Notably, pharmacological C5aR1 antagonism via PMX205, which is ineffective at reducing the amyloid plaque burden, was able to prevent cognitive decline.76 In support of our results in the rmCHI model, we previously reported that C5aR1 antagonism in a CCI model reduced peripheral immune cell infiltration in the injured brain but failed to improve cognitive performance.30 These apparent discrepancies may reflect fundamental differences in the mechanisms and types of inflammation that underlie acute traumatic brain injury versus chronic neurodegenerative disease. This evidence concerns the gene C5AR1 and amyloidosis.