Kathrin Doppler

Universitätsklinikum Würzburg

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Claudia Sommer

Universitätsklinikum Würzburg

Luise Appeltshauser

Universitätsklinikum Würzburg

Carmen Villmann

University of Würzburg

Jens Volkmann

Universitätsklinikum Würzburg

Frank Leypoldt

University Hospital Schleswig-Holstein

Christian Geis

Jena University Hospital

Andrea Kraft

Martha-Maria Hospital

Anastasia Kuzkina

Brigham and Women's Hospital

Harald Prüß

Charité - Universitätsmedizin Berlin

Heike L. Rittner

Universitätsklinikum Würzburg

Cooperative Institutions

Universitätsklinikum Würzburg

172

University of Würzburg

124

Charité - Universitätsmedizin Berlin

115

Ludwig-Maximilians-Universität München

110

Erasmus MC

German Center for Neurodegenerative Diseases

Heinrich Heine University Düsseldorf

Aarhus University Hospital

University of Lübeck

Klinik und Poliklinik für Neurologie

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

P 72 Antibody depletion in nodo-paranodopathy: Clinical and electrophysiological long-term follow-up

Clinical Neurophysiology (2022)

Luise Appeltshauser Helena Junghof Katharina Starz Claudia Sommer Kathrin Doppler

Electroneuronography

10.1016/j.clinph.2022.01.103

Cite

Citations (0)

The New Entity of Paranodopathies: A Target Structure with Therapeutic Consequences

Neurology International Open (2017)

Kathrin Doppler Claudia Sommer

Abstract Autoimmune neuropathies with autoantibodies against paranodal proteins have been described in the last few years. They comprise a subgroup of inflammatory neuropathies with IgG4 autoantibodies against the paranodal proteins neurofascin-155, contactin-1 and caspr-1. Although this subtype of autoimmune neuropathy represents less than 10% of all patients diagnosed with CIDP, it is of high interest as they show a different response to treatment. Even though there are no therapeutic studies available due to the limited number of patients identified so far, all case reports published so far report an excellent response to treatment with rituximab, and in most cases no response to treatment with IVIG, the standard therapy of CIDP. The typical clinical picture of patients with autoantibodies against paranodal proteins is characterized by an acute onset of a severe predominantly motor neuropathy, often accompanied by action tremor and sensory ataxia, with demyelinating features in the nerve conduction studies but an axonal histological phenotype. The latter may be explained by the pathogenetic concept of a paranodopathy/nodopathy, a disease of the paranode/node of Ranvier.

10.1055/s-0043-102455

Cite

Citations (1)

Complement deposition induced by binding of anti-contactin-1 auto-antibodies is modified by immunoglobulins

Experimental Neurology (2016)

Luise Appeltshauser Andreas Weishaupt Claudia Sommer Kathrin Doppler

Subclass

Complement C1q

C1-inhibitor

Complement

Pathophysiology

10.1016/j.expneurol.2016.10.006

Cite

Citations (43)

Neuropathische Schmerzen durch Nav1.7-Mutationen

Der Nervenarzt (2013)

Kathrin Doppler Claudia Sommer

NAV1

Erythromelalgia

Nociceptor

Pathophysiology

10.1007/s00115-012-3621-7

Cite

Citations (3)

Diabetische Neuropathie

Der Nervenarzt (2015)

Kathrin Doppler Karlheinz Reiners

Diabetic Neuropathy

10.1007/s00115-014-4127-2

Cite

Citations (4)

Anti-CNTN1 IgG3 induces acute conduction block and motor deficits in a passive transfer rat model

Journal of Neuroinflammation (2019)

Kathrin Doppler Yasmin Schuster Luise Appeltshauser Lydia Biko Carmen Villmann

Autoantibodies against the paranodal protein contactin-1 have recently been described in patients with severe acute-onset autoimmune neuropathies and mainly belong to the IgG4 subclass that does not activate complement. IgG3 anti-contactin-1 autoantibodies are rare, but have been detected during the acute onset of disease in some cases. There is evidence that anti-contactin-1 prevents adhesive interaction, and chronic exposure to anti-contactin-1 IgG4 leads to structural changes at the nodes accompanied by neuropathic symptoms. However, the pathomechanism of acute onset of disease and the pathogenic role of IgG3 anti-contactin-1 is largely unknown. In the present study, we aimed to model acute autoantibody exposure by intraneural injection of IgG of patients with anti-contacin-1 autoantibodies to Lewis rats. Patient IgG obtained during acute onset of disease (IgG3 predominant) and IgG from the chronic phase of disease (IgG4 predominant) were studied in comparison. Conduction blocks were measured in rats injected with the "acute" IgG more often than after injection of "chronic" IgG (83.3% versus 35%) and proved to be reversible within a week after injection. Impaired nerve conduction was accompanied by motor deficits in rats after injection of the "acute" IgG but only minor structural changes of the nodes. Paranodal complement deposition was detected after injection of the "acute IgG". We did not detect any inflammatory infiltrates, arguing against an inflammatory cascade as cause of damage to the nerve. We also did not observe dispersion of paranodal proteins or sodium channels to the juxtaparanodes as seen in patients after chronic exposure to anti-contactin-1. Our data suggest that anti-contactin-1 IgG3 induces an acute conduction block that is most probably mediated by autoantibody binding and subsequent complement deposition and may account for acute onset of disease in these patients. This supports the notion of anti-contactin-1-associated neuropathy as a paranodopathy with the nodes of Ranvier as the site of pathogenesis.

Pathogenesis

Multifocal motor neuropathy

Subclass

10.1186/s12974-019-1462-z

Cite

Citations (33)

Myogenesis in human denervated muscle biopsies

Muscle & Nerve (2007)

Kathrin Doppler Michel Mittelbronn Antje Bornemann

Electron microscopic studies of long-term denervated rat muscles have identified very small, immature myofibers that are believed to arise from detached satellite cells that have fused to form new fibers within the interstitial space. At present, it is unknown whether and to what extent equivalent fibers exist in denervated human muscle. Serial sections of muscle biopsies from 66 patients diagnosed with polyneuropathy or amyotrophic lateral sclerosis were immunolabeled with anti-NCAM and anti-neonatal myosin heavy chain monoclonal antibodies that are both neurally and developmentally regulated. We evaluated 200 myofibers in each section. Of the biopsy specimens, 75% contained small myofibers that showed a thin perinuclear cytoplasmic rim. Small fibers expressing neonatal myosin heavy chain (MHCn+) were found in all of these biopsies (100%) and NCAM+ fibers in 98%. The percentage of MHCn+ small fibers averaged 82% and NCAM+ small myofibers averaged 40%. The percentage of NCAM+ small fibers was significantly lower than that of MHCn+ fibers. In contrast, the percentage of MHCn+ vs. NCAM+ angular atrophic fibers did not show a significant difference. A substantial subset of neurogenic biopsies showed small fibers that differ from angular atrophic fibers both in size and expression pattern of MHCn and NCAM. Myogenesis appears to be a frequent finding in neurogenic atrophy.

10.1002/mus.20902

Cite

Citations (32)

Increased cutaneous miR-let-7d expression correlates with small nerve fiber pathology in patients with fibromyalgia syndrome

Pain (2016)

Mathias Leinders Kathrin Doppler Thomas Klein Maximiliane Deckart Heike L. Rittner

Fibromyalgia syndrome (FMS) is a chronic widespread pain condition probably comprising subgroups with different underlying pathomechanisms. There is increasing evidence for small nerve fiber impairment in subgroups of patients with FMS. MicroRNAs (miRNAs) regulate molecular factors determining nerve de- and re-generation. We investigated whether systemic and cutaneous miRNA expression in patients with FMS is related to small nerve fiber pathology. We confirmed previous findings of disturbed small fiber function and reduced intraepidermal nerve fiber density in subgroups of patients with FMS. We found 51 aberrantly expressed miRNAs in white blood cells of patients with FMS, of which miR-let-7d correlated with reduced small nerve fiber density in patients with FMS. Furthermore, we demonstrated miR-let-7d and its downstream target insulin-like growth factor-1 receptor as being aberrantly expressed in skin of patients with FMS with small nerve fiber impairment. Our study gives further evidence of small nerve fiber pathology in FMS subgroups and provides a missing link in the pathomechanism that may lead to small fiber loss in subgroups of patients with FMS.

Nerve fiber

Fibromyalgia syndrome

10.1097/j.pain.0000000000000668

Cite

Citations (65)

Diabetische Folgeerkrankungen

Springer eBooks (2014)

Kathrin Doppler Hans‐Peter Hammes A. Heidenreich D. Luft Karlheinz Reiners

10.1007/978-3-642-41358-2_8

Cite

Citations (0)

Autoantikörper bei Immunneuropathien — Biomarker für individualisierte Therapie

NeuroTransmitter (2019)

Luise Appeltshauser Kathrin Doppler

10.1007/s15016-019-6600-4

Cite

Citations (0)