NLRP3 and Hydrocephalus: In summary, we are the first to show that NLRP3-mediated dysfunction of the B-CSFB accelerated neurological deficits and hydrocephalus, at least in part, through the formation of LDs in the choroid plexus, which then interacted with mitochondria and increased mitochondrial ROS release to destroy tight junctions in the choroid plexus after ICH-IVH (Fig. 8).