Epilepsia open · 2021Article
- Emerging Role of C5 Complement Pathway in Peripheral Neuropathies: Current Treatments and Future Perspectives.Biomedicines · 2021Review
- Cytokines and Onchocerciasis-Associated Epilepsy, a Pilot Study and Review of the Literature.Pathogens (Basel, Switzerland) · 2021Article
- The Benefits of Complement Measurements for the Clinical Practice.Methods in molecular biology (Clifton, N.J.) · 2021Review
- The good, the bad, and the opportunities of the complement system in neurodegenerative disease.Journal of neuroinflammation · 2020Review
- Complement-Mediated Events in Alzheimer's Disease: Mechanisms and Potential Therapeutic Targets.Journal of immunology (Baltimore, Md. : 1950) · 2020Review
- Targeting Inflammatory Pathways in Alzheimer's Disease: A Focus on Natural Products and Phytomedicines.CNS drugs · 2019Review
- Article
- Therapeutic Inhibition of the Complement System in Diseases of the Central Nervous System.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
C5aR1, the proinflammatory receptor for C5a, is expressed in the central nervous system on microglia, endothelial cells, and neurons. Previous work demonstrated that the C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive deficits in two Alzheimer's Disease (AD) mouse models. However, the cellular mechanisms of this protection have not been definitively demonstrated. Here, primary cultured mouse neurons treated with exogenous C5a show reproducible loss of MAP-2 staining in a dose-dependent manner within 24 hr of treatment, indicative of injury to neurons. This injury is prevented by the C5aR1 antagonist PMX53, a close analog of PMX205. Furthermore, primary neurons derived from C5aR1 null mice exhibited no MAP-2 loss after exposure to the highest concentration of C5a tested. Primary mouse neurons treated with both 100 nM C5a and 5 µM fibrillar amyloid beta (fAβ), to model what occurs in the AD brain, showed increased MAP-2 loss relative to either C5a or fAβ alone. Blocking C5aR1 with PMX53 (100 nM) blocked the loss of MAP2 in these primary neurons to the level seen with fAβ alone. Similar experiments with primary neurons derived from C5aR1 null mice showed a loss of MAP-2 due to fAβ treatment. However, the addition of C5a to the cultures did not enhance the loss of MAP-2 and the addition of PMX53 to the cultures did not change the MAP-2 loss in response to fAβ. Thus, at least part of the beneficial effects of C5aR1 antagonist in AD mouse models may be due to protection of neurons from the toxic effects of C5a.
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