Abstract
Considerable prior work suggests basal ganglia dysfunction in Tourette syndrome (TS). Analysis of a small number of postmortem specimens suggests deficits of some striatal interneuron populations, including striatal cholinergic interneurons. To assess the integrity of striatal cholinergic interneurons in TS, we used [18F]FEOBV positron emission tomography (PET) to quantify striatal vesicular acetylcholine transporter (VAChT) expression, a measure of cholinergic terminal density, in human TS and control subjects. We found no evidence of striatal cholinergic deficits. Discrepant imaging and postmortem analysis results may reflect agonal or postmortem changes, medication effects, or significant disease heterogeneity.
Footnotes
The authors declare no competing financial interests.
This work was supported by the National Institutes of Health-National Institute of Neurological Disorders and Stroke Grant R21 NSNS088302.
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