Given our previously reported results, where pharmacological inhibition of C5a-C5aR1 signaling or genetic ablation of C5aR1 significantly rescue memory deficits in two mouse models of Alzheimer’s disease [21, 22], we further explored the potential beneficial effect of PMX205 on the appearance of dystrophic neurites (swollen dendrites and/or swollen axons that appears surrounding neuritic amyloid plaques) and microglial synaptic pruning. Here, C5 is linked to Alzheimer disease.