ArticleNPJ Parkinson's disease2026
Microglial low-affinity FcγR mediates the phagocytic elimination of dopaminergic neurons in Parkinson's disease degeneration.
Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- C-terminal Domain of the Heavy Chain of Tetanus Toxin Ameliorate Lipopolysaccharide Induced Hemiparkinsonism in Rats.Neurotoxicity research · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
It is postulated that microglial cells interact with dopaminergic (DA) neurons of the substantia nigra pars compacta (SNpc), playing a critical role in Parkinson's disease (PD) neurodegeneration. However, the specific mechanisms by which microglial reactivity is triggered remain unclear. Experimental models of PD in mice indicate that phagocytosis drives the elimination of degenerating neurons, suggesting that blocking this microglial function could preserve remaining DA neurons. Here, we pinpoint the role of Fcγ receptor (FcγR) as a potential trigger of microglial phagocytosis in PD. We found that FcγR is overexpressed in the SNpc of PD patients, alongside indications of phagocytic microglia. Likewise, experimental models of PD show equivalent results. Importantly, blocking FcγR in vivo and in vitro, with neutralizing antibodies, reduced the microglial-mediated elimination of DA cells. These results highlight FcγR as a critical factor inducing DA neuron phagocytosis in PD and suggest a novel immunotherapeutic strategy to prevent neuronal loss.
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