An example of the participation of glutamatergic transmission on AD physiopathology, indirectly regulated by albumin, is the inhibition of dementia symptoms for a limited period by the use of antagonist of the N-methyl-D-aspartate receptors or the use of glutamate transporters in patients with mild to moderate AD, which trials are now at days in phase 2 and 3 [65],[66]. This evidence concerns the gene ALB and Alzheimer disease.