Single cell RNAseq of SOD1 mouse spinal cords
Sequencing was performed to better understand the role of neuroinflammation and glial RIPK1 signaling in ALS pathogenesis in the SOD1G93A transgenic mouse model. Overall design: Starting on postnatal day 70, before noticeable motor deficits, female mice were treated prophylactically with the tool compound GSK'547 (RIPK1i), a highly selective CNS-penetrant RIPK1 kinase inhibitor. The inhibitor was initially dosed in chow and as motor symptoms became more severe, RIPK1i was administered via oral gavage. Spinal cords were removed at day 120 for analysis.