However, this is consistent with other report showing that the distinct DAO population does not exceed 5% of all oligodendrocytes [67], which is also consistently shared across multiple pathologies, including different models of Alzheimer’s disease (5xFAD amyloidosis model, P301L pure tauopathy model, and PS2/APP/P301L combined tauopathy/amyloidosis model), a multiple sclerosis model of experimental autoimmune encephalomyelitis, or following LPS-induced brain inflammation [67], with signature genes involved in phagocytosis and lactate shuttling functions [38–40]. This evidence concerns the gene APP and experimental autoimmune encephalomyelitis.