PET studies in Parkinson's disease motor and cognitive dysfunction

Abstract

Positron emission tomography (PET) has led to significant advances in the knowledge of the neurobiology and pathophysiology of Parkinson's disease (PD) and has also greatly contributed to the understanding of potential mechanisms involved in the development of treatment-induced complications. Initially, PET was mostly used to assess in vivo the severity of the nigrostriatal dopaminergic dysfunction and the resulting motor symptomatology in PD. It has been demonstrated that PET measurements of putaminal dopaminergic function, as measured by [(18)F]-Fluorodopa uptake, correlate well with stages of disease and symptom severity in PD patients, particularly with bradykinesia and rigidity. Analysis of metabolic changes across the brain has identified specific brain networks associated with the main motor features of the disease, including bradykinesia and tremor. In more recent years, the growing availability of new imaging radiotracers for monoaminergic and cholinergic neurons has enabled the evaluation of the non-dopaminergic brain pathways that are likely to be involved in the pathophysiology of non motor symptoms of PD, including depression, fatigue, sleep disorders, and cognitive impairment. Finally, β-amyloid imaging agents have been used to assess the influence of coexistent cortical Alzheimer pathology in PD. This review summarizes the findings from PET studies that have investigated pathophysiology and treatment of motor dysfunction and cognitive impairment in PD.