Metabolic disorders, such as reduced glucose utilization and mitochondrial dysfunction, are common characteristics of AD.[18] Emerging evidence indicates that MG activation is associated with early alterations in energy metabolism in the blood and cerebrospinal fluid of AD patients.[19] Furthermore, hypometabolism in the brain of 3xTg‐AD mice is associated with high expression of MG marker Iba‐1, rather than astrocyte marker GFAP,[20] suggesting that impaired MG energy metabolism plays a pivotal role in AD. This evidence concerns the gene AIF1 and Alzheimer disease.