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Article ; Online: From astrocyte destruction to axon injury: watching lesion evolution in experimental neuromyelitis optica.

Bradl, Monika

2022 Volume 145, Issue 5, Page(s) 1581–1583

MeSH term(s)	Aquaporin 4/metabolism ; Astrocytes/metabolism ; Axons/pathology ; Brain/pathology ; Humans ; Neuromyelitis Optica/pathology
Chemical Substances	Aquaporin 4
Language	English
Publishing date	2022-04-18
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac141
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Book: Gehirn und Nervensystem

Bradl, Monika / Weninger, Wolfgang Johann

MCW - Block 19 ; [mit pathologisch-histologischen Farbtafeln und Erläuterungen]

2015

Author's details	Wolfgang J. Weninger (Hg.) [Autorinnen und Autoren: Monika Bradl ...]
Keywords	Nervenkrankheit
Subject	Nervenkrankheiten ; Neurologische Erkrankung ; Neurologische Krankheit ; Nervensystem ; Nervensystemkrankheit ; Nervous disease
Language	German
Size	216 S. : Ill., graph. Darst., 240 mm x 170 mm
Edition	9., aktualisierte und erg. Aufl.
Publisher	Facultas
Publishing place	Wien
Publishing country	Austria
Document type	Book
HBZ-ID	HT018565909
ISBN	978-3-7089-1291-2 ; 3-7089-1291-8
Database	Catalogue ZB MED Medicine, Health

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2015 A 2281	available for loan (reading room)	Lesesaal EG

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Article ; Online: Multiple sclerosis: experimental models and reality.

Lassmann, Hans / Bradl, Monika

Acta neuropathologica

2016 Volume 133, Issue 2, Page(s) 223–244

Abstract: One of the most frequent statements, provided in different variations in the introduction of experimental studies on multiple sclerosis (MS), is that "Multiple sclerosis is a demyelinating autoimmune disease and experimental autoimmune encephalomyelitis ( ...

Abstract	One of the most frequent statements, provided in different variations in the introduction of experimental studies on multiple sclerosis (MS), is that "Multiple sclerosis is a demyelinating autoimmune disease and experimental autoimmune encephalomyelitis (EAE) is a suitable model to study its pathogenesis". However, so far, no single experimental model covers the entire spectrum of the clinical, pathological, or immunological features of the disease. Many different models are available, which proved to be highly useful for studying different aspects of inflammation, demyelination, remyelination, and neurodegeneration in the central nervous system. However, the relevance of results from such models for MS pathogenesis has to be critically validated. Current EAE models are mainly based on inflammation, induced by auto-reactive CD4
MeSH term(s)	Animals ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental ; Humans ; Multiple Sclerosis
Keywords	covid19
Language	English
Publishing date	2016-10-20
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-016-1631-4
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Article: Neurologic autoimmunity: mechanisms revealed by animal models.

Bradl, Monika / Lassmann, Hans

Handbook of clinical neurology

2016 Volume 133, Page(s) 121–143

Abstract: Over the last decade, neurologic autoimmunity has become a major consideration in the diagnosis and management of patients with many neurologic presentations. The nature of the associated antibodies and their targets has led to appreciation of the ... ...

Abstract	Over the last decade, neurologic autoimmunity has become a major consideration in the diagnosis and management of patients with many neurologic presentations. The nature of the associated antibodies and their targets has led to appreciation of the importance of the accessibility of the target antigen to antibodies, and a partial understanding of the different mechanisms that can follow antibody binding. This chapter will first describe the basic principles of autoimmune inflammation and tissue damage in the central and peripheral nervous system, and will then demonstrate what has been learnt about neurologic autoimmunity from circumstantial clinical evidence and from passive, active, and occasionally spontaneous or genetic animal models. It will cover neurologic autoimmune diseases ranging from disorders of neuromuscular transmission, peripheral and ganglionic neuropathy, to diseases of the central nervous system, where autoantibodies are either pathogenic and cause destruction or changes in function of their targets, where they are harmless bystanders of T-cell-mediated tissue damage, or are not involved at all. Finally, this chapter will summarize the relevance of current animal models for studying the different neurologic autoimmune diseases, and it will identify aspects where future animal models need to be improved to better reflect the disease reality experienced by affected patients, e.g., the chronicity or the relapsing/remitting nature of their disease.
MeSH term(s)	Animals ; Autoimmune Diseases of the Nervous System/immunology ; Autoimmune Diseases of the Nervous System/therapy ; Autoimmunity ; Disease Models, Animal ; Humans ; Neurology
Language	English
Publishing date	2016
Publishing country	Netherlands
Document type	Journal Article
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-63432-0.00008-6
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Article ; Online: Mechanisms for lesion localization in neuromyelitis optica spectrum disorders.

Bradl, Monika / Reindl, Markus / Lassmann, Hans

Current opinion in neurology

2018 Volume 31, Issue 3, Page(s) 325–333

Abstract: Purpose of review: Neuromyelitis optica spectrum disorders (NMOSD) are severe inflammatory diseases of the central nervous system (CNS), with the presence of aquaporin 4 (AQP4)-specific serum antibodies in the vast majority of patients, and with the ... ...

Abstract	Purpose of review: Neuromyelitis optica spectrum disorders (NMOSD) are severe inflammatory diseases of the central nervous system (CNS), with the presence of aquaporin 4 (AQP4)-specific serum antibodies in the vast majority of patients, and with the presence of myelin oligodendrocyte glycoprotein (MOG)-specific antibodies in approximately 40% of all AQP4-antibody negative NMOSD patients. Despite differences in antigen recognition, the preferred sites of lesions are similar in both groups of patients: They localize to the spinal cord and to the anterior visual pathway including retina, optic nerves, chiasm, and optic tracts, and - to lesser extent - also to certain predilection sites in the brain. Recent findings: The involvement of T cells in the formation of NMOSD lesions has been challenged for quite some time. However, several recent findings demonstrate the key role of T cells for lesion formation and localization. Studies on the evolution of lesions in the spinal cord of NMOSD patients revealed a striking similarity of early NMOSD lesions with those observed in corresponding T-cell-induced animal models, both in lesion formation and in lesion localization. Studies on retinal abnormalities in NMOSD patients and corresponding animals revealed the importance of T cells for the very early stages of retinal lesions which eventually culminate in damage to Müller cells and to the retinal nerve fiber layer. Finally, a study on cerebrospinal fluid (CSF) barrier pathology demonstrated that NMOSD immunopathology extends beyond perivascular astrocytic foot processes to include the pia, the ependyma, and the choroid plexus, and that diffusion of antibodies from the CSF could further influence lesion formation in NMOSD patients. Summary: The pathological changes observed in AQP4-antibody positive and MOG-antibody positive NMOSD patients are strikingly similar to those found in corresponding animal models, and many mechanisms which determine lesion localization in experimental animals seem to closely reflect the human situation.
MeSH term(s)	Aquaporin 4/immunology ; Autoantibodies ; Brain/immunology ; Brain/pathology ; Humans ; Myelin-Oligodendrocyte Glycoprotein/immunology ; Neuromyelitis Optica/immunology ; Neuromyelitis Optica/pathology ; Retina/immunology ; Retina/pathology ; Spinal Cord/immunology ; Spinal Cord/pathology
Chemical Substances	Aquaporin 4 ; Autoantibodies ; Myelin-Oligodendrocyte Glycoprotein
Language	English
Publishing date	2018-02-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1182686-1
ISSN	1473-6551 ; 1350-7540
ISSN (online)	1473-6551
ISSN	1350-7540
DOI	10.1097/WCO.0000000000000551
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Zs.A 2524: Show issues

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Article ; Online: Paths to hippocampal damage in neuromyelitis optica spectrum disorders.

Zakani, Mona / Nigritinou, Magdalini / Ponleitner, Markus / Takai, Yoshiki / Hofmann, Daniel / Hillebrand, Sophie / Höftberger, Romana / Bauer, Jan / Lasztoczi, Balint / Misu, Tatsuro / Kasprian, Gregor / Rommer, Paulus / Bradl, Monika

Neuropathology and applied neurobiology

2023 Volume 49, Issue 2, Page(s) e12893

Abstract: Aims: Many patients with neuromyelitis optica spectrum disorders (NMOSD) suffer from cognitive impairment affecting memory, processing speed and attention and suffer from depressive symptoms. Because some of these manifestations could trace back to the ... ...

Abstract	Aims: Many patients with neuromyelitis optica spectrum disorders (NMOSD) suffer from cognitive impairment affecting memory, processing speed and attention and suffer from depressive symptoms. Because some of these manifestations could trace back to the hippocampus, several magnetic resonance imaging (MRI) studies have been performed in the past, with a number of groups describing volume loss of the hippocampus in NMOSD patients, whereas others did not observe such changes. Here, we addressed these discrepancies. Methods: We performed pathological and MRI studies on the hippocampi of NMOSD patients, combined with detailed immunohistochemical analysis of hippocampi from experimental models of NMOSD. Results: We identified different pathological scenarios for hippocampal damage in NMOSD and its experimental models. In the first case, the hippocampus was compromised by the initiation of astrocyte injury in this brain region and subsequent local effects of microglial activation and neuronal damage. In the second case, loss of hippocampal volume was seen by MRI in patients with large tissue-destructive lesions in the optic nerves or the spinal cord, and the pathological work-up of tissue derived from a patient with such lesions revealed subsequent retrograde neuronal degeneration affecting different axonal tracts and neuronal networks. It remains to be seen whether remote lesions and associated retrograde neuronal degeneration on their own are sufficient to cause extensive volume loss of the hippocampus, or whether they act in concert with small astrocyte-destructive, microglia-activating lesions in the hippocampus that escape detection by MRI, either due to their small size or due to the chosen time window for examination. Conclusions: Different pathological scenarios can culminate in hippocampal volume loss in NMOSD patients.
MeSH term(s)	Humans ; Neuromyelitis Optica/pathology ; Spinal Cord/pathology ; Brain/pathology ; Magnetic Resonance Imaging ; Hippocampus/pathology ; Autoantibodies ; Aquaporin 4
Chemical Substances	Autoantibodies ; Aquaporin 4
Language	English
Publishing date	2023-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80371-6
ISSN	1365-2990 ; 0305-1846
ISSN (online)	1365-2990
ISSN	0305-1846
DOI	10.1111/nan.12893
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Zs.A 1241: Show issues

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Article: Müller cells and retinal axons can be primary targets in experimental neuromyelitis optica spectrum disorder.

Zeka, Bleranda / Lassmann, Hans / Bradl, Monika

Clinical & experimental neuroimmunology

2017 Volume 8, Issue Suppl Suppl 1, Page(s) 3–7

Abstract: Recent work from our laboratory, using different models of experimental neuromyelitis optica spectrum disorder (NMOSD), has led to a number of observations that might be highly relevant for NMOSD patients. For example: (i) in the presence of ... ...

Abstract	Recent work from our laboratory, using different models of experimental neuromyelitis optica spectrum disorder (NMOSD), has led to a number of observations that might be highly relevant for NMOSD patients. For example: (i) in the presence of neuromyelitis optica immunoglobulin G, astrocyte-destructive lesions can be initiated by CD4+ T cells when these cells recognize aquaporin 4 (AQP4), but also when they recognize other antigens of the central nervous system. The only important prerequisite is that the T cells have to be activated within the central nervous system by "their" specific antigen. Recently activated CD4+ T cells with yet unknown antigen specificity are also found in human NMOSD lesions. (ii) The normal immune repertoire might contain AQP4-specific T cells, which are highly encephalitogenic on activation. (iii) The retina might be a primary target of AQP4-specific T cells and neuromyelitis optica immunoglobulin G: AQP4-specific T cells alone are sufficient to cause retinitis with low-grade axonal pathology in the retinal nerve fiber/ganglionic cell layer. A thinning of these layers is also observed in NMOSD patients, where it is thought to be a consequence of optic neuritis. Neuromyelitis optica immunoglobulin G might target cellular processes of Müller cells and cause their loss of AQP4 reactivity, when AQP4-specific T cells open the blood-retina barrier in the outer plexiform layer. Patchy loss of AQP4 reactivity on Müller cells of NMOSD patients has been recently described. Cumulatively, our findings in experimental NMOSD suggest that both CD4+ T cell and antibody responses directed against AQP4 might play an important role in the pathogenesis of tissue destruction seen in NMOSD.
Language	English
Publishing date	2017-01-11
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1759-1961
ISSN	1759-1961
DOI	10.1111/cen3.12345
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Article ; Online: Experimental models of neuromyelitis optica.

Bradl, Monika / Lassmann, Hans

Brain pathology (Zurich, Switzerland)

2013 Volume 24, Issue 1, Page(s) 74–82

Abstract: For a long time, the most important inflammatory demyelinating diseases of the central nervous system (CNS), for example, multiple sclerosis (MS) and neuromyelitis optica (NMO), were extremely hard to differentiate, often with severe consequences for ... ...

Abstract	For a long time, the most important inflammatory demyelinating diseases of the central nervous system (CNS), for example, multiple sclerosis (MS) and neuromyelitis optica (NMO), were extremely hard to differentiate, often with severe consequences for affected patients. This changed with the discovery of NMO-immunoglobulin G (IgG), a specific autoantibody which was detected in the vast majority of NMO patients, and with the demonstration that this autoantibody targets aquaporin 4 (AQP4), a water channel found on astrocytes in the CNS. These findings paved the way for the generation of experimental models of NMO. This chapter will discuss the contribution of experimental models to NMO research and what key questions remain to be addressed.
MeSH term(s)	Animals ; Aquaporin 4/immunology ; Central Nervous System/immunology ; Central Nervous System/pathology ; Cytokines/therapeutic use ; Disease Models, Animal ; Humans ; Immunoglobulin G/immunology ; Neuromyelitis Optica/diagnosis ; Neuromyelitis Optica/drug therapy ; Neuromyelitis Optica/immunology
Chemical Substances	Aquaporin 4 ; Cytokines ; Immunoglobulin G
Language	English
Publishing date	2013-12-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.12098
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Zs.A 3585: Show issues

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Article ; Online: Dissection of complement and Fc-receptor-mediated pathomechanisms of autoantibodies to myelin oligodendrocyte glycoprotein.

Mader, Simone / Ho, Samantha / Wong, Hoi Kiu / Baier, Selia / Winklmeier, Stephan / Riemer, Carolina / Rübsamen, Heike / Fernandez, Iris Marti / Gerhards, Ramona / Du, Cuilian / Chuquisana, Omar / Lünemann, Jan D / Lux, Anja / Nimmerjahn, Falk / Bradl, Monika / Kawakami, Naoto / Meinl, Edgar

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 13, Page(s) e2300648120

Abstract: Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) have recently been established to define a new disease entity, MOG-antibody-associated disease (MOGAD), which is clinically overlapping with multiple sclerosis. MOG-specific antibodies (Abs) ...

Abstract	Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) have recently been established to define a new disease entity, MOG-antibody-associated disease (MOGAD), which is clinically overlapping with multiple sclerosis. MOG-specific antibodies (Abs) from patients are pathogenic, but the precise effector mechanisms are currently still unknown and no therapy is approved for MOGAD. Here, we determined the contributions of complement and Fc-receptor (FcR)-mediated effects in the pathogenicity of MOG-Abs. Starting from a recombinant anti-MOG (mAb) with human IgG1 Fc, we established MOG-specific mutant mAbs with differential FcR and C1q binding. We then applied selected mutants of this MOG-mAb in two animal models of experimental autoimmune encephalomyelitis. First, we found MOG-mAb-induced demyelination was mediated by both complement and FcRs about equally. Second, we found that MOG-Abs enhanced activation of cognate MOG-specific T cells in the central nervous system (CNS), which was dependent on FcR-, but not C1q-binding. The identification of complement-dependent and -independent pathomechanisms of MOG-Abs has implications for therapeutic strategies in MOGAD.
MeSH term(s)	Animals ; Humans ; Myelin-Oligodendrocyte Glycoprotein ; Autoantibodies ; Receptors, Fc ; Multiple Sclerosis ; Encephalomyelitis, Autoimmune, Experimental ; Complement System Proteins ; Antibodies, Monoclonal
Chemical Substances	Myelin-Oligodendrocyte Glycoprotein ; Autoantibodies ; Receptors, Fc ; Complement System Proteins (9007-36-7) ; Antibodies, Monoclonal
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2300648120
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Zs.A 1148: Show issues

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Article: Myelin Oligodendrocyte Glycoprotein: Deciphering a Target in Inflammatory Demyelinating Diseases.

Peschl, Patrick / Bradl, Monika / Höftberger, Romana / Berger, Thomas / Reindl, Markus

Frontiers in immunology

2017 Volume 8, Page(s) 529

Abstract: Myelin oligodendrocyte glycoprotein (MOG), a member of the immunoglobulin (Ig) superfamily, is a myelin protein solely expressed at the outermost surface of myelin sheaths and oligodendrocyte membranes. This makes MOG a potential target of cellular and ... ...

Abstract	Myelin oligodendrocyte glycoprotein (MOG), a member of the immunoglobulin (Ig) superfamily, is a myelin protein solely expressed at the outermost surface of myelin sheaths and oligodendrocyte membranes. This makes MOG a potential target of cellular and humoral immune responses in inflammatory demyelinating diseases. Due to its late postnatal developmental expression, MOG is an important marker for oligodendrocyte maturation. Discovered about 30 years ago, it is one of the best-studied autoantigens for experimental autoimmune models for multiple sclerosis (MS). Human studies, however, have yielded controversial results on the role of MOG, especially MOG antibodies (Abs), as a biomarker in MS. But with improved detection methods using different expression systems to detect Abs in patients' samples, this is meanwhile no longer the case. Using cell-based assays with recombinant full-length, conformationally intact MOG, several recent studies have revealed that MOG Abs can be found in a subset of predominantly pediatric patients with acute disseminated encephalomyelitis (ADEM), aquaporin-4 (AQP4) seronegative neuromyelitis optica spectrum disorders (NMOSD), monophasic or recurrent isolated optic neuritis (ON), or transverse myelitis, in atypical MS and in
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.00529
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