Dopaminergic Function and Dopamine Transporter Binding Assessed With Positron Emission Tomography in Parkinson Disease

Open Access
Publisher Website
Google Scholar
Abstract
EVALUATING neuroprotective treatments designed to slow down the progressive loss of dopaminergic neurons is a crucial step for the development of therapeutic strategies in Parkinson disease (PD). A major drawback faced by previous neuroprotection studies in PD was that the potential neuroprotective effect was indistinguishable from the symptomatic improvement provided by the drug on trial.1,2 To overcome this limitation, a biological marker of disease progression could be valuable to evaluate the efficacy of neuroprotective drugs. Until now, positron emission tomography (PET) using 18F-dopa has been the gold standard tool for measuring disease progression in patients with PD.3-5 However, 18F-dopa uptake reflects the density of striatal dopaminergic terminals6 and the conversion of 18F-dopa into 18F-dopamine in these terminals.5,7,8 It has been suggested that in PD, the loss of dopaminergic synapses was partially compensated for by increased dopamine metabolism in the surviving terminals (for review see Zigmond et al,9 Hornykiewicz,10 and Bezard and Gross11). Thus, 18F-dopa uptake might overestimate the number of striatal dopaminergic nerve terminals in these patients.12,13