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© 1994 Oxford University Press

OTHER

Linkage of a locus for autosomal dominant familial spastic paraplegia to chromosome 2p markers

Afif Hentati1, Margaret A. Pericak-Vance3, Felicia Lennon3, Brad Wasserman1, Faycal Hentati4, Tony Juneja1, Misha H. Angrist5, Wu-Yen Hung1, Rose-Mary Boustany3, Saeed Bohlega6, Zafar Iqbal1, Carl H. Huether7, Mongi Ben Hamida4 and Teepu Siddique1,2,*

1Department of Neurology Northwestern University Medical School 300 East Superior, Chicago, IL 60611 2Department of Cell and Molecular Biology, Northwestern University Medical School 300 East Superior, Chicago, IL 60611 3Division of Neurology, Duke University Medical Center Durham, NC 27710, USA 4Institut National de Neurologie, Tunis, Tunisia Cleveland, OH, USA 5Case Western Reserve University Cleveland, OH, USA 6Department of Medicine, King Faisal Specialist Hospital and Research Centre Riyadh, Saudi Arabia 7Department of Biological Sciences, University of Cincinnati, Cincinnati, OH 45221, USA

*To whom correspondence should be addressed

Received June 27, 1994; Revised July 26, 1994; Accepted July 26, 1994

‘Pure’ autosomal dominant familial spastic paraplegia (SPG) is a neurodegenerative disease which clinically manifests as spasticity of the lower limbs. Dominantly inherited SPG is known to be clinically heterogenous and has been classified into late-onset and early-onset types, based on the age of onset of symptoms. We tested five autosomal dominant SPG families for genetic linkage and established linkage to chromogene 2p markers (Z({theta}) = 3.65) with evidence of genetic locus heterogeneity. Three late-onset SPG families and one early-onset SPG family had high posterior probability of linkage (P>0.94) to chromosome 2p, while the fifth family (a very early-onset family) was not linked to chromosome 2 and showed high probability of linkage to chromosome 14q. These data provide a basis for a classification of SPG according to chromosome location rather than age of onset of symptoms.


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