The differences in the overexpression of GFAP and MAO-B (the latter demonstrated by 3H-DED) observed in these results, together with studies in mouse models of disease [33], led to the hypothesis that increases in GFAP or MAO-B in AD reflect distinct subtypes of astrocytes displaying different responses to AD pathology, in a region-specific manner [10,13]. Here, MAOB is linked to Alzheimer disease.