Background: As a variety of necessary nutrient, iron participate in many physiological processes. Iron deficiency can lead to many diseases. Recent studies demonstrated that iron accumulation in cells could produce toxicity, and impair the function of cells. Divalent metal transporter-1 (DMT1), as a kind of membrane protein transporting metal ions, plays a pivotal role in intestinal nonheme-iron absorption and iron acquisition by cells, and is a critical regulator of sustaining body’s iron balance. According to recent studies, when cerebral artery infarction occurs, the iron accumulation of neurons happens, and the level of neuron iron accumulation decrease and improve mammal’s cognitive state, if inhibit DMT1 by some effective approaches. Therefore, scholars think, after cerebral ischemia occurs, the expression of DMT1 increase, and induce iron much more, and further injury neurons, therefore, impair mammal’s cognitive function. Objective: To study the mechanisms of cognitive dysfunction induced by DMT1-mediated iron accumulation after brain ischemia. Contents: this review presents the mechanisms of iron absorbing and releasing for neurons, the molecular structures and physiological functions of DMT1, the effects of DMT1 to iron accumulation after cerebral ischemia, the effects and mechanisms of iron accumulation to cognition after brain ischemia. Perspective: To study the role of patho-physiological mechanisms of DMT1 after brain ischemia, and provide novel approach to relieve cognitive dysfunction after cerebral artery infarction.