AbstractSporadic Alzheimer’s disease (sAD) is associated with decreased glucose/energy metabolism in the brain. The majority of glucose utilization in the brain appears to be mediated through glucose transporter protein 1 and 3 (GLUT1 and GLUT3). Deficiency of GLUT1 and GLUT3 in the brain has been found in sAD patients post mortem; however this is not unique to the disease as it is associated with different clinical syndromes as well. In line with recent findings that insulin resistant brain state precedes and may possibly cause sAD, an experimental sAD model based on the central application of the streptozotocin (STZ-icv rat model), which is a selective GLUT2 substrate, has drawn attention to the possible significance of the brain GLUT2 in sAD etiopathogenesis. Important steps in the GLUT2 and sAD interplay are reviewed and discussed. It is concluded that increased vulnerability of GLUT2 expressing neurons may be involved in development of sAD.
Insulin-resistant brain state: The culprit in sporadic Alzheimer's disease?