Prevalence of neurofascin-155 antibodies in patients with multiple sclerosis

  title={Prevalence of neurofascin-155 antibodies in patients with multiple sclerosis},
  author={Oliver Stich and S A Perera and Benjamin Berger and Sven Jarius and Brigitte Wildemann and A. Baumgartner and Sebastian Rauer},
  journal={Journal of the Neurological Sciences},
From PNS to CNS: characteristics of anti-neurofascin 186 neuropathy in 16 cases
It is worth noting that quite a few patients show CNS-impaired signs only, and cranial MRI is essential for the screening of CNS involvement, and CSF white blood cell counts were found significantly elevated in CNS-involved patients compared with patients of PNS group.
Anti-neurofascin autoantibody and demyelination
Autoantibodies in chronic inflammatory demyelinating polyradiculoneuropathy.
The discovery of autoantibodies against nodal and paranodal proteins has proven useful in clinical practice, has uncovered novel pathophysiological mechanisms, clinical phenotypes, therapeutic response and prognosis within the CIDP disease spectrum and has boosted the search for other clinically relevant autoantIBodies.
Role of B cells and antibodies in multiple sclerosis.
Immunoadsorption and Plasma Exchange in Seropositive and Seronegative Immune-Mediated Neuropathies
Preliminary evidence suggests that GBS/CIDP patients without detectable IgG antibodies on routine diagnostic tests may nevertheless benefit from IA, and that an unbiased screening approach using myelinating co-cultures may assist in the detection of further autoantibodies which remain to be identified in such patients.
Nodes of Ranvier during development and repair in the CNS
The organization and function of CNS nodes of Ranvier are described and how these nodes change in demyelination and remyelinating disorders is considered, highlighting the impact of these changes on neuronal physiology in health and disease as well as the associated therapeutic implications.
Focal loss of the paranodal domain protein Neurofascin155 in the internal capsule impairs cortically induced muscle activity in vivo
Paranodal axoglial junctions are essential for rapid nerve conduction and the organization of axonal domains in myelinated axons. Neurofascin155 (Nfasc155) is a glial cell adhesion molecule that is


Neurofascin as a target for autoantibodies in peripheral neuropathies
Autoantibodies to NF are detected in a very small proportion of patients with AIDP and patients with CIDP, but may nevertheless be pathogenic in these cases.
Anti-neurofascin antibody in patients with combined central and peripheral demyelination
In anti-neurofascin antibody–positive CCPD patients, including those with a limited response to corticosteroids, IV immunoglobulin or plasma exchange alleviated the symptoms, recognition of this antibody may be important, because patients with CCPD who are antibody positive respond well to IV immunglobulinor plasma exchange.
Neurofascin IgG4 antibodies in CIDP associate with disabling tremor and poor response to IVIg
This study provides Class IV evidence that autoantibodies to NF155 identify a CIDP subtype characterized by severe neuropathy, poor response to IVIg, and disabling tremor.
Elevated levels of antibody to myelin oligodendrocyte glycoprotein is not specific for patients with multiple sclerosis.
The elevated presence of anti-MOG antibody is not specific for MS because a similar appearance was also demonstrated in patients with ONDs, and it is not clear whether this antibody is pathogenic in MS or, on the contrary, has a defensive role against further immune-mediated damage after myelin breakdown.
Neurological autoimmunity targeting aquaporin-4
Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology.
Data support an immunopathogenetic mechanism whereby B-cell follicles developing in the multiple sclerosis meninges exacerbate the detrimental effects of humoral immunity with a subsequent major impact on the integrity of the cortical structures.
Humoral autoimmunity in multiple sclerosis
Disruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosis.
The alterations in oligodendrocyte Nfasc155 expression that accompany inflammation and demyelination suggest an ongoing disruption to the axonal-oligodendROcyte complex within newly forming as well as established lesions in multiple sclerosis, resulting in destruction of the N fasc186+/Na+v nodal complex vital to successful fast neurotransmission in the CNS.
Nodal proteins are target antigens in Guillain‐Barré syndrome
The prevalence of antibodies against nodal adhesion molecules in patients with Guillain‐Barré syndrome or chronic inflammatory demyelinating polyneuropathy (CIDP) is investigated and results suggest that antibody attack against nodding antigens participates in the etiology of GBS.
Axonal transection in the lesions of multiple sclerosis.
Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.