Since copper homeostasis is already affectedin AD, appropriatecopper chelators should not further aggravate this condition by alteringCu2+ binding to proteins involved in copper trafficking,17 such as the human copper transporter 1 (hCtr1)18,19 and the human serum albumin (HSA),20 whichbind copper with high affinity. This evidence concerns the gene SLC31A1 and Alzheimer disease.