Nico Melzer

Summary

Affiliation: University Hospital
Country: Germany

Publications

  1. pmc Excitotoxic neuronal cell death during an oligodendrocyte-directed CD8+ T cell attack in the CNS gray matter
    Nico Melzer
    Department of Neurology, University of Munster, Albert Schweitzer Campus 1, Munster 48149, Germany
    J Neuroinflammation 10:121. 2013
  2. pmc Paraneoplastic and non-paraneoplastic autoimmunity to neurons in the central nervous system
    Nico Melzer
    Department of Neurology, Inflammatory Disorders of the Nervous System and Neurooncology, University of Munster, Albert Schweitzer Campus 1, 48149 Munster, Germany
    J Neurol 260:1215-33. 2013
  3. pmc TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation
    Nico Melzer
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Munster, Munster, Germany
    PLoS ONE 7:e47617. 2012
  4. doi request reprint CD4(+) T cells predominate in cerebrospinal fluid and leptomeningeal and parenchymal infiltrates in cerebral amyloid β-related angiitis
    Nico Melzer
    Departments of Neurology, Inflammatory Disorders of the Nervous System, and Neurooncology, University of Munster, Albert Schweitzer Campus 1, Munster, 48149 Germany
    Arch Neurol 69:773-7. 2012
  5. pmc Cytotoxic CD8+ T cells and CD138+ plasma cells prevail in cerebrospinal fluid in non-paraneoplastic cerebellar ataxia with contactin-associated protein-2 antibodies
    Nico Melzer
    Department of Neurology, Inflammatory Disorders of the Nervous System and Neurooncology, University of Munster, Albert Schweitzer Campus 1, Munster 48149, Germany
    J Neuroinflammation 9:160. 2012
  6. doi request reprint Neuron-directed autoimmunity in the central nervous system: entities, mechanisms, diagnostic clues, and therapeutic options
    Nico Melzer
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Munster, Munster, Germany
    Curr Opin Neurol 25:341-8. 2012
  7. doi request reprint Cytotoxic CD8+ T cell-neuron interactions: perforin-dependent electrical silencing precedes but is not causally linked to neuronal cell death
    Sven G Meuth
    Department of Neurology, University of Wurzburg, D 97070 Wurzburg, Germany
    J Neurosci 29:15397-409. 2009
  8. pmc TASK1 modulates inflammation and neurodegeneration in autoimmune inflammation of the central nervous system
    Stefan Bittner
    University of Wuerzburg, Department of Neurology, Josef Schneider Str 11, 97080 Wuerzburg, Germany
    Brain 132:2501-16. 2009
  9. doi request reprint Collateral neuronal apoptosis in CNS gray matter during an oligodendrocyte-directed CD8(+) T cell attack
    Kerstin Göbel
    Department of Neurology, University of Wurzburg, Germany
    Glia 58:469-80. 2010
  10. doi request reprint Altered neuronal expression of TASK1 and TASK3 potassium channels in rodent and human autoimmune CNS inflammation
    Sven G Meuth
    Department of Neurology, University of Wurzburg, Josef Schneider Strafe 11, 97080 Wurzburg, Germany
    Neurosci Lett 446:133-8. 2008

Collaborators

Detail Information

Publications20

  1. pmc Excitotoxic neuronal cell death during an oligodendrocyte-directed CD8+ T cell attack in the CNS gray matter
    Nico Melzer
    Department of Neurology, University of Munster, Albert Schweitzer Campus 1, Munster 48149, Germany
    J Neuroinflammation 10:121. 2013
    ....
  2. pmc Paraneoplastic and non-paraneoplastic autoimmunity to neurons in the central nervous system
    Nico Melzer
    Department of Neurology, Inflammatory Disorders of the Nervous System and Neurooncology, University of Munster, Albert Schweitzer Campus 1, 48149 Munster, Germany
    J Neurol 260:1215-33. 2013
    ....
  3. pmc TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation
    Nico Melzer
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Munster, Munster, Germany
    PLoS ONE 7:e47617. 2012
    ..Our findings suggest TRPM2 cation channels as a potential target for treating autoimmune CNS inflammation...
  4. doi request reprint CD4(+) T cells predominate in cerebrospinal fluid and leptomeningeal and parenchymal infiltrates in cerebral amyloid β-related angiitis
    Nico Melzer
    Departments of Neurology, Inflammatory Disorders of the Nervous System, and Neurooncology, University of Munster, Albert Schweitzer Campus 1, Munster, 48149 Germany
    Arch Neurol 69:773-7. 2012
    ..It has been suggested that ABRA is triggered by vascular deposition of A followed by an Aβ-directed (auto)immune response...
  5. pmc Cytotoxic CD8+ T cells and CD138+ plasma cells prevail in cerebrospinal fluid in non-paraneoplastic cerebellar ataxia with contactin-associated protein-2 antibodies
    Nico Melzer
    Department of Neurology, Inflammatory Disorders of the Nervous System and Neurooncology, University of Munster, Albert Schweitzer Campus 1, Munster 48149, Germany
    J Neuroinflammation 9:160. 2012
    ..CASPR-2 antibodies strongly labeling axons of cerebellar granule neurons have recently been identified in sera from nine patients with otherwise unexplained progressive cerebellar ataxia with mild to severe cerebellar atrophy...
  6. doi request reprint Neuron-directed autoimmunity in the central nervous system: entities, mechanisms, diagnostic clues, and therapeutic options
    Nico Melzer
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Munster, Munster, Germany
    Curr Opin Neurol 25:341-8. 2012
    ....
  7. doi request reprint Cytotoxic CD8+ T cell-neuron interactions: perforin-dependent electrical silencing precedes but is not causally linked to neuronal cell death
    Sven G Meuth
    Department of Neurology, University of Wurzburg, D 97070 Wurzburg, Germany
    J Neurosci 29:15397-409. 2009
    ..Thus, electrical silencing is an immediate consequence of MHC I-restricted interaction of CD8(+) T cells with neurons. This mechanism is clearly perforin-dependent and precedes, but is not causally linked, to neuronal cell death...
  8. pmc TASK1 modulates inflammation and neurodegeneration in autoimmune inflammation of the central nervous system
    Stefan Bittner
    University of Wuerzburg, Department of Neurology, Josef Schneider Str 11, 97080 Wuerzburg, Germany
    Brain 132:2501-16. 2009
    ..These data support the identification and characterization of TASK1 as potential molecular target for the therapy of inflammatory and degenerative central nervous system disorders...
  9. doi request reprint Collateral neuronal apoptosis in CNS gray matter during an oligodendrocyte-directed CD8(+) T cell attack
    Kerstin Göbel
    Department of Neurology, University of Wurzburg, Germany
    Glia 58:469-80. 2010
    ..Collateral neuronal apoptosis could contribute to substantial neuronal loss in gray matter lesions and cause persistent neurological impairment in both acute and chronic gray matter lesions in various inflammatory CNS disorders...
  10. doi request reprint Altered neuronal expression of TASK1 and TASK3 potassium channels in rodent and human autoimmune CNS inflammation
    Sven G Meuth
    Department of Neurology, University of Wurzburg, Josef Schneider Strafe 11, 97080 Wurzburg, Germany
    Neurosci Lett 446:133-8. 2008
    ..Thus, regulated expression of TASK channels might contribute to a molecular switch between death and survival of neurons in autoimmune CNS inflammation...
  11. pmc Glatiramer acetate attenuates pro-inflammatory T cell responses but does not directly protect neurons from inflammatory cell death
    Alexander M Herrmann
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Munster, Domagkstr 13, 48149 Munster, Germany
    Am J Pathol 177:3051-60. 2010
    ..Our data suggest that GA attenuates adaptive pro-inflammatory T cell responses, but does not exert direct neuroprotective effects...
  12. pmc CD4(+) CD25(+) FoxP3(+) regulatory T cells suppress cytotoxicity of CD8(+) effector T cells: implications for their capacity to limit inflammatory central nervous system damage at the parenchymal level
    Kerstin Göbel
    Department of neurology Inflammatory disorders of the nervous system and neurooncology, University of Muenster, Albert Schweitzer Campus 1, 48149 Muenster, Germany
    J Neuroinflammation 9:41. 2012
    ..CD4(+) CD25(+) forkhead box P3 (FoxP3)(+) regulatory T cells (T reg cells) are known to suppress adaptive immune responses, key control tolerance and autoimmunity...
  13. doi request reprint CD8+ T cells and neuronal damage: direct and collateral mechanisms of cytotoxicity and impaired electrical excitability
    Nico Melzer
    Department of Neurology, University of Wurzburg, Josef Schneider Strasse 11, 97080 Wurzburg, Germany
    FASEB J 23:3659-73. 2009
    ..Moreover, we discuss mechanisms of impaired electrical signaling and cell death of neurons as direct and collateral targets of CD8(+) T cells in the CNS...
  14. pmc A beta-lactam antibiotic dampens excitotoxic inflammatory CNS damage in a mouse model of multiple sclerosis
    Nico Melzer
    Department of Neurology, University of Wurzburg, Wurzburg, Germany
    PLoS ONE 3:e3149. 2008
    ..The mechanisms are reduction of T cell activation by modulation of cellular antigen-presentation and impairment of antigen-specific T cell migration into the CNS rather than or modulation of central glutamate homeostasis...
  15. doi request reprint CNS inflammation and neuronal degeneration is aggravated by impaired CD200-CD200R-mediated macrophage silencing
    Sven G Meuth
    University of Wuerzburg, Department of Neurology, Josef Schneider Strasse 11, 97080 Wuerzburg, Germany
    J Neuroimmunol 194:62-9. 2008
    ..CD200 and its receptor could also be detected on neurons and macrophages in human MS plaques. Therefore the CD200-CD200R pathway seems of critical relevance for macrophage-mediated damage in autoimmune inflammation of the CNS...
  16. pmc ALAIN01-Alemtuzumab in autoimmune inflammatory neurodegeneration: mechanisms of action and neuroprotective potential
    Tobias Ruck
    Department of Neurology, University of Munster, Albert Schweitzer Campus 1, 48149, Munster, Germany
    BMC Neurol 16:34. 2016
    ..Markers for risk stratification and treatment response improving patient selection and therapy guidance are a big unmet need for MS patients and health care providers...
  17. pmc Fatal atypical reversible posterior leukoencephalopathy syndrome: a case report
    Stefanie Kristin Golombeck
    Department of Neurology, University of Wuerzburg, Josef Schneider Straße 11, Wuerzburg, 97080, Germany
    J Med Case Rep 7:14. 2013
    ..abstract:..
  18. doi request reprint Fluctuating neuromuscular transmission defects and inverse acetazolamide response in episodic ataxia type 2 associated with the novel CaV2.1 single amino acid substitution R2090Q
    Nico Melzer
    Department of Neurology, Julius Maximilian University, Wurzburg, Germany
    J Neurol Sci 296:104-6. 2010
    ..Upon initiation of acetazolamide treatment she experienced a dose-dependent severe increase of attack frequency and severity along with a shorter attack duration, while she responded well to subsequent therapy with 4-aminopyridine...
  19. doi request reprint A pure cerebellar syndrome with corresponding ponto-cerebellar atrophy in acquired hepatocerebral degeneration
    Nico Melzer
    Department of Neurology, University of Wuerzburg, Josef Schneider Strasse 11, 97080 Wuerzburg, Germany
    J Neurol Sci 292:96-8. 2010
    ..We report a case of acquired hepatocerebral degeneration (AHCD) presenting as a pure cerebellar syndrome. Magnetic resonance imaging (MRI) showed the typical features of AHCD in conjunction with ponto-cerebellar atrophy...
  20. doi request reprint Distal-symmetric focal inflammatory myopathy distinct from focal myositis and polymyositis
    Nico Melzer
    Department of Neurology, University of Wurzburg, Josef Schneider Strabetae 11, 97080 Wurzburg, Germany
    Muscle Nerve 40:309-12. 2009
    ..Our findings add another entity to the spectrum of spatially restricted inflammatory myopathies. Muscle Nerve 40: 309-312, 2009...