In an initial clinical study that recruited various patients and healthy subjects, [18F]F-DED uptake patterns were consistent with MAO-B expression in neurological diseases, as follows: AD without tau and neurodegeneration (A+T-N-), high cortical binding; AD with tau and neurodegeneration (A+T+N+), relatively low cortical binding; PD, moderate global binding with enhanced signal in the basal ganglia; multiple system atrophy, strong cortical binding; and autoimmune encephalitis, strong cerebellar peduncles binding (Fig. 4. This evidence concerns the gene MAOB and Alzheimer disease.