The results of this research in both participants with sporadic Alzheimer’s disease and carriers of ADAD mutations support in this case our two-wave hypothesis of astrogliosis in Alzheimer’s disease and that changes in 11C-DED binding reflect an early reactive astrogliosis wave [2, 35], which shows functional changes, such as changes in mitochondrial function, in the form of MAO-B overexpression [36], while plasma GFAP might reflect a later state of astrocytes, which shows overexpression and/or release of GFAP from their cytoskeleton [37]. The gene discussed is GFAP; the disease is Alzheimer disease.