Altough recent studies have demonstrated that microglia and complement coordinate to eliminate synapses in certain pathological contexts and also that specific complement proteins can be targeted to improve aspects of behavior and neuropathology in Alzheimerʼs disease models30–32,34,36,149–151, our study is the first, to our knowledge, to show that (1) these mechanisms can selectively target specific synapses in a disease-relevant neuronal circuit and (2) that strategies that block this process and preserve this synaptic population can also prevent the development of cognitive deficits. Here, VTN is linked to Cognitive impairment.