LAUSR

It was Tesla who wrote “Let the future tell the truth, and evaluate each one according to his work and accomplishments.” As we celebrate the contribution of Dr. James Parkinson, the words of Tesla ring true because the behavioral motor symptoms that Parkinson described are still with us today. As we look forward and ponder what the next 200 years will unearth for Parkinson’s disease, it is no doubt that imaging tools will provide a window to visualize and quantify this complex disease. The imaging tools developed in the 20th century have provided critical insights and discoveries. Both molecular imaging and magnetic resonance imaging are teaching us a great deal about the structure, pathology, and function of the human nervous system. Indeed, both of these imaging methods available to us today stand on the shoulders of giants who have described so many critical discoveries. It was Hevesy who was awarded the Nobel Prize for the work on radioactive tracers. Bloch and Purcell shared the Nobel Prize for their work characterizing the measurement of magnetic resonance in bulk matter. Lauterbur and Mansfield won the Nobel Prize for their work on echo-planar imaging. All of these key insights and many others have led to advances in our understanding of the nervous system in Parkinson’s disease. The imaging advances in Parkinson’s disease have been occurring at a rapid pace in the past several decades. In molecular imaging, we have learned a great deal about the presynaptic and postsynaptic integrity of dopaminergic nerve terminals in the putamen and caudate. Diffusion magnetic resonance imaging and iron-sensitive magnetic resonance imaging reliably detect signal abnormalities in a key structure linked with pathology of Parkinson—the substantia nigra. Functional magnetic resonance imaging and network approaches to positron emission tomography have helped us understand that Parkinson’s disease affects networks beyond the nigrostriatal regions, including motor and nonmotor networks. Although Parkinson’s disease pathology has been described, we are just beginning to understand how imaging tools can help us obtain reliable measurements of signals related to pathology in living humans. Two articles in the current issue of Movement Disorders provide new findings that are giving us insight into how imaging tau could benefit our understanding of Parkinson’s disease. In the article by Hansen and colleagues, in vivo cortical tau was measured using F-AV-1451 positron emission tomography in Parkinson’s disease. It is noteworthy that F-AV-1451 binding in vivo is increased in the cortex in patients with Alzheimer’s disease and subcortically (basal ganglia, cerebellum mid-brain). In the phase of mild cognitive impairment preceding Alzheimer’s disease, taurelated pathology can be identified using tau neurofibrillary tangle tracer AV-1451. Mild cognitive impairment is frequent and heralds the development of frank dementia in a high proportion of patients with Parkinson’s disease (up to 80%). Thus, the study of Hansen and colleagues in Parkinson’s disease is a novel and interesting addition to this most relevant area. They separated patients into those with mild cognitive impairment (n 5 9) and those without mild cognitive impairment (n 5 17) and compared them with 23 controls. In the cohort of patients with Parkinson’s disease, no differences in tau pathology were detected between control and PD and between PD 6 mild cognitive impairment groups, and there was no correlation between cognitive measures and tau pathology using AV-1451. Although neuropathological studies frequently describe tau pathology in Parkinson’s disease patients postmortem, particularly in those with dementia, the tracer AV-1451 was not able to detect tau pathology in this cohort of -----------------------------------------------------------*Correspondence to: Dr. David E. Vaillancourt, University of Florida, Department of Applied Physiology and Kinesiology, P.O. Box 118205, Gainesville, FL 32611; [email protected]