While no associations between the measured FDG-PET binding and clinical measures in the asymptomatic carriers were reported, the authors argued that observed cerebral hypo-metabolism patterns might underlie certain motor symptoms such as akinesia and the increased dopaminergic activity in the caudate might reflect presynaptic dopamine transporter upregulation or increased endogenous dopamine secretion in GBA1 carriers [55]. This evidence concerns the gene SLC6A3 and Akinesia.