Normal Striatal Vesicular Acetylcholine Transporter Expression in Tourette Syndrome

Abstract

Considerable prior work suggests basal ganglia dysfunction in Tourette syndrome (TS). Analysis of a small number of post-mortem 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 to quantify striatal vesicular acetylcholine transporter expression, a measure of cholinergic terminal density, in human TS and control subjects. We found no evidence of striatal cholinergic deficits. Discrepant imaging and post-mortem analysis results may reflect agonal or post-mortem changes, medication effects, or significant disease heterogeneity.

Significance Statement Prior post-mortem analyses suggest loss of striatal cholinergic interneurons in Tourette syndrome (TS). We evaluated this possibility with [¹⁸F]FEOBV PET, a ligand for the vesicular acetylcholine transporter and measure of cholinergic terminal integrity. We studied TS and matched control subjects. There were no differences between TS and control subjects in striatal [¹⁸F]FEOBV binding, indicating intact striatal cholinergic neurons in TS.