Multiple Sclerosis (MS) is a neurodegenerative disease where the immune system is thought to attack the myelin sheath of neurons. Microglia constitute part of the innate immune response to demyelination; however, their role is not fully understood. Previously, microglia were thought to switch from a M1 (pro-inflammatory) to a M2 (regenerative) phenotype to promote remyelination (Miron et al. 2013). However, the M1 to M2 spectrum of phenotypes has been rejected in favor for a diverse array of microglia populations (Ransohoff 2016), which undergo necroptosis and repopulation in favor of a regenerative phenotype in a demyelinated environment (Lloyd et al. 2019). We propose that in the central nervous system (CNS), microglia promote remyelination. We use a fate-mapping strategy to fluorescently label microglia with the endogenous microglial marker TdTomato. We then inject the spinal cord of mice with lysophosphatidylcholine (LPC), which causes demyelination and then we analyze the cells present in the lesion with immunohistochemistry (IHC) and confocal imaging. We will determine the contribution of microglia through their relative abundance (in comparison to macrophages) with IHC and we will further characterize the microglial phenotype by looking at the previously established markers of the M1 and M2 phenotypes with flow cytometry. We expect to see increased microglial density at the site of the demyelinating lesion, and we expect to see remyelination-associated populations of microglia that predominate at the lesion area. Microglial research in MS mouse models is important in further understanding the innate immune response that leads to the development of MS, for a better understanding of the cause of MS and in developing treatments.