Many studies have also reported changes in the astrocytic secretome profile occurring in response to AD pathophysiology [20,21], including, among others, the increased production of both plasma and CSF levels of Glial Fibrillary Acidic Protein (GFAP)—the main intermediate filament protein in mature astrocytes—[22,23] and β-S100, a calcium-binding protein tied to neurotoxic astrocytic activity [24,25]. This evidence concerns the gene GFAP and Alzheimer disease.