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From the Departments of Molecular and Medical Genetics (Drs. Carrero-Valenzuela, Payami, and Litt, and S. Shattuc), Neurology (Drs. Payami and Nutt, and S. Shattuc), and Biochemistry and Molecular Biology (Dr. Litt), Oregon Health Sciences University, Portland, OR; the Department of Neurology (Dr. Johnson and E. Stenroos), UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ; the Neurogenetics Unit (Dr. Schalling and K. Lindblad), Department of Molecular Medicine, Karolinska Hospital, Stockholm, Sweden; and INSERM U289 (Dr. Brice), Hopital de la Salpetriere, Paris, France.
Supported in part by grants from the American Parkinson's Disease Association and the National Center for Human Genome Research (NIH grant RO1-HG00022), the Swedish Medical Research Council (grant B9S-13XB-10909-02B), and EC Biomed 1 (grant Gene CT93-0060) and by a NARSAD Young Investigator Award to M.S.
Received December 12, 1994. Accepted in final form February 3, 1995.
Address correspondence and reprint requests to Dr. Michael Litt, Department of Biochemistry, L333, Oregon Health Sciences University, Portland, OR 97201-3098; e-mail: litt@ohsu.edu.
In some kindreds, familial Parkinson's disease (PD) exhibits genetic anticipation.Thus, we postulated that familial PD in certain kindreds may be associated with a CAG repeat expansion. However, using the repeat expansion detection method, we found no significant increase in the frequency of CAG repeat expansion among 46 unrelated PD probands compared with controls. Nor did we find evidence for CAG repeat expansion between generations in 11 different PD families that exhibit anticipation in age at onset.
NEUROLOGY 1995;45: 1760-1763
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