This review discusses the polarization states of microglia, the immune cells of the nervous system, and their relationship to mitochondrial metabolism. Microglia exhibit two primary phenotypes: M1, which is pro-inflammatory and activated by cytokines like LPS and IFN-γ, and M2, which is anti-inflammatory and activated by cytokines like IL-4 and IL-13. The M1 phenotype is associated with increased glycolysis and reduced mitochondrial function, while the M2 phenotype is characterized by decreased glycolysis and increased oxidative metabolism. Metabolic reprogramming plays a crucial role in regulating the innate inflammatory response, with cells shifting from oxidative phosphorylation to aerobic glycolysis to meet energy demands during activation. The review also highlights the dynamic nature of polarization, where cells can transition between M1 and M2 states, and the potential implications of these metabolic shifts in neurodegenerative disorders. Experimental data from primary microglia and the BV-2 microglia cell line support the findings, showing that LPS-induced M1 polarization leads to a glycolytic burst and mitochondrial dysfunction, while IL-4/IL-13-induced M2 polarization maintains an oxidative metabolic state. The review concludes by discussing the broader implications of metabolic shifts in microglial function and the potential for therapeutic interventions targeting these metabolic changes.This review discusses the polarization states of microglia, the immune cells of the nervous system, and their relationship to mitochondrial metabolism. Microglia exhibit two primary phenotypes: M1, which is pro-inflammatory and activated by cytokines like LPS and IFN-γ, and M2, which is anti-inflammatory and activated by cytokines like IL-4 and IL-13. The M1 phenotype is associated with increased glycolysis and reduced mitochondrial function, while the M2 phenotype is characterized by decreased glycolysis and increased oxidative metabolism. Metabolic reprogramming plays a crucial role in regulating the innate inflammatory response, with cells shifting from oxidative phosphorylation to aerobic glycolysis to meet energy demands during activation. The review also highlights the dynamic nature of polarization, where cells can transition between M1 and M2 states, and the potential implications of these metabolic shifts in neurodegenerative disorders. Experimental data from primary microglia and the BV-2 microglia cell line support the findings, showing that LPS-induced M1 polarization leads to a glycolytic burst and mitochondrial dysfunction, while IL-4/IL-13-induced M2 polarization maintains an oxidative metabolic state. The review concludes by discussing the broader implications of metabolic shifts in microglial function and the potential for therapeutic interventions targeting these metabolic changes.