Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the presence of alpha-synuclein pathology. The resulting dopamine deficiency leads to motor symptoms such as bradykinesia, rigidity and tremor, accompanied by a broad range of non-motor features. The adenosine A2A receptor (A2AR), which is co-localized with dopamine D2 receptors in the striatum, plays a critical role in regulating basal ganglia neurotransmission. Modulation of A2ARs has been shown to influence motor control making it an important therapeutic target in PD. However,in vivo data on how A2AR expression changes with disease progression and dopaminergic medication remain limited. In this thesis, A2AR availability was examined in patients withPD using positron emission tomography (PET) with the selective A2AR radioligand [¹¹C]TMSX. The aims were to (1) assess the effect of short-term cessation of dopaminergicmedication on striatal A2AR availability, (2) compare A2AR binding between healthy controls, early- and moderate-stage PD, and (3) explore A2AR expression in cerebral gray and white matter regions. Quantitative PET analyses were performed using reference tissue models to estimate distribution volume ratios across brain regions. The results showed A2AR availability in the putamen and pallidum was comparable between on and after short termcessation of dopaminergic medication. However, the results in caudate were not equal between both states. Furthermore, patients with early-stage PD showed a decrease in caudate and moderate-stage PD exhibited increased A2AR binding in the pallidum compared tohealthy controls, indicating progressive receptor alterations with disease severity. Finally, we showed A2AR alterations in cerebral gray and white matter regions, implying thatadenosinergic signaling may contribute to extra-striatal and potentially, neuroinflammatory aspects of PD. These findings demonstrate that [¹¹C]TMSX PET imaging can be used to characterize A2A receptor availability in vivo and that A2AR expression is dynamically alteredby disease progression. The results provide new insights into disease stage dependent changes in A2AR availability in patients with PD.