Possible factors include altered blood vessels and stroke [6], insufficient neurovascular coupling and/or inadequate glucose delivery to capillaries [7, 28], reduced glucose transport across the blood brain barrier [38], as well as intrinsic changes in metabolism within neurons, such as changes in oxidative phosphorylation [20, 39] and mechanistic target of rapamycin (mTor) and other regulatory alterations [40-42]. This evidence concerns the gene MTOR and stroke disorder.