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Ludger Schöls

Researcher at University of Tübingen

Publications -  391
Citations -  17866

Ludger Schöls is an academic researcher from University of Tübingen. The author has contributed to research in topics: Ataxia & Spinocerebellar ataxia. The author has an hindex of 67, co-authored 338 publications receiving 14915 citations. Previous affiliations of Ludger Schöls include German Center for Neurodegenerative Diseases & Goethe University Frankfurt.

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Journal ArticleDOI

Autosomal dominant cerebellar ataxias: clinical features, genetics, and pathogenesis.

TL;DR: The identification of ataxia genes raises hope that essential pathogenetic mechanisms causing SCA will become more and more apparent, and will enable the development of rational therapies for this group of disorders, which currently can only be treated symptomatically.
MonographDOI

Leitlinien für Diagnostik und Therapie in der Neurologie

H. C. Diener, +101 more
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The natural history of degenerative ataxia: a retrospective study in 466 patients.

TL;DR: In FRDA, the time until confinement to wheelchair was shorter in patients with earlier disease onset, suggesting that patients with long GAA repeats and early disease onset have a poor prognosis, and in MSA, later age of onset increased the risk of rapid progression and death.
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Oxidative stress in patients with Friedreich ataxia

TL;DR: Oral treatment with 5 mg/kg/day of the antioxidant idebenone for 8 weeks significantly decreased urinary 8OH2'dG concentrations, indicating that 8OH 2'dG may be useful in monitoring therapeutic interventions in patients with FRDA.
Journal ArticleDOI

A Pan‐European Study of the C9orf72 Repeat Associated with FTLD: Geographic Prevalence, Genomic Instability, and Intermediate Repeats

Julie van der Zee, +88 more
- 01 Feb 2013 - 
TL;DR: In vitro reporter gene expression studies demonstrated significantly decreased transcriptional activity of C9orf72 with increasing number of normal repeat units, indicating that intermediate repeats might act as predisposing alleles and in favor of the loss‐of‐function disease mechanism.