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  1. Artikel ; Online: The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34.

    Berglund, Rasmus / Cheng, Yufei / Piket, Eliane / Adzemovic, Milena Z / Zeitelhofer, Manuel / Olsson, Tomas / Guerreiro-Cacais, Andre Ortlieb / Jagodic, Maja

    Nature communications

    2024  Band 15, Heft 1, Seite(n) 383

    Abstract: Microglia harness an unutilized health-promoting potential in age-related neurodegenerative and neuroinflammatory diseases, conditions like progressive multiple sclerosis (MS). Our research unveils an microglia population emerging in the cortical brain ... ...

    Abstract Microglia harness an unutilized health-promoting potential in age-related neurodegenerative and neuroinflammatory diseases, conditions like progressive multiple sclerosis (MS). Our research unveils an microglia population emerging in the cortical brain regions of aging mice, marked by ERK1/2, Akt, and AMPK phosphorylation patterns and a transcriptome indicative of activated autophagy - a process critical for cellular adaptability. By deleting the core autophagy gene Ulk1 in microglia, we reduce this population in the central nervous system of aged mice. Notably, this population is found dependent on IL-34, rather than CSF1, although both are ligands for CSF1R. When aging mice are exposed to autoimmune neuroinflammation, the loss of autophagy-dependent microglia leads to neural and glial cell death and increased mortality. Conversely, microglial expansion mediated by IL-34 exhibits a protective effect. These findings shed light on an autophagy-dependent neuroprotective microglia population as a potential target for treating age-related neuroinflammatory conditions, including progressive MS.
    Mesh-Begriff(e) Animals ; Mice ; Microglia ; Central Nervous System ; Neuroglia ; Autophagy/genetics ; Interleukins
    Chemische Substanzen Interleukins
    Sprache Englisch
    Erscheinungsdatum 2024-01-09
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-44556-6
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Effect of Vitamin D on Experimental Autoimmune Neuroinflammation Is Dependent on Haplotypes Comprising Naturally Occurring Allelic Variants of CIITA (

    Hochmeister, Sonja / Aeinehband, Shahin / Dorris, Charles / Berglund, Rasmus / Haindl, Michaela T / Velikic, Vid / Gustafsson, Sven A / Olsson, Tomas / Piehl, Fredrik / Jagodic, Maja / Zeitelhofer, Manuel / Adzemovic, Milena Z

    Frontiers in neurology

    2020  Band 11, Seite(n) 600401

    Abstract: An increasing body of evidence associates low vitamin D levels with increased risk of multiple sclerosis (MS), suggesting the possibility of a gene-environment interaction for this environmental factor in MS pathogenesis. Moreover, it has been shown that ...

    Abstract An increasing body of evidence associates low vitamin D levels with increased risk of multiple sclerosis (MS), suggesting the possibility of a gene-environment interaction for this environmental factor in MS pathogenesis. Moreover, it has been shown that vitamin D downregulates major histocompatibility complex (MHC) class II expression in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. We here report about the impact of a dietary vitamin D supplementation on EAE in the rat strains having functionally relevant allelic variations in the
    Sprache Englisch
    Erscheinungsdatum 2020-11-13
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2020.600401
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Microglial autophagy-associated phagocytosis is essential for recovery from neuroinflammation.

    Berglund, Rasmus / Guerreiro-Cacais, Andre Ortlieb / Adzemovic, Milena Z / Zeitelhofer, Manuel / Lund, Harald / Ewing, Ewoud / Ruhrmann, Sabrina / Nutma, Erik / Parsa, Roham / Thessen-Hedreul, Melanie / Amor, Sandra / Harris, Robert A / Olsson, Tomas / Jagodic, Maja

    Science immunology

    2020  Band 5, Heft 52

    Abstract: Multiple sclerosis (MS) is a leading cause of incurable progressive disability in young adults caused by inflammation and neurodegeneration in the central nervous system (CNS). The capacity of microglia to clear tissue debris is essential for maintaining ...

    Abstract Multiple sclerosis (MS) is a leading cause of incurable progressive disability in young adults caused by inflammation and neurodegeneration in the central nervous system (CNS). The capacity of microglia to clear tissue debris is essential for maintaining and restoring CNS homeostasis. This capacity diminishes with age, and age strongly associates with MS disease progression, although the underlying mechanisms are still largely elusive. Here, we demonstrate that the recovery from CNS inflammation in a murine model of MS is dependent on the ability of microglia to clear tissue debris. Microglia-specific deletion of the autophagy regulator
    Sprache Englisch
    Erscheinungsdatum 2020-08-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abb5077
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Fatal demyelinating disease is induced by monocyte-derived macrophages in the absence of TGF-β signaling.

    Lund, Harald / Pieber, Melanie / Parsa, Roham / Grommisch, David / Ewing, Ewoud / Kular, Lara / Han, Jinming / Zhu, Keying / Nijssen, Jik / Hedlund, Eva / Needhamsen, Maria / Ruhrmann, Sabrina / Guerreiro-Cacais, André Ortlieb / Berglund, Rasmus / Forteza, Maria J / Ketelhuth, Daniel F J / Butovsky, Oleg / Jagodic, Maja / Zhang, Xing-Mei /
    Harris, Robert A

    Nature immunology

    2018  Band 19, Heft 5, Seite(n) 1–7

    Abstract: The cytokine transforming growth factor-β (TGF-β) regulates the development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-β is not critical for microglia survival but is required for the maintenance of the ... ...

    Abstract The cytokine transforming growth factor-β (TGF-β) regulates the development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-β is not critical for microglia survival but is required for the maintenance of the microglia-specific homeostatic gene signature
    Mesh-Begriff(e) Animals ; Brain/immunology ; Brain/metabolism ; Brain/pathology ; Demyelinating Diseases/immunology ; Demyelinating Diseases/metabolism ; Demyelinating Diseases/pathology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Signal Transduction ; Spinal Cord/immunology ; Spinal Cord/metabolism ; Spinal Cord/pathology ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/metabolism
    Chemische Substanzen Transforming Growth Factor beta
    Sprache Englisch
    Erscheinungsdatum 2018-04-16
    Erscheinungsland United States
    Dokumenttyp Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-018-0091-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Acute treatment with valproic acid and l-thyroxine ameliorates clinical signs of experimental autoimmune encephalomyelitis and prevents brain pathology in DA rats.

    Castelo-Branco, Gonçalo / Stridh, Pernilla / Guerreiro-Cacais, André Ortlieb / Adzemovic, Milena Z / Falcão, Ana Mendanha / Marta, Monica / Berglund, Rasmus / Gillett, Alan / Hamza, Kedir Hussen / Lassmann, Hans / Hermanson, Ola / Jagodic, Maja

    Neurobiology of disease

    2014  Band 71, Seite(n) 220–233

    Abstract: Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the central nervous system (CNS) in young adults. Chronic treatments with histone deacetylase inhibitors (HDACis) have been reported to ameliorate experimental ... ...

    Abstract Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the central nervous system (CNS) in young adults. Chronic treatments with histone deacetylase inhibitors (HDACis) have been reported to ameliorate experimental autoimmune encephalomyelitis (EAE), a rodent model of MS, by targeting immune responses. We have recently shown that the HDAC inhibition/knockdown in the presence of thyroid hormone (T3) can also promote oligodendrocyte (OL) differentiation and expression of myelin genes in neural stem cells (NSCs) and oligodendrocyte precursors (OPCs). In this study, we found that treatment with an HDACi, valproic acid (VPA), and T3, alone or in combination, directly affects encephalitogenic CD4+ T cells. VPA, but not T3, compromised their proliferation, while both molecules reduced the frequency of IL-17-producing cells. Transfer of T3, VPA and VPA/T3 treated encephalitogenic CD4+ T cells into naïve rats induced less severe EAE, indicating that the effects of these molecules are persistent and do not require their maintenance after the initial stimuli. Thus, we investigated the effect of acute treatment with VPA and l-thyroxine (T4), a precursor of T3, on myelin oligodendrocyte glycoprotein-induced EAE in Dark Agouti rats, a close mimic of MS. We found that a brief treatment after disease onset led to sustained amelioration of EAE and prevention of inflammatory demyelination in the CNS accompanied with a higher expression of myelin-related genes in the brain. Furthermore, the treatment modulated immune responses, reduced the number of CD4+ T cells and affected the Th1 differentiation program in the brain. Our data indicate that an acute treatment with VPA and T4 after the onset of EAE can produce persistent clinically relevant therapeutic effects by limiting the pathogenic immune reactions while promoting myelin gene expression.
    Mesh-Begriff(e) Analysis of Variance ; Animals ; Brain/drug effects ; Brain/pathology ; CD11b Antigen/metabolism ; CD4-Positive T-Lymphocytes/drug effects ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/etiology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Enzyme Inhibitors/therapeutic use ; Flow Cytometry ; Interleukin-17/metabolism ; Ki-67 Antigen/metabolism ; Myelin Basic Protein/immunology ; Myelin Basic Protein/toxicity ; Peptide Fragments/immunology ; Peptide Fragments/toxicity ; Rats ; Thyroxine/therapeutic use ; Valproic Acid/therapeutic use
    Chemische Substanzen CD11b Antigen ; Enzyme Inhibitors ; Interleukin-17 ; Ki-67 Antigen ; Myelin Basic Protein ; Peptide Fragments ; myelin basic protein 68-88 ; Valproic Acid (614OI1Z5WI) ; Thyroxine (Q51BO43MG4)
    Sprache Englisch
    Erscheinungsdatum 2014-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2014.08.019
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4444: Hefte anzeigen Standort:
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