Other important features of the rat i.c.v. STZ model that resemble findings in brains from AD patients are as follows: memory deficits, progressive cholinergic abnormalities (Kamat, 2015[26]), loss of GLUT2 expression, glucose hypometabolism, and other pathophysiological changes, such as processing of amyloid precursor protein (APP), as well as changes in synaptic function, protein kinases, and insulin signaling (Grieb, 2016[21]). This evidence concerns the gene SLC2A2 and Alzheimer disease.