The pathophysiological hallmarks of AD involve the extracellular accumulation of amyloid-beta (Aβ) as plaques, intracellular accumulation of phosphorylated Tau as neurofibrillary tangles, and elevated levels of glial fibrillary acidic protein (GFAP) surrounding Aβ plaques [4]. Here, GFAP is linked to Alzheimer disease.