Hyperactivation of the complement system is associated with severe inflammatory responses in the CNS, companied by synapse and neuron loss in human AD, and also in tauopathy (e.g., FTD in the PS19 model), as best studied in the two seminal works [43, 44]: C1q - the initiating factor of the classical complement pathway, followed by activated C3-C3R [45]. The gene discussed is C3; the disease is tauopathy.