Dissertation defence (Clinical Neuroscience): MBBS, MSc Imran Waggan
MBBS, MSc Imran Waggan defends the dissertation in Clinical Neuroscience titled “Adenosine A2A receptors in Parkinson’s disease: Insights from in vivo brain PET imaging” at the University of Turku on 21 August 2026 at 12.00 (University of Turku, Medisiina D, Lauren 2 hall, Kiinamyllynkatu 10, Turku).
Opponent: Professor Charalampos (Haris) Tzoulis, MD, PhD, Director (Neuro-SysMed Center of Excellence for Clinical Research Department of Neurology, Haukeland University Hospital Bergen, Norway)
Custos: Professor Laura Airas, MD, PhD (Clinical Neurosciences, University of Turku Neurocenter, Turku University Hospital Turku PET Centre, University of Turku and Turku University Hospital Turku)
Summary of the Doctoral Dissertation:
Parkinson's disease is a condition that slowly affects a person's ability to move. People with Parkinson's often experience shaking, stiffness, and slower movements, along with other symptoms that are less visible but equally challenging. These problems happen because certain brain cells that produce dopamine, a chemical that helps control movement, gradually stop working and die.
This dissertation looked at a different part of the brain's chemistry that is closely connected to dopamine: a receptor called the adenosine A2A receptor. Receptors act like docking stations on brain cells, picking up chemical signals and passing them on. The A2A receptor sits right next to dopamine receptors in a brain area called the striatum, which plays a central role in movement control. Because these two receptor types work so closely together, A2A receptors are seen as a promising target for future Parkinson's treatments. However, until now, little was known about how these receptors change as the Parkinson's disease progresses.
Using a brain imaging method called PET, combined with a special tracer that attaches specifically to A2A receptors, this research measured receptor levels in the brains of people with Parkinson's disease and compared them to healthy individuals. Three main things were discovered. First, briefly stopping Parkinson's medication did not change A2A receptor levels in putamen and pallidum, important regions in Parkinson's pathology. This suggests that the medication's short-term effect on this receptor is more limited. Second, receptor levels were not the same across all stages of the disease. People in the early stages of Parkinson's showed lower receptor levels in one brain region, while those in the moderate stages showed higher levels in another. This tells us that these receptors change dynamically as the disease develops, rather than simply increasing or decreasing in one direction. Third, changes in A2A receptors were also detected outside the striatum, in other parts of the brain not traditionally linked to Parkinson's. This points to a possible connection between this receptor system and inflammation processes in the brain.
This research provides new evidence, gathered directly from living patients rather than from animal models or laboratory studies, about how A2A receptors behave at different stages of Parkinson's disease. This kind of information has been very limited until now.
Understanding how these receptors change over time helps researchers and doctors better understand what is happening inside the brains of people with Parkinson's disease. It also supports the case for A2A receptors as a target for new medications. Some drugs that act on this receptor are already used to help manage Parkinson's symptoms, and this research adds valuable knowledge that could help refine how and when such treatments are used in the future.
