Article

Complement C3aR deletion does not attenuate neurodegeneration in a tauopathy model or alter acute inflammation-induced gene expression changes in the brain

2025-06-17

Abstract excerpt

Aberrant activation of the classical complement pathway in the brain is implicated in contributing to synapse loss and neurodegeneration in various neurodegenerative conditions. Given that C3aR is a druggable target in the complement pathway, we evaluated the potential of C3aR KO to rescue neurodegeneration in a tauopathy model and neuroinflammatory responses in an acute endotoxemia model. We found that C3aR KO di...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: b8acd122-72d4-53f2-8317-febc68eccc7d
DOI: 10.1101/2025.06.16.660026

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Complement C3aR deletion does not attenuate neurodegeneration in a tauopathy model or alter acute inflammation-induced gene expression changes in the brainDOI 10.1101/2025.06.16.660026Read

Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s DiseaseSemantic proximity Read

The good, the bad, and the opportunities of the complement system in neurodegenerative diseaseSemantic proximity Read

Complement therapeutics in neurodegenerative diseasesSemantic proximity Read

Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice.Semantic proximity Read

Complement and microglia mediate early synapse loss in Alzheimer mouse modelsSemantic proximity Read

Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice.Semantic proximity Read

Targeting complement in neurodegeneration: challenges, risks, and strategiesSemantic proximity Read

Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's diseaseSemantic proximity Read

Complement in the pathogenesis of Alzheimer’s diseaseSemantic proximity Read

Microglia, Alzheimer's Disease, and ComplementSemantic proximity Read

Glial-specific and inducible full body C3 deficiency does not affect amyloid pathology in the AppNL-G-F mouse model of Alzheimer’s diseaseSemantic proximity Read

Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer’s DiseaseSemantic proximity Read