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Preclinical research demonstrates accelerated progression via C5a-C5aR1 microglial activation in Alzheimer models, indicating therapeutic value in C5aR1 inhibition.
C5a-C5aR1 signaling in AD largely exerts its effects by enhancing microglial activation pathways that accelerate disease progression. While C5a may have neuroprotective effects via C5aR2, engagement of C5a with C5aR1 is detrimental in AD models. These data support specific pharmacological inhibition of C5aR1 as a potential therapeutic strategy to treat AD.
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Carvalho et al. (2022) studied this question.
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