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Neurology 2002;59:445-448
© 2002 American Academy of Neurology
Brief Communications

Dopamine transmission in DYT1 dystonia: A biochemical and autoradiographical study

S. J. Augood, PhD, Z. Hollingsworth, MPH, D. S. Albers, PhD, L. Yang, MD, J.-C. Leung, BS, B. Muller, MD, C. Klein, MD, X. O. Breakefield, PhD and D. G. Standaert, MD, PhD

From the Center for Aging, Genetics, and Neurodegeneration (Drs. Augood, and Standaert, and Z. Hollingsworth) and the Neurogenetics Unit (Dr. Breakefield and J.-C. Leung), Massachusetts General Hospital and Harvard Medical School, Charlestown, MA; Department of Neurology and Neurosciences (Drs. Albers and Yang), Weill Medical College of Cornell University, New York, NY; and Department of Neurology (Drs. Muller and Klein), Medical University of Lübeck, Germany.

Address correspondence and reprint requests to Dr. Sarah J. Augood, Center for Aging, Genetics and Neurodegeneration, Massachusetts General Hospital, CNY 114-2300, 114 16th Street, Charlestown, MA 02129; e-mail: augood{at}helix.mgh.harvard.edu

Indices of dopamine transmission were measured in the postmortem striatum of DYT1 dystonia brains. A significant increase in the striatal 3,4-dihydroxyphenylacetic acid/dopamine ratio was found. Quantitative autoradiography revealed no differences in the density of dopamine transporter or vesicular monoamine transporter-2 binding; however, there was a trend toward a reduction in D1 receptor and D2 receptor binding. One brain with DYT1 parkinsonism was similarly evaluated and marked reductions in striatal dopamine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid content as well as the density of binding of all four dopaminergic ligands were measured.




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