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Fig. 8 | Molecular Neurodegeneration

Fig. 8

From: Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss

Fig. 8

Proposed mechanism by which C5aR1 stimulation contributes to AD progression. Aβ fibrils activate complement resulting in cleavage of C3 and C5. Amyloid deposited C3b/iC3b should lead to more efficient phagocytosis by microglia/macrophages, while generated C5a recruits and alters the function of microglia. C5a induces an inflammatory polarization of the microglia, potentially synergizing with TLRs, which results in production of neurotoxic inflammatory products while suppressing beneficial phagocytosis and degradation pathways thereby contributing to neuronal damage and cognitive deficits. Targeting C5a and its receptor C5aR1 will not interfere with the beneficial effects of upstream complement components

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Molecular Neurodegeneration

ISSN: 1750-1326