MAOB and Alzheimer disease: These trends might be explained by non-specific binding of [11C]-L-deprenyl-D2, resulting in different binding capacity at baseline, or by differences in K1, and may be reflective of MAO-B activity, as the binding capacity was highest in the striatum and lower in the cortical regions in both patients with AD and EC subjects in the present study as well in others [23, 25].