Literature DB >> 19345147

Mutations in THAP1 (DYT6) in early-onset dystonia: a genetic screening study.

Susan B Bressman1, Deborah Raymond, Tania Fuchs, Gary A Heiman, Laurie J Ozelius, Rachel Saunders-Pullman.   

Abstract

BACKGROUND: Mutations in THAP1 were recently identified as the cause of DYT6 primary dystonia; a founder mutation was detected in Amish-Mennonite families, and a different mutation was identified in another family of European descent. To assess more broadly the role of this gene, we screened for mutations in families that included one family member who had early-onset, non-focal primary dystonia.
METHODS: We identified 36 non-DYT1 multiplex families in which at least one person had non-focal involvement at an age of onset that was younger than 22 years. All three coding exons of THAP1 were sequenced, and the clinical features of individuals with mutations were compared with those of individuals who were negative for mutations in THAP1. Genotype-phenotype differences were also assessed.
FINDINGS: Of 36 families, nine (25%) had members with mutations in THAP1, and most were of German, Irish, or Italian ancestry. One family had the Amish-Mennonite founder mutation, whereas the other eight families each had novel, potentially truncating or missense mutations. The clinical features of the families with mutations conformed to the previously described DYT6 phenotype; however, age at onset was extended from 38 years to 49 years. Compared with non-carriers, mutation carriers were younger at onset and their dystonia was more likely to begin in brachial, rather than cervical, muscles, become generalised, and include speech involvement. Genotype-phenotype differences were not found.
INTERPRETATION: Mutations in THAP1 underlie a substantial proportion of early-onset primary dystonia in non-DYT1 families. The clinical features that are characteristic of affected individuals who have mutations in THAP1 include limb and cranial muscle involvement, and speech is often affected. FUNDING: Dystonia Medical Research Foundation; Bachmann-Strauss Dystonia and Parkinson Foundation; National Institute of Neurological Disorders and Stroke; Aaron Aronov Family Foundation.

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Year:  2009        PMID: 19345147      PMCID: PMC3712754          DOI: 10.1016/S1474-4422(09)70081-X

Source DB:  PubMed          Journal:  Lancet Neurol        ISSN: 1474-4422            Impact factor:   44.182


  21 in total

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3.  Idiopathic dystonia among Ashkenazi Jews: evidence for autosomal dominant inheritance.

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10.  The DYT1 gene on 9q34 is responsible for most cases of early limb-onset idiopathic torsion dystonia in non-Jews.

Authors:  P L Kramer; G A Heiman; T Gasser; L J Ozelius; D de Leon; M F Brin; R E Burke; J Hewett; A L Hunt; C Moskowitz
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Review 4.  Inherited isolated dystonia: clinical genetics and gene function.

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5.  Dimerization of the DYT6 dystonia protein, THAP1, requires residues within the coiled-coil domain.

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Review 7.  Primary dystonia: molecules and mechanisms.

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8.  Identification and functional analysis of novel THAP1 mutations.

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Review 9.  Update on the pathology of dystonia.

Authors:  David G Standaert
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10.  Novel THAP1 sequence variants in primary dystonia.

Authors:  J Xiao; Y Zhao; R W Bastian; J S Perlmutter; B A Racette; S D Tabbal; M Karimi; R C Paniello; Z K Wszolek; R J Uitti; J A Van Gerpen; D K Simon; D Tarsy; P Hedera; D D Truong; K P Frei; S Dev Batish; A Blitzer; R F Pfeiffer; S Gong; M S LeDoux
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