Rolf Schroder

Summary

Affiliation: University of Bonn
Country: Germany

Publications

  1. ncbi request reprint Mutant valosin-containing protein causes a novel type of frontotemporal dementia
    Rolf Schroder
    Department of Neurology, University Hospital Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Ann Neurol 57:457-61. 2005
  2. ncbi request reprint Beyond LGMD1A: myotilin is a component of central core lesions and nemaline rods
    R Schroder
    Department of Neurology, University of Bonn, 53105 Bonn, Germany
    Neuromuscul Disord 13:451-5. 2003
  3. pmc A mutation in the dimerization domain of filamin c causes a novel type of autosomal dominant myofibrillar myopathy
    Matthias Vorgerd
    Department of Neurology, Neuromuscular Center Ruhrgebiet, Ruhr University Bochum, Bochum, Germany
    Am J Hum Genet 77:297-304. 2005
  4. ncbi request reprint Different early pathogenesis in myotilinopathy compared to primary desminopathy
    Dirk Fischer
    Muskellabor, Department of Neurology, University of Bonn, Bonn, Germany
    Neuromuscul Disord 16:361-7. 2006
  5. ncbi request reprint On noxious desmin: functional effects of a novel heterozygous desmin insertion mutation on the extrasarcomeric desmin cytoskeleton and mitochondria
    Rolf Schroder
    Department of Neurology, University Hospital Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    Hum Mol Genet 12:657-69. 2003
  6. doi request reprint Health-related quality of life in ALS, myasthenia gravis and facioscapulohumeral muscular dystrophy
    Yaroslav Winter
    Department of Neurology, Philipps University Marburg, Rudolf Bultmannstr 8, Marburg, Germany
    J Neurol 257:1473-81. 2010
  7. ncbi request reprint Disorganization of the desmin cytoskeleton and mitochondrial dysfunction in plectin-related epidermolysis bullosa simplex with muscular dystrophy
    Rolf Schroder
    Department of Neurology, University of Bonn, Germany
    J Neuropathol Exp Neurol 61:520-30. 2002
  8. ncbi request reprint Primary longitudinal adhesion structures: plectin-containing precursors of costameres in differentiating human skeletal muscle cells
    Rolf Schroder
    Department of Neurology, University of Bonn, 53105 Bonn, Germany
    Histochem Cell Biol 118:301-10. 2002
  9. doi request reprint Clinical, genetic, and cardiac magnetic resonance imaging findings in primary desminopathies
    Katharina Strach
    Department of Radiology, University Hospital Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    Neuromuscul Disord 18:475-82. 2008
  10. ncbi request reprint Clinical and morphological phenotype of the filamin myopathy: a study of 31 German patients
    Rudolf A Kley
    Department of Neurology, Neuromuscular Center Ruhrgebiet, Ruhr University Bochum, Bochum, Germany
    Brain 130:3250-64. 2007

Detail Information

Publications31

  1. ncbi request reprint Mutant valosin-containing protein causes a novel type of frontotemporal dementia
    Rolf Schroder
    Department of Neurology, University Hospital Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Ann Neurol 57:457-61. 2005
    ..We demonstrate that mutant VCP causes a novel type of frontotemporal dementia characterized by neuronal nuclear inclusions containing ubiquitin and VCP...
  2. ncbi request reprint Beyond LGMD1A: myotilin is a component of central core lesions and nemaline rods
    R Schroder
    Department of Neurology, University of Bonn, 53105 Bonn, Germany
    Neuromuscul Disord 13:451-5. 2003
    ....
  3. pmc A mutation in the dimerization domain of filamin c causes a novel type of autosomal dominant myofibrillar myopathy
    Matthias Vorgerd
    Department of Neurology, Neuromuscular Center Ruhrgebiet, Ruhr University Bochum, Bochum, Germany
    Am J Hum Genet 77:297-304. 2005
    ..As a consequence of this malfunction, the muscle fibers of our patients display massive cytoplasmic aggregates containing filamin c and several Z-disk-associated and sarcolemmal proteins...
  4. ncbi request reprint Different early pathogenesis in myotilinopathy compared to primary desminopathy
    Dirk Fischer
    Muskellabor, Department of Neurology, University of Bonn, Bonn, Germany
    Neuromuscul Disord 16:361-7. 2006
    ..These findings suggest that unrelated molecular pathways may result in seemingly similar disease phenotypes at late disease stages...
  5. ncbi request reprint On noxious desmin: functional effects of a novel heterozygous desmin insertion mutation on the extrasarcomeric desmin cytoskeleton and mitochondria
    Rolf Schroder
    Department of Neurology, University Hospital Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    Hum Mol Genet 12:657-69. 2003
    ..As a consequence, the intermediate filament pathology-induced mitochondrial dysfunction may contribute to the degeneration/regeneration process leading to progressive muscle dysfunction in human desminopathies...
  6. doi request reprint Health-related quality of life in ALS, myasthenia gravis and facioscapulohumeral muscular dystrophy
    Yaroslav Winter
    Department of Neurology, Philipps University Marburg, Rudolf Bultmannstr 8, Marburg, Germany
    J Neurol 257:1473-81. 2010
    ..In addition to the treatment of motor symptoms, greater attention should be paid to the treatment of depression, which was found to be among the independent predictors of the HRQoL in ALS and MG...
  7. ncbi request reprint Disorganization of the desmin cytoskeleton and mitochondrial dysfunction in plectin-related epidermolysis bullosa simplex with muscular dystrophy
    Rolf Schroder
    Department of Neurology, University of Bonn, Germany
    J Neuropathol Exp Neurol 61:520-30. 2002
    ..Beyond EBS-MD, our data may contribute to the understanding of other myopathies characterized by sarcoplasmic IF accumulations such as desminopathies or alpha-B-crystallinopathies...
  8. ncbi request reprint Primary longitudinal adhesion structures: plectin-containing precursors of costameres in differentiating human skeletal muscle cells
    Rolf Schroder
    Department of Neurology, University of Bonn, 53105 Bonn, Germany
    Histochem Cell Biol 118:301-10. 2002
    ..After the occurrence of spontaneous contractions, these structures reorient and mature costameres are assembled...
  9. doi request reprint Clinical, genetic, and cardiac magnetic resonance imaging findings in primary desminopathies
    Katharina Strach
    Department of Radiology, University Hospital Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    Neuromuscul Disord 18:475-82. 2008
    ..Therefore, cardiac MRI may serve as a screening tool to identify patients at risk, which might benefit from early pharmacological and/or interventional (e.g. implantable cardioverter-defibrillator devices) therapy...
  10. ncbi request reprint Clinical and morphological phenotype of the filamin myopathy: a study of 31 German patients
    Rudolf A Kley
    Department of Neurology, Neuromuscular Center Ruhrgebiet, Ruhr University Bochum, Bochum, Germany
    Brain 130:3250-64. 2007
    ..Therapy is so far limited to symptomatic treatment. The German filaminopathy cohort, the largest group of patients studied so far, shares phenotypic features with LGMD and presents with characteristic histopathological findings of MFM...
  11. doi request reprint Cardiac conduction disturbances and differential effects on atrial and ventricular electrophysiological properties in desmin deficient mice
    Jan Wilko Schrickel
    Department of Medicine Cardiology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    J Interv Card Electrophysiol 28:71-80. 2010
    ..The aim of the present study was to characterize electrophysiological cardiac properties in a desmin-deficient mouse model...
  12. ncbi request reprint On symptomatic heterozygous alpha-sarcoglycan gene mutation carriers
    Dirk Fischer
    Muskellabor, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Ann Neurol 54:674-8. 2003
    ..This finding may be attributed to an additional negative variation in a yet unknown modifier gene essential to the function of the sarcoglycan complex in shoulder girdle muscles...
  13. doi request reprint Socioeconomic burden of amyotrophic lateral sclerosis, myasthenia gravis and facioscapulohumeral muscular dystrophy
    Karsten Schepelmann
    Department of Neurology, Philipps University Marburg, Marburg, Germany
    J Neurol 257:15-23. 2010
    ..The socioeconomic burden of NMDs in Germany is considerable. Further studies evaluating both the health-economic and clinical effects of NMD treatment as well as disease management programs and benchmarking activities are necessary...
  14. ncbi request reprint Pax7 distribution in human skeletal muscle biopsies and myogenic tissue cultures
    Jens Reimann
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Cell Tissue Res 315:233-42. 2004
    ..Most of these were found to be the nuclei of cells engaged in focal regenerative processes, but Pax7 re-expression by myonuclei "in distress" cannot be ruled out entirely...
  15. doi request reprint Concerted action of two novel tRNA mtDNA point mutations in chronic progressive external ophthalmoplegia
    Cornelia Kornblum
    Department of Neurology, University of Bonn Medical Center, Bonn, D 53105, Germany
    Biosci Rep 28:89-96. 2008
    ..Thus homoplasmic mutations may influence the functional consequences of pathogenic heteroplasmic mtDNA mutations...
  16. ncbi request reprint IFN-beta1a (Rebif) modifies the expression of microfilament-associated cell-cell contacts in C6 glioma cells
    Michael Harzheim
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    J Interferon Cytokine Res 23:83-9. 2003
    ..This effect may also contribute to the therapeutic action of IFN-beta1a in MS...
  17. doi request reprint Suprascapular nerve entrapment by a spinoglenoid cyst
    Alexander Semmler
    Department of Neurology, University Bonn, Germany
    Neurology 70:890. 2008
  18. ncbi request reprint Distinct neuromuscular phenotypes in myotonic dystrophy types 1 and 2 : a whole body highfield MRI study
    Cornelia Kornblum
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    J Neurol 253:753-61. 2006
    ..In contrast, MRI was no reliable indicator for skeletal muscle involvement in mildly affected DM2 patients since myalgia and mild paresis were usually not reflected by MRI signal alterations...
  19. ncbi request reprint Consequences of a novel caveolin-3 mutation in a large German family
    Dirk Fischer
    Department of Neurology, University of Bonn, Germany
    Ann Neurol 53:233-41. 2003
    ..Different clinical phenotypes in caveolinopathies may be attributed to so far unidentified modifying factors/genes in the individual genetic background of affected patients...
  20. ncbi request reprint Mitochondrial dysfunction in myofibrillar myopathy
    Jens Reimann
    Department of Neurology, University of Bonn, Germany
    Neuropathol Appl Neurobiol 29:45-51. 2003
    ..Together with data from observations in desmin- and plectin-deficient mice, our results support the view that desmin intermediate filament pathology in these cases is closely linked to mitochondrial dysfunction in skeletal muscle...
  21. ncbi request reprint Enhanced heterogeneity of myocardial conduction and severe cardiac electrical instability in annexin A7-deficient mice
    Jan W Schrickel
    Department of Medicine Cardiology, University of Bonn, Germany
    Cardiovasc Res 76:257-68. 2007
    ..We investigated the impact of annexin A7 on cardiac electrophysiological properties using an annexin A7-deficient mouse strain (annexin A7(-/-))...
  22. ncbi request reprint Metabolic consequences of a novel missense mutation of the mtDNA CO I gene
    Dmitry A Varlamov
    Department of Epileptology, University of Bonn Medical Center, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    Hum Mol Genet 11:1797-805. 2002
    ..This is due to a 2-fold increase of COX flux control on muscle fiber respiration and a 30% decrease of COX metabolic threshold, supporting the concept of tight COX control of oxidative phosphorylation in skeletal muscle...
  23. pmc Grey and white matter loss along cerebral midline structures in myotonic dystrophy type 2
    Martina Minnerop
    Department of Neurology, University Hospital of Bonn, Sigmund Freud Strasse 25, Bonn, Germany
    J Neurol 255:1904-9. 2008
    ..The reduced size of the corpus callosum further extends the spectrum of white matter changes in DM2 and may represent the morphological substrate of neuropsychological abnormalities previously described in this disorder...
  24. ncbi request reprint The expression of microfilament-associated cell-cell contacts in brain endothelial cells is modified by IFN-beta1a (Rebif)
    Michael Harzheim
    Department of Neurology, University of Bonn, Germany
    J Interferon Cytokine Res 24:711-6. 2004
    ..This action of IFN-beta1a may contribute to its beneficial effects in MS therapy...
  25. ncbi request reprint Variability of the recessive oculopharyngeal muscular dystrophy phenotype
    Alexander Semmler
    Department of Neurology, University Hospital Bonn, Germany
    Muscle Nerve 35:681-4. 2007
    ..We conclude that the apparent rarity of the autosomal-recessive form of OPMD may be due to the fact that genetic testing is generally administered only to patients with typical clinical features or a positive family history...
  26. ncbi request reprint Expression, localization and functional divergence of alphaB-crystallin and heat shock protein 27 in core myopathies and neurogenic atrophy
    Dirk Fischer
    Department of Neurology, University Hospital Bonn, Rheinische Friedrich Wilhelms Universitat, Sigmund Freud Str 25, 53105 Bonn, Germany
    Acta Neuropathol 104:297-304. 2002
    ..The latter findings imply a functional diversity of both shsps with a preferential association of hsp 27 with the actin microfilament system and alphaBC with the intermyofibrillar desmin cytoskeleton in human skeletal muscle...
  27. ncbi request reprint On the early diagnosis of IVIg-responsive chronic multifocal acquired motor axonopathy
    Dirk Fischer
    Department of Neurology, University of Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Neurol 251:1204-7. 2004
    ..Our findings indicate that paraspinal EMG and anti-GD1a antibodies can facilitate the early identification of treatable, IVIg responsive, patients with MAMA...
  28. ncbi request reprint Diagnostic value of muscle MRI in differentiating LGMD2I from other LGMDs
    Dirk Fischer
    Dept of Neurology, University of Bonn, Sigmund Freud Str 25, 53105 Bonn, Germany
    J Neurol 252:538-47. 2005
    ..Our results indicate that muscular MRI is a powerful tool for differentiating LGMD2I from other forms of autosomal recessive LGMDs and dystrophinopathies...
  29. ncbi request reprint Hsp27-2D-gel electrophoresis is a diagnostic tool to differentiate primary desminopathies from myofibrillar myopathies
    Christoph S Clemen
    Department of Neurology, Medical Faculty, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, FRG
    FEBS Lett 579:3777-82. 2005
    ..They indicated a shift of the main hsp27-spot to alkaline pH degrees, which may help to differentiate primary desminopathies from other myopathies with structural pathology of the desmin cytoskeleton...
  30. ncbi request reprint Diagnostic value of mitochondrial DNA mutation analysis in juvenile unilateral ptosis
    Thorsten Okulla
    Department of Neurology, University of Bonn, Sigmund Freud Str 25, 53105, Bonn, Germany
    Graefes Arch Clin Exp Ophthalmol 243:380-2. 2005
    ..To highlight the diagnostic relevance of mitochondrial DNA (mtDNA) mutation analysis in acquired juvenile unilateral upper eyelid ptosis...
  31. ncbi request reprint Cranial magnetic resonance imaging in genetically proven myotonic dystrophy type 1 and 2
    Cornelia Kornblum
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    J Neurol 251:710-4. 2004
    ..Our findings indicate a high frequency of central nervous system (CNS) involvement in both disorders. However, temporopolar pathology, previously associated with intellectual dysfunction, seems to be restricted to DM1...