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Cholinergic vesicular transporters in progressive supranuclear palsy

From the Departments of Radiology (Division of Nuclear Medicine) (Drs. Suzuki and Frey), Neurology (Drs. Albin and Frey), and The Mental Health Research Institute (Dr. Frey and T. Desmond), University of Michigan, Ann Arbor; Geriatrics Research, Education, and Clinical Center (Dr. Albin), Ann Arbor Veteran’s Administration Medical Center, MI; and Department of Neurology (Dr. Suzuki), Jikei University School of Medicine, Tokyo, Japan.

Address correspondence and reprint requests to Dr. K.A. Frey, University of Michigan Hospitals, Room B1G 412/0028 AGH, 1500 East Medical Center Drive, Ann Arbor, MI 48109; e-mail: kfrey{at}umich.edu

Objective: To determine the status of cholinergic and monoaminergic vesicular transporter binding sites in progressive supranuclear palsy (PSP).

Methods: The authors determined autoradiographically the regional expression of acetylcholine vesicular transporter (VAChT) and monoamine vesicular transporter type 2 (VMAT2) binding sites in postmortem basal ganglia samples from subjects with PSP. Comparison neurochemical measures included choline acetyltransferase (ChAT) enzyme activity and benzodiazepine (BZ) binding sites.

Results: VAChT expressions and ChAT activities in caudate nucleus and putamen were markedly decreased in PSP, whereas BZ binding was unaffected, consistent with selective losses of striatal cholinergic interneurons. VMAT2 density was reduced significantly in the caudate nucleus, putamen, and substantia nigra pars compacta, consistent with degeneration of dopaminergic nigrostriatal projection neurons in PSP. In the globus pallidus, BZ receptor binding sites were reduced, whereas VMAT2 and VAChT binding sites were unchanged, indicating losses of intrinsic pallidal neurons and synapses.

Conclusions: These results confirm selective and marked degenerations of basal ganglia cholinergic and dopaminergic terminals in PSP. Striatal VAChT reduction may provide a unique neurochemical imaging marker for distinction of PSP from other types of basal ganglia neurodegeneration.

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