Effect of microglia depletion on white and gray matter inflammation in myelin mutant mice

This thesis aimed to characterize microglia phenotype following CSF1R inhibitor PLX5622 treatment in the catatonia mouse model Cnp knockout (Cnp-/-). Prior research established Cnp-/- mice as a translational model for catatonia and associated neuroinflammation, and demonstrated the efficacy of PLX5622 administration in alleviating the behavioral and inflammatory symptoms. This study analyzed microglial activation and marker expression across one and two treatment paradigms using immunohistochemistry and FACS. Results revealed leftover, highly pro-inflammatory microglia after PLX5622, with upregulation of CD68, MHCII, and CD11c, and downregulation of Tmem119. Both treatment regimes showed similar effectiveness, supporting the therapeutic potential of PLX5622 for reversing catatonia-associated pathology. Optimization and further exploration of depletion and repopulating cell dynamics remain warranted.