Indeed, the initial studies using [11C]-Deuterium-l-Deprenyl ([11C]-DED)—an irreversible MAO-B inhibitor derived from the anti-parkinsonian drug selegiline—did not reveal clear differences between CTRL and sporadic AD individuals and pointed to an increased uptake in pre-symptomatic autosomal dominant AD mutation carriers with decreased uptake toward their expected age of onset [5, 41, 43]. Here, MAOB is linked to Alzheimer disease.