The latter effect is likely due to the abnormal elevated amounts of C5a (produced under the GFAP promoter) binding to C5aR2, which has been shown to possess anti-inflammatory properties [57], thus pointing to the benefit of specific inhibition of C5aR1 as a potential therapeutic target for Alzheimer’s disease. This evidence concerns the gene C5AR1 and early-onset autosomal dominant Alzheimer disease.