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Joel Gelernter, MD; Andrew J. Pakstis, PhD; David L. Pauls, PhD; Roger Kurlan, MD; Steven T. Gancher, MD; Olivier Civelli, PhD; David Grandy, PhD; Kenneth K. Kidd, PhD

Arch Gen Psychiatry. 1990;47(11):1073-1077.

Abstract
• Gilles de la Tourette syndrome has an important genetic component; the pathophysiology of this disorder may involve the dopamine system. We tested a D₂-dopamine receptor (locus DRD2, recognized by probe hD2G1) for genetic linkage with Gilles de la Tourette syndrome. Using a genetic linkage map of the region of DRD2 on the long arm of chromosome 11 and restriction fragment length polymorphism data from a total of four markers (DRD2 itself, D11S84, D11S29,and PBGD), we were able to exclude linkage of this candidate gene and Gilles de la Tourette syndrome in two extended kindreds segregating for Gilles de la Tourette syndrome. This rules out causation of Gilles de la Tourette syndrome by mutation in DRD2 in the kindreds studied under the genetic assumptions we employed; use of the map and multipoint linkage analyses also allowed us to exclude a Gilles de la Tourette syndrome susceptibility locus from a larger genetic region.

Author Affiliations
From the Departments of Psychiatry (Drs Gelernter and Kidd) and Human Genetics (Drs Pakstis, Kidd, and Pauls) and the Child Study Center (Dr Pauls), Yale University School of Medicine, New Haven, Conn; the Department of Neurology, University of Rochester (NY) (Dr Kurlan); and Oregon Health Sciences University, Portland (Drs Gancher, Civelli, and Grandy).

Footnotes
Accepted for publication December 7, 1989.

Presented in part before the American Psychiatric Association Annual Meeting, San Francisco, Calif, May 11, 1989; and the First World Congress on Psychiatric Genetics, Cambridge, England, August 4, 1989.

Reprint requests to Department of Psychiatry, Yale University School of Medicine, 1-309 SHM, New Haven, CT 06510 (Dr Gelernter).

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