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  1. Book ; Online: Neuro-Immune Connections to Enable Repair in CNS Disorders

    Vanmierlo, Tim / Broux, Bieke / Van Horssen, Jack / Hellings, Niels

    2020  

    Keywords Medicine ; Immunology ; neuroimmunology ; central nervous system ; immune system ; CNS repair ; CNS disorders
    Size 1 electronic resource (243 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230660
    ISBN 9782889660070 ; 2889660079
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book ; Thesis: Heparan sulfate proteoglycans and vascular pathology in Alzheimer's disease

    Horssen, Jacobus van

    2005  

    Author's details door Jacobus van Horssen
    Language English
    Size 167 S. : Ill.
    Publishing country Netherlands
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Nijmegen, Radboud Univ., Diss., 2004
    HBZ-ID HT014589302
    ISBN 90-9018832-0 ; 978-90-9018832-4
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2005 E 2375 order for loan Magazin

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  3. Article: Editorial: Redox-signaling in neurodegenerative diseases: biomarkers, targets, and therapies.

    Carvalho, Andreia N / Branco, Vasco / van Horssen, Jack / Saso, Luciano

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1198669

    Language English
    Publishing date 2023-04-20
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1198669
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Editorial: Neuro-Immune Connections to Enable Repair in CNS Disorders.

    Vanmierlo, Tim / van Horssen, Jack / Hellings, Niels / Broux, Bieke

    Frontiers in immunology

    2020  Volume 11, Page(s) 1425

    MeSH term(s) Animals ; Central Nervous System Diseases/immunology ; Central Nervous System Diseases/pathology ; Humans ; Nerve Regeneration/immunology ; Neuroimmunomodulation/physiology
    Language English
    Publishing date 2020-07-24
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.01425
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Breaching Brain Barriers: B Cell Migration in Multiple Sclerosis.

    Rodriguez-Mogeda, Carla / Rodríguez-Lorenzo, Sabela / Attia, Jiji / van Horssen, Jack / Witte, Maarten E / de Vries, Helga E

    Biomolecules

    2022  Volume 12, Issue 6

    Abstract: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) known for the manifestation of demyelinated lesions throughout the CNS, leading to neurodegeneration. To date, not all pathological mechanisms that drive disease ... ...

    Abstract Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) known for the manifestation of demyelinated lesions throughout the CNS, leading to neurodegeneration. To date, not all pathological mechanisms that drive disease progression are known, but the clinical benefits of anti-CD20 therapies have put B cells in the spotlight of MS research. Besides their pathological effects in the periphery in MS, B cells gain access to the CNS where they can contribute to disease pathogenesis. Specifically, B cells accumulate in perivascular infiltrates in the brain parenchyma and the subarachnoid spaces of the meninges, but are virtually absent from the choroid plexus. Hence, the possible migration of B cells over the blood-brain-, blood-meningeal-, and blood-cerebrospinal fluid (CSF) barriers appears to be a crucial step to understanding B cell-mediated pathology. To gain more insight into the molecular mechanisms that regulate B cell trafficking into the brain, we here provide a comprehensive overview of the different CNS barriers in health and in MS and how they translate into different routes for B cell migration. In addition, we review the mechanisms of action of diverse therapies that deplete peripheral B cells and/or block B cell migration into the CNS. Importantly, this review shows that studying the different routes of how B cells enter the inflamed CNS should be the next step to understanding this disease.
    MeSH term(s) Blood-Brain Barrier/pathology ; Brain/pathology ; Cell Movement/physiology ; Central Nervous System/pathology ; Humans ; Multiple Sclerosis/pathology
    Language English
    Publishing date 2022-06-07
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom12060800
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Oxidative stress and its impact on neurons and glia in multiple sclerosis lesions.

    Lassmann, Hans / van Horssen, Jack

    Biochimica et biophysica acta

    2015  Volume 1862, Issue 3, Page(s) 506–510

    MeSH term(s) Animals ; Brain/metabolism ; Brain/pathology ; Humans ; Iron/analysis ; Iron/metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Mitochondria/metabolism ; Mitochondria/pathology ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Nerve Fibers, Myelinated/metabolism ; Nerve Fibers, Myelinated/pathology ; Neuroglia/metabolism ; Neuroglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Oxidative Stress
    Chemical Substances Iron (E1UOL152H7)
    Language English
    Publishing date 2015-10-08
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2015.09.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis.

    Spaas, Jan / Goulding, Richie P / Keytsman, Charly / Fonteyn, Lena / van Horssen, Jack / Jaspers, Richard T / Eijnde, Bert O / Wüst, Rob C I

    Journal of cachexia, sarcopenia and muscle

    2022  Volume 13, Issue 5, Page(s) 2537–2550

    Abstract: Background: Patients with multiple sclerosis (MS) experience reduced exercise tolerance that substantially reduces quality of life. The mechanisms underpinning exercise intolerance in MS are not fully clear. This study aimed to determine the ... ...

    Abstract Background: Patients with multiple sclerosis (MS) experience reduced exercise tolerance that substantially reduces quality of life. The mechanisms underpinning exercise intolerance in MS are not fully clear. This study aimed to determine the contributions of the cardiopulmonary system and peripheral muscle in MS-induced exercise intolerance before and after exercise training.
    Methods: Twenty-three patients with MS (13 women) and 20 age-matched and sex-matched healthy controls (13 women) performed a cardiopulmonary exercise test. Muscle fibre type composition, size, succinate dehydrogenase (SDH) activity, capillarity, and gene expression and proteins related to mitochondrial density were determined in vastus lateralis muscle biopsies. Nine MS patients (five women) were re-examined following a 12 week exercise training programme consisting of high-intensity cycling interval and resistance training.
    Results: Patients with MS had lower maximal oxygen uptake compared with healthy controls (V̇O
    Conclusions: Skeletal muscle oxidative phenotype (mitochondrial complex I and II content, SDH activity) is lower in patients with MS, contributing to reduced exercise tolerance. However, skeletal muscle mitochondria appeared resistant to the beneficial effects of exercise training, suggesting that other physiological systems, at least in part, drive the improvements in exercise capacity following exercise training in MS.
    MeSH term(s) Exercise ; Exercise Tolerance/physiology ; Female ; Humans ; Male ; Multiple Sclerosis/metabolism ; Muscle, Skeletal/metabolism ; Oxidative Stress ; Oxygen/metabolism ; Oxygen Consumption/physiology ; PPAR gamma/metabolism ; Phenotype ; Quality of Life ; Succinate Dehydrogenase/metabolism
    Chemical Substances PPAR gamma ; Succinate Dehydrogenase (EC 1.3.99.1) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2022-08-04
    Publishing country Germany
    Document type Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2586864-0
    ISSN 2190-6009 ; 2190-5991
    ISSN (online) 2190-6009
    ISSN 2190-5991
    DOI 10.1002/jcsm.13050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Extended interval dosing of ocrelizumab modifies the repopulation of B cells without altering the clinical efficacy in multiple sclerosis.

    Rodriguez-Mogeda, Carla / van Lierop, Zoë Y G J / van der Pol, Susanne M A / Coenen, Loet / Hogenboom, Laura / Kamermans, Alwin / Rodriguez, Ernesto / van Horssen, Jack / van Kempen, Zoé L E / Uitdehaag, Bernard M J / Teunissen, Charlotte E / Witte, Maarten E / Killestein, Joep / de Vries, Helga E

    Journal of neuroinflammation

    2023  Volume 20, Issue 1, Page(s) 215

    Abstract: Background: Recent studies suggest that extended interval dosing of ocrelizumab, an anti-B cell therapy, does not affect its clinical effectiveness in most patients with multiple sclerosis (MS). However, it remains to be established whether certain B ... ...

    Abstract Background: Recent studies suggest that extended interval dosing of ocrelizumab, an anti-B cell therapy, does not affect its clinical effectiveness in most patients with multiple sclerosis (MS). However, it remains to be established whether certain B cell subsets are differentially repopulated after different dosing intervals and whether these subsets relate to clinical efficacy.
    Methods: We performed high-dimensional single-cell characterization of the peripheral immune landscape of patients with MS after standard (SID; n = 43) or extended interval dosing (EID; n = 37) of ocrelizumab and in non-ocrelizumab-treated (control group, CG; n = 28) patients with MS, using mass cytometry by time of flight (CyTOF).
    Results: The first B cells that repopulate after both ocrelizumab dosing schemes were immature, transitional and regulatory CD1d
    Conclusions: Taken together, our data highlight that extending the dosing interval of ocrelizumab does not lead to increased repopulation of effector B cells. We show that the increase of CD20 expression on B cell subsets in EID might lead to longer depletion or less repopulation of B cells after the next infusion of ocrelizumab. Lastly, even though extending the ocrelizumab interval dosing alters B cell repopulation, it does not affect the clinical efficacy of ocrelizumab in our cohort of patients with MS.
    MeSH term(s) Humans ; Multiple Sclerosis ; Antibodies, Monoclonal, Humanized/therapeutic use ; B-Lymphocytes ; Treatment Outcome ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Immunologic Factors/therapeutic use
    Chemical Substances ocrelizumab (A10SJL62JY) ; Antibodies, Monoclonal, Humanized ; Immunologic Factors
    Language English
    Publishing date 2023-09-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-023-02900-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Inflammation and mitochondrial dysfunction: A vicious circle in neurodegenerative disorders?

    van Horssen, Jack / van Schaik, Pauline / Witte, Maarten

    Neuroscience letters

    2017  Volume 710, Page(s) 132931

    Abstract: Experimental evidence supports an intricate association between inflammation and mitochondrial dysfunction as main contributors of neurological diseases. Inflammatory mediators produced by activated microglia and infiltrated immune cells trigger ... ...

    Abstract Experimental evidence supports an intricate association between inflammation and mitochondrial dysfunction as main contributors of neurological diseases. Inflammatory mediators produced by activated microglia and infiltrated immune cells trigger intracellular signalling cascades that can alter cellular mitochondrial metabolism. Cytokines, particularly tumor necrosis factor-alpha, impede mitochondrial oxidative phosphorylation and associated ATP production and instigate mitochondrial reactive oxygen species production. This culminates in mitochondrial membrane permeabilization, altered mitochondrial dynamics and might ultimately result in cell death. When severely injured mitochondria are not appropriately removed by mitophagy they can release their contents into the cytosol and extracellular environment and thereby amplify the inflammatory process. Here we provide a comprehensive overview on how inflammatory mediators impair mitochondrial metabolism and discuss how defective mitochondria can elicit and potentiate an inflammatory response.
    MeSH term(s) Animals ; Cell Death ; Cytokines ; Humans ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Mice ; Microglia/metabolism ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Diseases/pathology ; Mitophagy ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/physiopathology ; Reactive Oxygen Species ; Signal Transduction ; Tumor Necrosis Factor-alpha
    Chemical Substances Cytokines ; Inflammation Mediators ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2017-06-28
    Publishing country Ireland
    Document type Journal Article ; Review
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2017.06.050
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1166: Show issues Location:
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  10. Article ; Online: Neuron-specific activation of necroptosis signaling in multiple sclerosis cortical grey matter.

    Picon, Carmen / Jayaraman, Anusha / James, Rachel / Beck, Catriona / Gallego, Patricia / Witte, Maarten E / van Horssen, Jack / Mazarakis, Nicholas D / Reynolds, Richard

    Acta neuropathologica

    2021  Volume 141, Issue 4, Page(s) 585–604

    Abstract: Sustained exposure to pro-inflammatory cytokines in the leptomeninges is thought to play a major role in the pathogenetic mechanisms leading to cortical pathology in multiple sclerosis (MS). Although the molecular mechanisms underlying neurodegeneration ... ...

    Abstract Sustained exposure to pro-inflammatory cytokines in the leptomeninges is thought to play a major role in the pathogenetic mechanisms leading to cortical pathology in multiple sclerosis (MS). Although the molecular mechanisms underlying neurodegeneration in the grey matter remain unclear, several lines of evidence suggest a prominent role for tumour necrosis factor (TNF). Using cortical grey matter tissue blocks from post-mortem brains from 28 secondary progressive MS subjects and ten non-neurological controls, we describe an increase in expression of multiple steps in the TNF/TNF receptor 1 signaling pathway leading to necroptosis, including the key proteins TNFR1, FADD, RIPK1, RIPK3 and MLKL. Activation of this pathway was indicated by the phosphorylation of RIPK3 and MLKL and the formation of protein oligomers characteristic of necrosomes. In contrast, caspase-8 dependent apoptotic signaling was decreased. Upregulation of necroptotic signaling occurred predominantly in macroneurons in cortical layers II-III, with little expression in other cell types. The presence of activated necroptotic proteins in neurons was increased in MS cases with prominent meningeal inflammation, with a 30-fold increase in phosphoMLKL+ neurons in layers I-III. The density of phosphoMLKL+ neurons correlated inversely with age at death, age at progression and disease duration. In vivo induction of chronically elevated TNF and INFγ levels in the CSF in a rat model via lentiviral transduction in the meninges, triggered inflammation and neurodegeneration in the underlying cortical grey matter that was associated with increased neuronal expression of TNFR1 and activated necroptotic signaling proteins. Exposure of cultured primary rat cortical neurons to TNF induced necroptosis when apoptosis was inhibited. Our data suggest that neurons in the MS cortex are dying via TNF/TNFR1 stimulated necroptosis rather than apoptosis, possibly initiated in part by chronic meningeal inflammation. Neuronal necroptosis represents a pathogenetic mechanism that is amenable to therapeutic intervention at several points in the signaling pathway.
    MeSH term(s) Adult ; Aged ; Animals ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Female ; Gray Matter/metabolism ; Gray Matter/pathology ; Humans ; Male ; Middle Aged ; Multiple Sclerosis, Chronic Progressive/pathology ; Necroptosis/physiology ; Neurons/pathology ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Signal Transduction/physiology ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2021-02-10
    Publishing country Germany
    Document type Journal Article ; 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/s00401-021-02274-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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