Glia

Cover image for Vol. 66 Issue 1

Edited By: Bruce R. Ransom and Helmut Kettenmann

Impact Factor: 6.2

ISI Journal Citation Reports © Ranking: 2016: 25/259 (Neurosciences)

Online ISSN: 1098-1136

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2016 Impact Factor:
GLIA is pleased to announce its new Impact Factor is 6.2!

2017 Release of Journal Citation Reports®. Source: Thomson Reuters 2016 Citation Data







Recently Published Articles

  1. Neuregulin-1 promotes remyelination and fosters a pro-regenerative inflammatory response in focal demyelinating lesions of the spinal cord

    Hardeep Kataria, Arsalan Alizadeh, Ghazaleh M. Shahriary, Shekoofeh Saboktakin Rizi, Ryan Henrie, Kallivalappil T. Santhosh, James A. Thliveris and Soheila Karimi-Abdolrezaee

    Version of Record online: 17 NOV 2017 | DOI: 10.1002/glia.23264

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    Main Points

    Neuregulin-1 promotes remyelination in focal demyelinating lesions of spinal cord: We demonstrate that Neuregulin-1 (Nrg-1) is downregulated in lysolecithin induced focal demyelinating lesion of the spinal cord which could be an underlying cause of myelin thinning in remyelinated axons. Restoration of Nrg-1 levels in the demyelinated spinal cord lesions promoted generation and maturation of new oligodendrocytes. Nrg-1 therapy remarkably reduced the expression of oligodendrocyte inhibitory factor Chondroitin sulfate proteoglycans (CSPGs) and promoted a pro-regenerative inflammatory response characterized by induced interleukin-10 (IL-10) expression in LPC-demyelinating lesion. Importantly, Nrg-1 treatment accelerated endogenous remyelination by both oligodendrocyte and Schwann cell populations in LPC demyelinating foci resulting in significant improvement in myelin thickness in newly remyelinated spinal cord axons. Our complimentary in vitro assessments elucidated that Nrg-1 specifically mediates it effects through activation of ErbB2 and ErbB4 receptors. In conclusion, Nrg-1 promotes a pro-regenerative microenvironment that fosters oligodendrocyte replacement and enhances remyelination process in demyelinating lesions of the central nervous system.

  2. A critical role of TRPM2 channel in Aβ42-induced microglial activation and generation of tumor necrosis factor-α

    Sharifah Alawieyah Syed Mortadza, Joan A Sim, Veronika E Neubrand and Lin-Hua Jiang

    Version of Record online: 16 NOV 2017 | DOI: 10.1002/glia.23265

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    Main Points

    • TRPM2 channel is critical for Aβ42-induced microglial activation and generation of TNF-α.
    • PKC/NOX-mediated ROS generation and activation of the PYK2/MEK/ERK signaling pathway mediate Aβ42-induced TRPM2 channel activation.
  3. Sex differences in the phagocytic and migratory activity of microglia and their impairment by palmitic acid

    Natalia Yanguas-Casás, Andrea Crespo-Castrillo, Maria L. de Ceballos, Julie A. Chowen, Iñigo Azcoitia, Maria Angeles Arevalo and Luis M. Garcia-Segura

    Version of Record online: 15 NOV 2017 | DOI: 10.1002/glia.23263

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    Main Points

    • Male microglia in vitro show higher migration but lower phagocytic activity than female microglia in basal conditions and after interferon-γ (IFNγ) stimulation.
    • Palmitic acid abolishes migration and phagocytosis of male and female microglia stimulated with IFNγ.
  4. Microglia from offspring of dams with allergic asthma exhibit epigenomic alterations in genes dysregulated in autism

    Annie Vogel Ciernia, Milo Careaga, Janine M. LaSalle and Paul Ashwood

    Version of Record online: 14 NOV 2017 | DOI: 10.1002/glia.23261

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    Main Points

    • Maternal allergic asthma induces changes in DNA methylation and transcription in juvenile offspring microglia
    • Differentially methylated regions are enriched for functions and transcription factor binding motifs involved in inflammation and microglial development
    • Differentially expressed genes and differentially methylated regions are enriched for genes dysregulated in autism spectrum disorders
  5. Systemic immune-checkpoint blockade with anti-PD1 antibodies does not alter cerebral amyloid-β burden in several amyloid transgenic mouse models

    Martine Latta-Mahieu, Bradford Elmer, Alexis Bretteville, Yaming Wang, Mati Lopez-Grancha, Philippe Goniot, Nicolas Moindrot, Paul Ferrari, Véronique Blanc, Nathalie Schussler, Emmanuel Brault, Valérie Roudières, Véronique Blanchard, Zhi-Yong Yang, Pascal Barneoud, Philippe Bertrand, Bart Roucourt, Sofie Carmans, Astrid Bottelbergs, Liesbeth Mertens, Cindy Wintmolders, Peter Larsen, Caroline Hersley, Tyler McGathey, Margaret M. Racke, Ling Liu, Jirong Lu, Michael J O'Neill, David R. Riddell, Andreas Ebneth, Gary J. Nabel and Laurent Pradier

    Version of Record online: 14 NOV 2017 | DOI: 10.1002/glia.23260

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    Main Points

    • Treatment with anti-PD1 had previously been shown to reduce brain amyloid load in transgenic mice.
    • We failed to reproduce this effect in three different animal models.
    • At this stage, limited evidence supports use of anti-PD1 therapy in Alzheimer's disease.

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