ArticleCell death & disease2026
Complement receptor 3 (CR3)-dependent microglial synapse elimination drives Parkinson's disease pathogenesis in systemic inflammation.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Csf1r-mediated depletion of myeloid cells prevents dopaminergic neuron loss during chronic colitis.Journal of neuroinflammation · 2026Article
- The potential role of aberrant microglial synaptic pruning in the neurodevelopmental pathogenesis of tourette syndrome.Frontiers in neuroscience · 2026Review
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Authors and funding
16 authors.
Funding
Abstract
Although systemic inflammation has been implicated in PD pathogenesis, the underlying mechanisms remain poorly understood. In this study, we investigate the pathological events in a systemic inflammation-induced PD mouse model. We demonstrate that synaptic loss in the midbrain occurs as early as 1 day after the final lipopolysaccharide (LPS) administration, preceding dopaminergic (DA) neuron degeneration, which was observed only at later stages (14 days). Early microglial activation in the midbrain is detected, accompanied by excessive synaptic engulfment, suggesting a critical role of microglia-dependent synapse elimination in PD pathogenesis. Furthermore, we identify the complement receptor 3 (CR3) as a key mediator of microglial synaptic engulfment, revealing that its inhibition rescues synaptic integrity and prevents neurodegeneration. Our results contribute to a deeper understanding of early events of PD progression driven by systemic inflammation and provide early intervention strategies targeting microglial complement signaling to halt PD progression.
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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 Socratic graph.