LAUSR

Adenosine A1 receptors (A1Rs) interact negatively with dopamine D1 receptors (D1Rs) in neurons of the basal ganglia's direct pathway, while adenosine A2A receptors (A2ARs) negatively interact with dopamine D2 receptors (D2Rs) in indirect‐pathway neurons. The aim of this study was to investigate the cerebral density of A1Rs in Parkinson's disease (PD) in its early stages, using PET scans with the radioligand 8‐dicyclopropylmethyl‐1‐11C‐methyl‐3‐propylxanthine (11C‐MPDX). We studied 10 drug‐naïve patients with early PD. Each patient was also examined for dopamine transporters (DATs) and D2Rs by PET using 11C‐2‐β‐carbomethoxy‐3‐β‐(4‐fluorophenyl)‐tropane (11C‐CFT) and 11C‐raclopride (11C‐RAC), respectively. Ten elderly, healthy volunteers were recruited as controls for 11C‐MPDX PET scanning and eight elderly volunteers were recruited as controls for 11C‐CFT and 11C‐RAC PET scanning. The PET scans revealed a decrease in the uptake ratio index (URI) of 11C‐CFT and an increase in the URI of 11C‐RAC in patients. In the temporal lobe, the binding potential for 11C‐MPDX was higher in the patient group than in healthy subjects, but not in the other regions examined, including the striatum. In patients, we observed motor‐symptom asymmetry and a relationship between parkinsonism and the striatal density of DATs, but not A1R density. In the putamen of early PD, asymmetrical down‐regulation of A2ARs is likely a compensatory mechanism in response to a decrease in dopamine. However, our study suggests that A1Rs are unaltered in the putamen of early PD.