Title : Variations in neural and cardiac responses to reward processing in parkinson’s disease with depressive symptoms
Abstract:
Parkinson’s disease (PD) is the second most common and fastest-growing neurodegenerative disease in the world. Although commonly recognized as a motor disorder, non-motor symptoms such as apathy and anhedonia are equally as prevalent. Depressive symptoms may result from neurological and autonomic nervous system changes in PD, such as reduced dopamine release in brain regions damaged during the disease process. It could also be the result of abnormalities in dopamine transmission between the ventral tegmental area (VTA) and nucleus accumbens (NAcc), both of which are crucial areas for reward anticipation and consumption. Abnormal dopamine transmission between these regions may contribute to anhedonia, a core symptom of depression. This study aims to understand the connection between depression and Parkinson’s disease during reward anticipation and consumption using fMRI. We will examine the blood oxygen level-dependent signal in dopaminergic brain regions, such as the nucleus accumbens (NAcc), ventral tegmental area (VTA), and substantia nigra (SN) during reward-related tasks. We anticipate that in PD, where there is cell death in dopaminergic brain regions such as the SN, we anticipate that (1) there will be reduced BOLD activity during reward anticipation and consumption. In addition to reduced neural activity in regions responsible for reward, we also anticipate (2) reward responses to be tied to lower cardiac activity and (3) a lower speed and rate of responses during reward tasks for participants with PD compared to healthy controls. Understanding these neural and physiological responses could provide insight into the underlying mechanisms of depression in PD and inform potential therapeutic approaches.
