In the context of AD different studies have demonstrated that Hepc expression levels decrease in AD human and in the APP-transgenic mouse [160], while the Hepc treatment on cultured microvascular endothelial cells and neurons generated a reduction of iron import (TfR1 and DMT1) and export (Fpn1) proteins with a consequence reduction of iron intake in neurons [166]. This evidence concerns the gene SLC40A1 and Alzheimer disease.