SLC9A1 and stroke disorder: We detected increased C1q/PSD95 co-localization in the Nhe1 cKO brains at 3 d post-stroke, where C1q, the initiating protein in the classical complement cascade, can selectively target synaptosomes expressing proteins involved in apoptotic processes that need to be eliminated by microglia, and thus has emerged as a critical mediator for synaptic refinement and plasticity25,27,28.