Microglia are critical immune cells in the central nervous system, functioning as tissue-resident macrophages that influence brain development, maintenance, and response to injury. They can adopt M1 or M2 phenotypes based on environmental cues, with M1 being pro-inflammatory and M2 involved in tissue repair. Recent studies highlight the role of metabolic reprogramming in microglial activation, particularly the shift from oxidative phosphorylation to aerobic glycolysis during M1 polarization. This metabolic switch is crucial for energy production and survival under inflammatory conditions. M1 polarization is associated with increased production of pro-inflammatory cytokines, reactive oxygen species, and nitric oxide, while M2 polarization is linked to anti-inflammatory functions and tissue repair. The metabolic state of microglia is influenced by factors such as LPS, IFN-γ, and IL-4/IL-13, which drive distinct metabolic pathways. Studies using BV-2 microglia and primary microglia have shown that LPS induces M1 polarization with increased glycolysis and lactate production, while IL-4/IL-13 promotes M2 polarization with reduced glycolysis and increased oxidative metabolism. These metabolic shifts are critical for microglial function in neurodegenerative diseases and tissue repair. The interplay between microglial polarization and mitochondrial metabolism is a key area of research, with implications for understanding and treating neurological disorders.Microglia are critical immune cells in the central nervous system, functioning as tissue-resident macrophages that influence brain development, maintenance, and response to injury. They can adopt M1 or M2 phenotypes based on environmental cues, with M1 being pro-inflammatory and M2 involved in tissue repair. Recent studies highlight the role of metabolic reprogramming in microglial activation, particularly the shift from oxidative phosphorylation to aerobic glycolysis during M1 polarization. This metabolic switch is crucial for energy production and survival under inflammatory conditions. M1 polarization is associated with increased production of pro-inflammatory cytokines, reactive oxygen species, and nitric oxide, while M2 polarization is linked to anti-inflammatory functions and tissue repair. The metabolic state of microglia is influenced by factors such as LPS, IFN-γ, and IL-4/IL-13, which drive distinct metabolic pathways. Studies using BV-2 microglia and primary microglia have shown that LPS induces M1 polarization with increased glycolysis and lactate production, while IL-4/IL-13 promotes M2 polarization with reduced glycolysis and increased oxidative metabolism. These metabolic shifts are critical for microglial function in neurodegenerative diseases and tissue repair. The interplay between microglial polarization and mitochondrial metabolism is a key area of research, with implications for understanding and treating neurological disorders.