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Search for the PARK3 founder haplotype in a large cohort of patients with Parkinson's disease from Northern Germany

Published online by Cambridge University Press:  01 July 1999

C. KLEIN ,
P. VIEREGGE ,
J. HAGENAH ,
M. SIEBERER ,
E. DOYLE ,
H. JACOBS ,
T. GASSER ,
X. O. BREAKEFIELD ,
N. J. RISCH  and
L. J. OZELIUS
C. KLEIN
Affiliation:
Molecular Neurogenetics Unit, Massachusetts General Hospital, and Departments of Neurology and Genetics and Neuroscience Program, Harvard Medical School, Boston, Massachusetts 02114, USA
P. VIEREGGE
Affiliation:
Department of Neurology, Medical University of Lübeck, 23538 Lübeck, Germany
J. HAGENAH
Affiliation:
Department of Neurology, Medical University of Lübeck, 23538 Lübeck, Germany
M. SIEBERER
Affiliation:
Department of Neurology, Medical University of Lübeck, 23538 Lübeck, Germany
E. DOYLE
Affiliation:
Molecular Neurogenetics Unit, Massachusetts General Hospital, and Departments of Neurology and Genetics and Neuroscience Program, Harvard Medical School, Boston, Massachusetts 02114, USA
H. JACOBS
Affiliation:
Department of Neurology, Medical University of Lübeck, 23538 Lübeck, Germany
T. GASSER
Affiliation:
Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians University, Munich, Germany
X. O. BREAKEFIELD
Affiliation:
Molecular Neurogenetics Unit, Massachusetts General Hospital, and Departments of Neurology and Genetics and Neuroscience Program, Harvard Medical School, Boston, Massachusetts 02114, USA
N. J. RISCH
Affiliation:
Department of Genetics, Stanford University, Stanford, California 94305, USA
L. J. OZELIUS
Affiliation:
Molecular Neurogenetics Unit, Massachusetts General Hospital, and Departments of Neurology and Genetics and Neuroscience Program, Harvard Medical School, Boston, Massachusetts 02114, USA
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Abstract

A founder haplotype on chromosome 2p for autosomal dominant Parkinson's disease (PD) has been postulated for two families of Northern European descent, and a new mutation in the α-synuclein gene (Ala30Pro) has been found in a German PD family. We evaluated 85 German PD patients and 85 ethnically matched controls for shared markers on chromosome 2p and for the new α-synuclein mutation. We found no evidence for linkage disequilibrium, suggesting that the putative founder mutation on chromosome 2p is not a common cause of PD in the local population. Furthermore, no patient carried the Ala30Pro change, supporting earlier findings that mutations in the α-synuclein gene are extremely rare.

Type
Research Article
Information
Annals of Human Genetics , Volume 63 , Issue 4 , July 1999 , pp. 285 - 291
Copyright
© University College London 1999

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