In addition to enhanced potential for brain permeability, an advantage of a selective small-molecule C5aR1 antagonist vs eculizumab for long-term treatment of diseases such as AD is that, while the antagonist blocks the C5aR1-mediated effects of C5a, the generation of C5b by the uninhibited cleavage of C5 is still able to initiate the assembly of the bacteriolytic C5b-9 complex upon infection-mediated complement activation, avoiding the need for vaccination against specific bacterial strains. This evidence concerns the gene C5AR1 and Alzheimer disease.