H Lassmann

Summary

Affiliation: Medical University of Vienna
Country: Austria

Publications

  1. ncbi request reprint Neuropathology of multiple sclerosis-new concepts
    Barbara Kornek
    Brain Research Institute, Division of Neuroimmunology, A 1090 Vienna, Austria
    Brain Res Bull 61:321-6. 2003
  2. ncbi request reprint Multiple sclerosis: is there neurodegeneration independent from inflammation?
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Wien, Austria
    J Neurol Sci 259:3-6. 2007
  3. doi request reprint Axonal and neuronal pathology in multiple sclerosis: what have we learnt from animal models
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Exp Neurol 225:2-8. 2010
  4. pmc Disease-specific molecular events in cortical multiple sclerosis lesions
    Marie Therese Fischer
    Department of Neuroimmunology, Centre for Brain Research, Medical University of Vienna, Austria
    Brain 136:1799-815. 2013
  5. doi request reprint Progressive multiple sclerosis: pathology and pathogenesis
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Wien, Austria
    Nat Rev Neurol 8:647-56. 2012
  6. doi request reprint Pathology and disease mechanisms in different stages of multiple sclerosis
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria Electronic address
    J Neurol Sci 333:1-4. 2013
  7. pmc Presence of six different lesion types suggests diverse mechanisms of tissue injury in neuromyelitis optica
    Tatsuro Misu
    Department of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, Sendai, Japan
    Acta Neuropathol 125:815-27. 2013
  8. doi request reprint The birth of oligodendrocytes in the anatomical and neuropathological literature: the seminal contribution of Pio del Rio-Hortega. 1921
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Austria
    Clin Neuropathol 31:435-6. 2012
  9. pmc DQB1*0602 rather than DRB1*1501 confers susceptibility to multiple sclerosis-like disease induced by proteolipid protein (PLP)
    Nathali Kaushansky
    Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel
    J Neuroinflammation 9:29. 2012
  10. pmc NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury
    Marie T Fischer
    Centre for Brain Research, Medical University of Vienna, A 1090 Wien, Austria
    Brain 135:886-99. 2012

Detail Information

Publications107 found, 100 shown here

  1. ncbi request reprint Neuropathology of multiple sclerosis-new concepts
    Barbara Kornek
    Brain Research Institute, Division of Neuroimmunology, A 1090 Vienna, Austria
    Brain Res Bull 61:321-6. 2003
    ..In this short review, possible paraclinical markers for tissue destruction on the basis of the main features of myelin destruction are discussed. Furthermore, the importance of early axonal damage in multiple sclerosis is highlighted...
  2. ncbi request reprint Multiple sclerosis: is there neurodegeneration independent from inflammation?
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Wien, Austria
    J Neurol Sci 259:3-6. 2007
    ..However, the patterns of inflammation differ between different disease stages. This may in part explain, why anti-inflammatory or immunosuppressive treatments fail in progressive multiple sclerosis...
  3. doi request reprint Axonal and neuronal pathology in multiple sclerosis: what have we learnt from animal models
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Exp Neurol 225:2-8. 2010
    ....
  4. pmc Disease-specific molecular events in cortical multiple sclerosis lesions
    Marie Therese Fischer
    Department of Neuroimmunology, Centre for Brain Research, Medical University of Vienna, Austria
    Brain 136:1799-815. 2013
    ..Our study provides new insights into the complex mechanisms of neurodegeneration and regeneration in the cortex of patients with multiple sclerosis...
  5. doi request reprint Progressive multiple sclerosis: pathology and pathogenesis
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Wien, Austria
    Nat Rev Neurol 8:647-56. 2012
    ....
  6. doi request reprint Pathology and disease mechanisms in different stages of multiple sclerosis
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria Electronic address
    J Neurol Sci 333:1-4. 2013
    ..New data suggest that mitochondrial injury, mediated through oxidative injury, is in the center of the pathogenetic events leading to brain damage in multiple sclerosis patients. ..
  7. pmc Presence of six different lesion types suggests diverse mechanisms of tissue injury in neuromyelitis optica
    Tatsuro Misu
    Department of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, Sendai, Japan
    Acta Neuropathol 125:815-27. 2013
    ..Our data underline the primary assault of astrocytes in NMO lesions, but also indicate that different mechanisms of tissue injury operate in parallel in the same patient and even within the same lesion...
  8. doi request reprint The birth of oligodendrocytes in the anatomical and neuropathological literature: the seminal contribution of Pio del Rio-Hortega. 1921
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Austria
    Clin Neuropathol 31:435-6. 2012
    ..1921; 2: 16-43 and del Río-Hortega P. Are the glia with very few processes homologous with Schwann cells? Clin Neuropathol. 2012; 31: 460-462, originally published in Bol de la Soc Esp de Biol. 1922; X: 25-28...
  9. pmc DQB1*0602 rather than DRB1*1501 confers susceptibility to multiple sclerosis-like disease induced by proteolipid protein (PLP)
    Nathali Kaushansky
    Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel
    J Neuroinflammation 9:29. 2012
    ....
  10. pmc NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury
    Marie T Fischer
    Centre for Brain Research, Medical University of Vienna, A 1090 Wien, Austria
    Brain 135:886-99. 2012
    ..Our data suggest that the inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in demyelination and free radical-mediated tissue injury in the pathogenesis of multiple sclerosis...
  11. pmc Temporal expression and cellular origin of CC chemokine receptors CCR1, CCR2 and CCR5 in the central nervous system: insight into mechanisms of MOG-induced EAE
    Sana Eltayeb
    Department of Clinical Neuroscience, Center for Molecular Medicine, Neuroimmunology Unit, Karolinska Institute, Stockholm, Sweden
    J Neuroinflammation 4:14. 2007
    ....
  12. pmc Inflammation induced by innate immunity in the central nervous system leads to primary astrocyte dysfunction followed by demyelination
    Rakhi Sharma
    Centre for Brain Research, Medical University of Vienna, Vienna, Austria
    Acta Neuropathol 120:223-36. 2010
    ..Similar structural abnormalities were also seen in a subset of active lesions in multiple sclerosis. Our studies suggest that astrocyte injury may be an important early step in the cascade of lesion formation in brain inflammation...
  13. doi request reprint Models of multiple sclerosis: new insights into pathophysiology and repair
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Austria
    Curr Opin Neurol 21:242-7. 2008
    ..The purpose of this review is to discuss the relevance of different models for multiple sclerosis and new insights into pathophysiology of the disease obtained from experimental studies...
  14. doi request reprint Mechanisms of inflammation induced tissue injury in multiple sclerosis
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    J Neurol Sci 274:45-7. 2008
    ..The relative contribution of the different immune reactions may in part explain the inter-individual and stage dependent heterogeneity of multiple sclerosis lesions...
  15. ncbi request reprint Experimental models of multiple sclerosis
    H Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Rev Neurol (Paris) 163:651-5. 2007
    ..In addition, proper selection of the best suited EAE model for a specific study is essential...
  16. doi request reprint Mechanisms of neurodegeneration shared between multiple sclerosis and Alzheimer's disease
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Wien, Austria
    J Neural Transm 118:747-52. 2011
    ..Anti-oxidant and mitochondria protective therapeutic strategies may be beneficial both in multiple sclerosis and Alzheimer's disease in particular in early stages of the disease...
  17. doi request reprint Review: the architecture of inflammatory demyelinating lesions: implications for studies on pathogenesis
    H Lassmann
    Center for Brain Research, Medical University of Vienna, Wien, Austria
    Neuropathol Appl Neurobiol 37:698-710. 2011
    ..In addition, these data also imply that molecules, identified in these studies, must be confirmed and validated in the correct context of lesion initiation and/or progression...
  18. doi request reprint Pathophysiology of inflammation and tissue injury in multiple sclerosis: what are the targets for therapy
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    J Neurol Sci 306:167-9. 2011
    ..Finally, it is suggested that neuroprotective strategies, which target mitochondrial injury and its downstream effects on neurons and axons are promising future therapeutic options...
  19. ncbi request reprint Multiple sclerosis pathology: evolution of pathogenetic concepts
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Brain Pathol 15:217-22. 2005
    ....
  20. ncbi request reprint The immunopathology of multiple sclerosis: an overview
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Vienna, Austria
    Brain Pathol 17:210-8. 2007
    ..This heterogeneity is reflected by different clinical manifestations of the disease, such as relapsing or progressive MS, and also explains at least in part the relation of MS to other inflammatory demyelinating diseases...
  21. pmc Epstein-Barr virus in the multiple sclerosis brain: a controversial issue--report on a focused workshop held in the Centre for Brain Research of the Medical University of Vienna, Austria
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Brain 134:2772-86. 2011
    ..It further highlights that unequivocal proof of Epstein-Barr virus infection in multiple sclerosis lesions is still lacking, due to issues related to the sensitivity and specificity of the detection methods...
  22. ncbi request reprint New concepts on progressive multiple sclerosis
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Curr Neurol Neurosci Rep 7:239-44. 2007
    ..This process seems to be driven by the aberrant formation of ectopic lymphatic tissue within the brain compartment...
  23. doi request reprint The pathologic substrate of magnetic resonance alterations in multiple sclerosis
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Neuroimaging Clin N Am 18:563-76, ix. 2008
    ..All types of changes in the MS brain and spinal cord occur on the background of inflammation; the type of inflammation, however, differs between different stages and forms of the disease...
  24. doi request reprint The molecular basis of neurodegeneration in multiple sclerosis
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Wien, Austria
    FEBS Lett 585:3715-23. 2011
    ..However, mitochondrial injury, resulting in energy failure, is a key element of neurodegeneration in MS and is apparently driven by radical production in activated microglia...
  25. ncbi request reprint Transition from enhanced T cell infiltration to inflammation in the myelin-degenerative central nervous system
    Roland Grundtner
    Medical University Vienna, Center for Brain Research, Division of Neuroimmunology, Spitalgasse 4, A 1090 Vienna, Austria
    Neurobiol Dis 28:261-75. 2007
    ..The activation of the tethered cells may trigger the formation of inflammatory foci and could pave the way for inflammation in degenerative CNS disease...
  26. pmc The relation between inflammation and neurodegeneration in multiple sclerosis brains
    Josa M Frischer
    Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Brain 132:1175-89. 2009
    ..It further indicates that the disease processes of multiple sclerosis may die out in aged patients with long-standing disease...
  27. ncbi request reprint Clinical and pathological topics of multiple sclerosis
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Rinsho Shinkeigaku 49:715-8. 2009
    ..Future therapeutic interventions will have to target inflammation, which is compartmentalized in the central nervous system. In addition, however, neuroprotective therapies may be necessary...
  28. doi request reprint The cholinergic anti-inflammatory system limits T cell infiltration into the neurodegenerative CNS, but cannot counteract complex CNS inflammation
    Eva Maria Nicolussi
    Medical University Vienna, Center for Brain Research, Department of Neuroimmunology, Spitalgasse 4, Vienna, Austria
    Neurobiol Dis 35:24-31. 2009
    ..We found that the cholinergic anti-inflammatory pathway limits the site-directed influx of activated T cells into the lesioned facial motor nucleus, but cannot counteract CNS inflammation in EAE...
  29. ncbi request reprint Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions
    R Hoftberger
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Wien, Austria
    Brain Pathol 14:43-50. 2004
    ..MHC class II molecules were expressed on microglia and macrophages, but not on astrocytes. These data indicate that in MS lesions all cells of the central nervous system are potential targets for Class I MHC restricted cytotoxic T-cells...
  30. ncbi request reprint Mitochondrial damage and histotoxic hypoxia: a pathway of tissue injury in inflammatory brain disease?
    F Aboul-Enein
    Center for Brain Research, Medical University of Vienna, Austria
    Acta Neuropathol 109:49-55. 2005
    ....
  31. ncbi request reprint Lack of adrenoleukodystrophy protein enhances oligodendrocyte disturbance and microglia activation in mice with combined Abcd1/Mag deficiency
    Martina Dumser
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090, Vienna, Austria
    Acta Neuropathol 114:573-86. 2007
    ..Furthermore, the age at which this occurs precedes by far the onset of axonal degeneration in Abcd1-deficient mice, implying that oligodendrocyte/myelin disturbances may precede axonopathy in X-ALD...
  32. ncbi request reprint Remyelination is extensive in a subset of multiple sclerosis patients
    Peter Patrikios
    Center for Brain Research, Medical University of Vienna, Vienna, Austria
    Brain 129:3165-72. 2006
    ..These results suggest that the variable and patient-dependent extent of remyelination must be considered in the design of future clinical trials aimed at promoting CNS repair...
  33. pmc The "window of susceptibility" for inflammation in the immature central nervous system is characterized by a leaky blood-brain barrier and the local expression of inflammatory chemokines
    Lucia Schoderboeck
    Medical University Vienna, Center for Brain Research, Department of Neuroimmunology, Spitalgasse 4, A 1090 Wien, Austria
    Neurobiol Dis 35:368-75. 2009
    ..Changes in the chemokine expression profile along with a leaky blood-brain barrier pave the ground for an accelerated development of CNS inflammation...
  34. ncbi request reprint Hypoxia-like tissue injury as a component of multiple sclerosis lesions
    Hans Lassmann
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    J Neurol Sci 206:187-91. 2003
    ..Both, vascular pathology as well as metabolic disturbances induced by toxins of activated macrophages and microglia may be responsible for such lesions in multiple sclerosis...
  35. ncbi request reprint Astrocytes are a specific immunological target in Rasmussen's encephalitis
    Jan Bauer
    Division of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Ann Neurol 62:67-80. 2007
    ..An in vitro study, however, suggested glutamate receptor 3 (GluR3) antibody-mediated astrocytic loss. Therefore, we investigated astrocytic apoptosis and loss in situ...
  36. pmc Complementary contribution of CD4 and CD8 T lymphocytes to T-cell infiltration of the intact and the degenerative spinal cord
    Monika Bradl
    Department of Neuroimmunology, Brain Research Institute, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Am J Pathol 166:1441-50. 2005
    ..This could indicate that CD4+ and CD8+ T cells might fulfill complementary roles in the intact and the diseased organ...
  37. ncbi request reprint Stem cell and progenitor cell transplantation in multiple sclerosis: the discrepancy between neurobiological attraction and clinical feasibility
    Hans Lassmann
    Center for Brain Research, Medical University Vienna, Spitalgasse 4, A 1090 Wien, Austria
    J Neurol Sci 233:83-6. 2005
    ..In light of this complex situation, it is concluded that clinical trials of stem- or progenitor cell transplantation in multiple sclerosis are currently premature...
  38. ncbi request reprint The CD4-Th1 model for multiple sclerosis: a critical [correction of crucial] re-appraisal
    Hans Lassmann
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Trends Immunol 25:132-7. 2004
  39. ncbi request reprint Transient axonal injury in the absence of demyelination: a correlate of clinical disease in acute experimental autoimmune encephalomyelitis
    Fahmy Aboul-Enein
    Department of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090, Vienna, Austria
    Acta Neuropathol 111:539-47. 2006
    ..Our studies suggest that nitric oxide and its metabolites contribute to axonal pathology and possibly also to subsequent neurological dysfunction in EAE...
  40. pmc After injection into the striatum, in vitro-differentiated microglia- and bone marrow-derived dendritic cells can leave the central nervous system via the blood stream
    Sonja Hochmeister
    Department of Neuroimmunology, Center for Brain Research, Medical University Vienna, Vienna, Austria
    Am J Pathol 173:1669-81. 2008
    ..Moreover, we also found these cells in both mesenteric lymph nodes and spleens. Hence, microglia- and bone marrow-derived DCs can leave the CNS via the blood stream...
  41. doi request reprint Progressive multiple sclerosis
    Monika Bradl
    Department of Neuroimmunology, Medical University Vienna, Center for Brain Research, Vienna, Austria
    Semin Immunopathol 31:455-65. 2009
    ....
  42. pmc Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity?
    Christina Marik
    Centre for Brain Research, Medical University of Vienna, Austria
    Brain 130:2800-15. 2007
    ..The findings indicate that mechanisms associated with innate immunity may play a role in the formation of hypoxia-like demyelinating lesions in MS...
  43. ncbi request reprint Multiple sclerosis and Alzheimer's disease
    Assunta Dal Bianco
    Center for Brain Research, Medical University of Vienna, Austria
    Ann Neurol 63:174-83. 2008
    ..To what extent chronic inflammation in the cortex of MS patients influences the development of AD lesions is so far unresolved...
  44. pmc Oligodendrocytes: biology and pathology
    Monika Bradl
    Department of Neuroimmunology, Center for Brain Research, Medical University Vienna, Vienna, Austria
    Acta Neuropathol 119:37-53. 2010
    ..Finally, we will lay out the different pathways leading to oligodendrocyte and myelin loss in human CNS diseases, and we will reveal the different principles leading to the restoration of myelin sheaths or to a failure to do so...
  45. ncbi request reprint Correlations between mental state and quantitative neuropathology in the Vienna Longitudinal Study on Dementia
    C Bancher
    Ludwig Boltzmann Institute of Clinical Neurobiology, Vienna, Austria
    Eur Arch Psychiatry Clin Neurosci 246:137-46. 1996
    ..This pathology may be induced by a mismetabolism of the beta-amyloid precursor proteins or their interaction with cytoskeletal proteins related to neuronal degeneration...
  46. ncbi request reprint Experimental models of neuromyelitis optica
    Hans Lassmann
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A 1090 Wien, Austria
    Rinsho Shinkeigaku 49:900-1. 2009
    ....
  47. ncbi request reprint Mechanisms of demyelination and tissue destruction in multiple sclerosis
    Hans Lassmann
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Clin Neurol Neurosurg 104:168-71. 2002
  48. ncbi request reprint Fulminant central nervous system demyelination associated with interferon-alpha therapy and hepatitis C virus infection
    R Hoftberger
    Institute of Neurology, Medical University of Vienna, Austria
    Mult Scler 13:1100-6. 2007
    ..Additionally, the presence of HCV RNA within the demyelinated lesion indicates a possible role in triggering or propagating disease...
  49. ncbi request reprint Distribution of a calcium channel subunit in dystrophic axons in multiple sclerosis and experimental autoimmune encephalomyelitis
    B Kornek
    Department of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A 1090 Vienna, Austria
    Brain 124:1114-24. 2001
    ..Our data suggest that calcium influx through voltage-dependent calcium channels is one possible candidate mechanism for axonal degeneration in inflammatory demyelinating disorders...
  50. ncbi request reprint Heterogeneity of multiple sclerosis pathogenesis: implications for diagnosis and therapy
    H Lassmann
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Spitalgasse 4, A 1090, Wien, Austria
    Trends Mol Med 7:115-21. 2001
    ..This might, at least in part, explain the heterogeneity in genetic susceptibility, clinical presentation and response to treatment observed between individuals...
  51. ncbi request reprint Dysferlin is a new marker for leaky brain blood vessels in multiple sclerosis
    Sonja Hochmeister
    Division of Neuroimmunology, Center for Brain Research, Medical University of Vienna, Vienna, Austria
    J Neuropathol Exp Neurol 65:855-65. 2006
    ..Hence, dysferlin is not only a marker for leaky brain vessels, but also reveals dissociation of perivascular inflammatory infiltrates and blood-brain barrier disturbance in multiple sclerosis...
  52. ncbi request reprint Widespread demyelination in the cerebellar cortex in multiple sclerosis
    Alexandra Kutzelnigg
    Center for Brain Research, Medical University of Vienna, Austria
    Brain Pathol 17:38-44. 2007
    ..Our data identify cortical demyelination as a potential substrate of cerebellar dysfunction in MS...
  53. ncbi request reprint Recent neuropathological findings in MS--implications for diagnosis and therapy
    Hans Lassmann
    Brain Research Institute, University of Vienna, Division of Neuroimmunology, Spitalgasse 4, 1090, Vienna, Austria
    J Neurol 251:IV2-5. 2004
    ..Since the pathogenetic pathways of demyelination and tissue damage vary between different MS patients, their identification by paraclinical markers is of critical importance for diagnosis and therapeutic management...
  54. ncbi request reprint Tissue preconditioning may explain concentric lesions in Baló's type of multiple sclerosis
    Christine Stadelmann
    Brain Research Center, Medical University of Vienna, Vienna, Austria
    Brain 128:979-87. 2005
    ..Due to their neuroprotective effects, the rim of periplaque tissue, where these proteins are expressed, may be resistant to further damage in an expanding lesion and may therefore remain as a layer of preserved myelinated tissue...
  55. ncbi request reprint Cortical demyelination and diffuse white matter injury in multiple sclerosis
    Alexandra Kutzelnigg
    Center for Brain Research, Medical University of Vienna, Vienna, Austria
    Brain 128:2705-12. 2005
    ..With chronicity, diffuse inflammation accumulates throughout the whole brain, and is associated with slowly progressive axonal injury in the NAWM and cortical demyelination...
  56. pmc Squamous cell carcinoma: infiltrating monocyte/macrophage subpopulations express functional mature phenotype
    C Neuchrist
    Institute of General and Experimental Pathology, Vienna, Austria
    Br J Cancer 62:748-53. 1990
    ..Thus, the majority of tumour-infiltrating mononuclear phagocytes were found to possess a rather mature phenotype. The number of Mo/M phi with mature phenotype within the tumours correlated with T lymphocyte infiltration in the tissue...
  57. ncbi request reprint Presence of D110 antigen expressing immunocompetent cells in glioblastoma associates with prolonged survival
    M Preusser
    Institute of Neurology, Medical University Vienna, Vienna, Austria
    Neuropathol Appl Neurobiol 30:608-14. 2004
    ..We conclude that D110 immunoreactivity in glioblastoma does not seem to be related to tissue hypoxia. D110 identifies immunocompetent cells, which positively influence survival of glioblastoma patients...
  58. ncbi request reprint Neuroma prevention by end-to-side neurorraphy: an experimental study in rats
    Oskar C Aszmann
    Division of Plastic and Reconstructive Surgery, Department of Surgery, and Division of Neuroimmunology, Department of Neuroscience, Medical School, University of Vienna, Vienna, Austria
    J Hand Surg Am 28:1022-8. 2003
    ....
  59. pmc Mutation in the Scyl1 gene encoding amino-terminal kinase-like protein causes a recessive form of spinocerebellar neurodegeneration
    Wolfgang M Schmidt
    Neuromuscular Research Department, Center of Anatomy and Cell Biology, Medical University of Vienna, Wahringer Strasse 13, A 1090 Vienna, Austria
    EMBO Rep 8:691-7. 2007
    ..We show that the pathology of mdf comprises cerebellar atrophy, Purkinje cell loss and optic nerve atrophy, and therefore defines a new animal model for neurodegenerative diseases with cerebellar involvement in humans...
  60. ncbi request reprint Cortical lesions and brain atrophy in MS
    Alexandra Kutzelnigg
    Department of Neuroimmunology, Center for Brain Research Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria
    J Neurol Sci 233:55-9. 2005
    ..In this review, we discuss the possibility that disease involvement of grey matter structures may significantly contribute to clinical disability in multiple sclerosis patients...
  61. ncbi request reprint Neuropathology of CNS disease in Langerhans cell histiocytosis
    Nicole Grois
    Langerhans Cell Histiocytosis Study Reference Center, Children Cancer Research Institute, St Anna Children s Hospital, Kinderspitalgasse 6, A 1090 Vienna, Austria
    Brain 128:829-38. 2005
    ....
  62. ncbi request reprint Cortical demyelination in multiple sclerosis: a substrate for cognitive deficits?
    Alexandra Kutzelnigg
    Center for Brain Research, Medical University of Vienna, Spitalgasse 4 A 1090, Vienna, Austria
    J Neurol Sci 245:123-6. 2006
    ..These data indicate that cortical lesions have to be considered as an additional pathological substrate for cognitive dysfunction in MS patients...
  63. ncbi request reprint Rasmussen's encephalitis: a role for autoimmune cytotoxic T lymphocytes
    Jan Bauer
    Brain Research Institute, Division of Neuroimmunology, University of Vienna, Vienna, Austria
    Curr Opin Neurol 15:197-200. 2002
    ..Specific attention is given to the recent recognition of cytotoxicity by CD8+/granzyme-B-positive T lymphocytes as a new pathogenic mechanism of neuronal damage...
  64. doi request reprint Neuromyelitis optica: pathogenicity of patient immunoglobulin in vivo
    Monika Bradl
    Department of Neuroimmunology, Medical University Vienna, Center for Brain Research, Vienna, Austria
    Ann Neurol 66:630-43. 2009
    ..A diagnostic hallmark of this disease is the presence of serum autoantibodies against the water channel aquaporin-4 (AQP-4) on astrocytes...
  65. pmc Oxidative damage in multiple sclerosis lesions
    Lukas Haider
    Centre for Brain Research, Medical University of Vienna, A 1090 Vienna, Austria
    Brain 134:1914-24. 2011
    ..Our data suggest profound oxidative injury of oligodendrocytes and neurons to be associated with active demyelination and axonal or neuronal injury in multiple sclerosis...
  66. ncbi request reprint Cortical, subcortical and spinal alterations in neuroimmunological diseases
    Hans Lassmann
    Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090, Wien, Austria
    J Neurol 254:II15-7. 2007
    ..Aim of this short review is to discuss the main factors determining lesional topography in brain inflammation and to illustrate these patterns of tissue injury with clinical examples...
  67. doi request reprint The protein tyrosine kinase Tec regulates a CD44highCD62L- Th17 subset
    Nicole Boucheron
    Division of Immunobiology, Institute of Immunology, Medical University of Vienna, Vienna, Austria
    J Immunol 185:5111-9. 2010
    ..pneumoniae. Taken together, our data indicated a critical role for Tec in T cell-intrinsic signaling pathways that regulate the in vivo generation of CD44(high)CD62L(-) effector/memory Th17 populations...
  68. ncbi request reprint Brain damage when multiple sclerosis is diagnosed clinically
    Hans Lassmann
    Brain Research Institute, University of Vienna, A 1090, Vienna, Austria
    Lancet 361:1317-8. 2003
  69. ncbi request reprint CD134 plays a crucial role in the pathogenesis of EAE and is upregulated in the CNS of patients with multiple sclerosis
    Susanna Carboni
    Serono Pharmaceutical Research Institute, 14, Chemin Aulx, 1228 Plan les Ouates, Switzerland
    J Neuroimmunol 145:1-11. 2003
    ....
  70. ncbi request reprint Comparison of myelin, axon, lipid, and immunopathology in the central nervous system of differentially myelin-compromised mutant mice: a morphological and biochemical study
    Gabriele Loers
    Zentrum fur Molekulare Neurobiologie Hamburg, Universitat Hamburg, D 20251 Hamburg, Germany
    Mol Cell Neurosci 27:175-89. 2004
    ..The combined observations point to differences, but also similarities in the relation of myelin, axon, and immunopathology with genotype, and to a common aggravation of the phenotype with age...
  71. ncbi request reprint Deficiency of the complement regulator CD59a enhances disease severity, demyelination and axonal injury in murine acute experimental allergic encephalomyelitis
    Richard James Mead
    Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Heath Park, Cardiff, UK
    Lab Invest 84:21-8. 2004
    ..These findings are relevant to some types of human demyelination, where abundant deposits of MAC are found in association with pathology...
  72. ncbi request reprint Comparing the pathogenesis of experimental autoimmune encephalomyelitis in CD4-/- and CD8-/- DBA/1 mice defines qualitative roles of different T cell subsets
    Khairul Bariah Abdul-Majid
    Neuroimmunology Unit, Karolinska Hospital, SE 171 76 Stockholm, Sweden
    J Neuroimmunol 141:10-9. 2003
    ..We interpret our findings such that in an ontogenic lack of CD4(+) T cells, EAE is mediated by CD8(+) and elevated levels of alphabetaCD4(-)CD8(-) cells, and that CNS damage is partly enacted by the activity of CD8(+) T cells...
  73. ncbi request reprint The role of nitric oxide in multiple sclerosis
    Kenneth J Smith
    Neuroinflammation Research Group, Guy s, King s, and St Thomas School of Medicine, King s College, London SE1 1UL, UK
    Lancet Neurol 1:232-41. 2002
    ....
  74. ncbi request reprint Effector stage CC chemokine receptor-1 selective antagonism reduces multiple sclerosis-like rat disease
    Sana Eltayeb
    Neuroimmunology Unit, Department of Medicine, Karolinska Institutet, SE 171 76 Stockholm, Sweden
    J Neuroimmunol 142:75-85. 2003
    ..Thus, we demonstrate therapeutic targeting of CCR1-dependent leukocyte recruitment to the central nervous system in a multiple sclerosis (MS)-like rat model...
  75. ncbi request reprint New loci regulating rat myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis
    Kristina Becanovic
    Neuroimmunology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden
    J Immunol 170:1062-9. 2003
    ..Furthermore, we detected a locus-specific parent-of-origin effect with suggestive linkage in Eae17. Further genetic and functional dissection of these loci may disclose critical disease-regulating molecular mechanisms...
  76. doi request reprint Pivotal advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis
    Asa Andersson
    Department of Clinical Neurosciences, Neuroimmunology Unit, Karolinska University Hospital at Solna, Karolinska Institutet, Stockholm, Sweden
    J Leukoc Biol 84:1248-55. 2008
    ..Significant expression of HMGB1 and its receptors on accumulating activated macrophages and resident microglia may thus provide a positive feedback loop that amplifies the inflammatory response during MS and EAE pathogenesis...
  77. ncbi request reprint Endoplasmic reticulum stress in PLP-overexpressing transgenic rats: gray matter oligodendrocytes are more vulnerable than white matter oligodendrocytes
    Jan Bauer
    Division of Neuroimmunology, Brain Research Institute, University of Vienna, Austria
    J Neuropathol Exp Neurol 61:12-22. 2002
    ..These results indicate that gray matter oligodendrocyte differ from white matter oligodendrocytes in their capacity to stabilize metabolic disturbances by an unfolded protein response...
  78. ncbi request reprint BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective interactions between immune and neuronal cells?
    Christine Stadelmann
    Institute for Neuropathology, Charite, Humboldt University, Berlin, Germany
    Brain 125:75-85. 2002
    ....
  79. ncbi request reprint Destruction of neurons by cytotoxic T cells: a new pathogenic mechanism in Rasmussen's encephalitis
    Christian G Bien
    Department of Epileptology, University of Bonn, Bonn, Germany
    Ann Neurol 51:311-8. 2002
    ..This study directly shows, for what we believe is the first time, that a cytotoxic T-cell mechanism contributes to loss of neurons in human brain disease...
  80. ncbi request reprint Multiple sclerosis: a study of CXCL10 and CXCR3 co-localization in the inflamed central nervous system
    Torben L Sørensen
    The MS Clinic, Department of Neurology, University of Copenhagen, Glostrup Hospital, 2600 Glostrup, Denmark
    J Neuroimmunol 127:59-68. 2002
    ..These data suggest a critical role for CXCL10 and CXCR3 in the accumulation of T cells in the CNS of MS patients...
  81. ncbi request reprint A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica
    Claudia F Lucchinetti
    Department of Neurology, Mayo Clinic, Rochester, MN, USA
    Brain 125:1450-61. 2002
    ..Based on this study, future therapeutic strategies designed to limit the deleterious effects of complement activation, eosinophil degranulation and neutrophil/macrophage/microglial activation are worthy of further investigation...
  82. ncbi request reprint Cytotoxic T lymphocytes in autoimmune and degenerative CNS diseases
    Harald Neumann
    Neuroimmunology Unit, European Neuroscience Institute Göttingen, Waldweg 33, 37073 Gottingen, Germany
    Trends Neurosci 25:313-9. 2002
    ..In MS, damage of axons is closely linked to the CD8(+) CTLs, and protection against CTL-mediated damage should be considered as a new therapeutic approach in MS and other neuroinflammatory diseases...
  83. ncbi request reprint A comparative analysis of B cell-mediated myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis pathogenesis in B cell-deficient mice reveals an effect on demyelination
    Lars Svensson
    Medical Inflammation Research, Lund University, Lund, Sweden
    Eur J Immunol 32:1939-46. 2002
    ..The contribution of B cells to pathogenesis appears to be mainly through demyelination rather than through inflammation...
  84. ncbi request reprint Differential expression of the chemokine receptors CX3CR1 and CCR1 by microglia and macrophages in myelin-oligodendrocyte-glycoprotein-induced experimental autoimmune encephalomyelitis
    Dan Sunnemark
    Department of Molecular Sciences, Local Discovery Research Area CNS and Pain Control, AstraZeneca AB, Sodertalje, Sweden
    Brain Pathol 13:617-29. 2003
    ..This has great relevance for the possibility of therapeutic intervention in demyelinating diseases such as multiple sclerosis, for example by targeting signaling events leading to monocyte recruitment...
  85. pmc The activation status of neuroantigen-specific T cells in the target organ determines the clinical outcome of autoimmune encephalomyelitis
    Naoto Kawakami
    Department of Neuroimmunology, Max Planck Institute for Neurobiology, 82152 Martinsried, Germany
    J Exp Med 199:185-97. 2004
    ..Low-level reactivation of weakly pathogenic T cells was not due to anergy because these cells could be activated by specific antigen in situ as well as after isolation ex vivo...
  86. ncbi request reprint Selective and antigen-dependent effects of myelin degeneration on central nervous system inflammation
    Fahmy Aboul-Enein
    Medizinische Universität Wien, Institut für Hirnforschung, Abteilung Neuroimmunologie, Austria
    J Neuropathol Exp Neurol 63:1284-96. 2004
    ....
  87. ncbi request reprint Autologous haematopoietic stem cell transplantation fails to stop demyelination and neurodegeneration in multiple sclerosis
    Imke Metz
    Department of Neuropathology, Georg August University, Gottingen, Germany
    Brain 130:1254-62. 2007
    ....
  88. pmc Combined immunostimulation and conditional cytotoxic gene therapy provide long-term survival in a large glioma model
    Sumia Ali
    Molecular Medicine and Gene Therapy Unit, University of Manchester, Manchester, United Kingdom
    Cancer Res 65:7194-204. 2005
    ..We propose that combined Flt3L and HSV1-TK adenoviral-mediated gene therapy may provide an effective antiglioma treatment with increased efficacy in clinical trials of glioma...
  89. ncbi request reprint CCR5Delta32 polymorphism effects on CCR5 expression, patterns of immunopathology and disease course in multiple sclerosis
    Orhun H Kantarci
    Department of Neurology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    J Neuroimmunol 169:137-43. 2005
    ..Furthermore it does not segregate with patterns of immunopathology in MS. We did not find an association between CCR5*Delta32 mutation and disease severity and age of onset in MS...
  90. ncbi request reprint Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis
    Shanu F Roemer
    Department of Neurology, Mayo Clinic, College of Medicine, 200 First St SW, Rochester, MN 55905, USA
    Brain 130:1194-205. 2007
    ..These findings strongly support a role for a complement activating AQP4-specific autoantibody as the initiator of the NMO lesion, and further distinguish NMO from MS...
  91. pmc Instant effect of soluble antigen on effector T cells in peripheral immune organs during immunotherapy of autoimmune encephalomyelitis
    Francesca Odoardi
    Max Planck Institute for Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany
    Proc Natl Acad Sci U S A 104:920-5. 2007
    ..This specific blockage almost completely abrogated CNS inflammation and clinical disease. These findings highlight the speed and efficiency of antigen recognition in vivo and add to our understanding of T cell-mediated autoimmunity...
  92. ncbi request reprint Neural precursors attenuate autoimmune encephalomyelitis by peripheral immunosuppression
    Ofira Einstein
    Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah Hebrew University Medical Center, Jerusalem, Israel
    Ann Neurol 61:209-18. 2007
    ..Although stem cell therapy was introduced initially for cell replacement, we examine here whether NPCs possess immunomodulatory effects...
  93. ncbi request reprint Epitope specificity of autoreactive T and B cells associated with experimental autoimmune encephalomyelitis and optic neuritis induced by oligodendrocyte-specific protein in SJL/J mice
    Nathali Kaushansky
    Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel
    J Immunol 177:7364-76. 2006
    ....
  94. ncbi request reprint Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis
    Nadine Hövelmeyer
    Laboratory for Molecular Immunology, Institute for Genetics, University of Cologne, Cologne, Germany
    J Immunol 175:5875-84. 2005
    ..Although only moderate reduction of lymphocyte infiltration into CNS tissue was observed, the absence of these receptors appears to confer protection from demyelination and development of clinical disease...
  95. ncbi request reprint Steroid-responsive encephalopathy associated with autoimmune thyroiditis and primary CNS demyelination
    Don J Mahad
    Department of Neurosciences, Mail Code NC30, The Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    J Neurol Sci 228:3-5. 2005
    ..We report a case of SREAT with biopsy proven (on two occasions) primary CNS demyelination and radiological evidence of steroid responsiveness, identifying primary CNS demyelination as a complication of autoimmune thyroid disease...
  96. ncbi request reprint Cellular FLIP (long isoform) overexpression in T cells drives Th2 effector responses and promotes immunoregulation in experimental autoimmune encephalomyelitis
    Vivian Tseveleki
    Laboratory of Molecular Genetics, Hellenic Pasteur Institute, National Center for Scientific Research Demokritos, Athens, Greece
    J Immunol 173:6619-26. 2004
    ..Our results show that the constitutive overexpression of c-FLIP(L) in T cells is sufficient to drive Th2 polarization of effector T cell responses and indicate that it might function as a key regulator of Th cell differentiation...
  97. ncbi request reprint Multiple sclerosis: T-cell receptor expression in distinct brain regions
    Andreas Junker
    Institute for Clinical Neuroimmunology, Ludwig Maximilians University, D 81377 Munich, Germany
    Brain 130:2789-99. 2007
    ..These experiments revealed that at least some of the pervasive T-cell clones belonged to the CD8+ compartment, supporting the pathogenic relevance of this T-cell subset...
  98. ncbi request reprint MHC gene related effects on microglia and macrophages in experimental autoimmune encephalomyelitis determine the extent of axonal injury
    Maria K Storch
    Department of Neurology, University of Graz, Austria
    Brain Pathol 12:287-99. 2002
    ..Thus, our studies document a genetic influence of the MHC-region on the relative contribution of macrophages versus microglia in the pathogenesis of EAE...
  99. ncbi request reprint Expression of chemokine receptors CCR1 and CCR5 reflects differential activation of mononuclear phagocytes in pattern II and pattern III multiple sclerosis lesions
    Don J Mahad
    Department of Neurosciences, The Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    J Neuropathol Exp Neurol 63:262-73. 2004
    ..As judged by mononuclear phagocyte chemokine receptor expression, there appear to be distinct tissue environments in pattern II and III MS lesions...
  100. pmc Fibrin depletion decreases inflammation and delays the onset of demyelination in a tumor necrosis factor transgenic mouse model for multiple sclerosis
    Katerina Akassoglou
    Department of Pharmacology, University of California at San Diego, La Jolla, CA 92093 0636, USA
    Proc Natl Acad Sci U S A 101:6698-703. 2004
    ..Design of therapeutic strategies based on fibrin depletion could potentially benefit the clinical course of demyelinating diseases such as multiple sclerosis...
  101. ncbi request reprint Cutting edge: Multiple sclerosis-like lesions induced by effector CD8 T cells recognizing a sequestered antigen on oligodendrocytes
    Amit Saxena
    Institut National de la Sante et de la Recherche Medicale, Unite 563, Toulouse, France
    J Immunol 181:1617-21. 2008
    ..These results provide new insights with regard to CNS tissue damage mediated by CD8 T cells and for understanding the role of CD8 T cells in MS...