Lack of mutations in the epsilon-sarcoglycan gene in patients with different subtypes of Primary dystonias
Identifieur interne : 000D00 ( PascalFrancis/Curation ); précédent : 000C99; suivant : 000D01Lack of mutations in the epsilon-sarcoglycan gene in patients with different subtypes of Primary dystonias
Auteurs : Kathrin Grundmann [Allemagne] ; Ulrike Laubis-Herrmann [Allemagne] ; Dirk Dressier [Allemagne] ; Juliane Vollmer-Haase [Allemagne] ; Peter Bauer [Allemagne] ; Manfred Stuhrmann [Allemagne] ; Thorsten Schulte [Allemagne] ; Ludger Schöls [Allemagne] ; Helge Topka [Allemagne] ; Olaf Riess [Allemagne]Source :
- Movement disorders [ 0885-3185 ] ; 2004.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
Primary dystonias represent a clinically and genetically heterogeneous group of movement disorders. Mutations in the e-sarcoglycan (SGCE) gene have been found recently to cause myoclonus-dystonia (MD). Considerable clinical variation of SGCE mutation carriers leads to the hypothesis that mutations in the SGCE gene might also be relevant for other subtypes of dystonias. To determine the contribution of mutations in the SGCE gene in patients with different subtypes of dystonias, we analyzed the coding sequence of the SGCE gene in a group of 296 patients with a clinical phenotype of primary dystonia and in 2 patients with a clinical phenotype of myoclonus-dystonia. Patients with mutations in the DYT1 gene were excluded. We could not detect a mutation in the SGCE gene in any of the 298 patients. Our results suggest that mutations in the SGCE gene cannot be held responsible for other subtypes of primary dystonia.
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<front><div type="abstract" xml:lang="en">Primary dystonias represent a clinically and genetically heterogeneous group of movement disorders. Mutations in the e-sarcoglycan (SGCE) gene have been found recently to cause myoclonus-dystonia (MD). Considerable clinical variation of SGCE mutation carriers leads to the hypothesis that mutations in the SGCE gene might also be relevant for other subtypes of dystonias. To determine the contribution of mutations in the SGCE gene in patients with different subtypes of dystonias, we analyzed the coding sequence of the SGCE gene in a group of 296 patients with a clinical phenotype of primary dystonia and in 2 patients with a clinical phenotype of myoclonus-dystonia. Patients with mutations in the DYT1 gene were excluded. We could not detect a mutation in the SGCE gene in any of the 298 patients. Our results suggest that mutations in the SGCE gene cannot be held responsible for other subtypes of primary dystonia.</div>
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<fC07 i1="04" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21><s1>004</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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