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Licensed Unlicensed Requires Authentication Published by De Gruyter August 16, 2013

Molecular triggers of neuroinflammation in mouse models of demyelinating diseases

  • Benoit Barrette

    Benoit Barrette finished his PhD in 2008 at the CHUL research center (Quebec city, Canada) under the supervision of Steve Lacroix, professor at the department of Neurosciences (Université Laval). He studied Schwann cell neuroinflammatory molecular triggers released during wallerian degeneration and could demonstrate that inflammatory response is required to support the axonal regeneration after a peripheral nerve injury. He joined the Klaus-Armin Nave’s laboratory as a post-doc to work with the first mouse model in which inflammatory demyelination and lymphocyte infiltration is caused by a primary oligodendrocyte defect impairing the peroxisome biogenesis. By using this model, his task is to decipher the role played by the different lymphocyte populations and the innate immune response in the neuropathology’s progression.

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    , Klaus-Armin Nave

    Klaus-Armin Nave is director of the Department of Neurogenetics at the Max-Planck-Institute of Experimental Medicine in Goettingen, Germany. He obtained his PhD from U.C. San Diego and completed a post-doctoral fellowship at the Salk Institute. His research focus is on mechanisms of myelination and mouse models of human myelin diseases. His specific interest is the role of oligodendrocytes in maintaining axonal integrity, a function that is independent of myelination.

    and Julia M. Edgar

    Julia Edgar is a lecturer in the Institute of Infection, Immunity and Inflammation at the University of Glasgow and associate member of the Department of Neurogenetics at the Max Planck Institute of Experimental Medicine in Goettingen, Germany. She obtained her PhD from the University of Edinburgh in 1999 and undertook her post-doctoral training in the laboratory of Ian Griffiths at the University of Glasgow. She is interested in how disorders of the central nervous system myelin sheath affect axonal health and in particular, how the oligodendrocyte exerts axonal protection.

From the journal Biological Chemistry

Abstract

Myelinating cells wrap axons with multi-layered myelin sheaths for rapid impulse propagation. Dysfunctions of oligodendrocytes or Schwann cells are often associated with neuroinflammation, as observed in animal models of leukodystrophies and peripheral neuropathies, respectively. The neuroinflammatory response modulates the pathological changes, including demyelination and axonal injury, but also remyelination and repair. Here we discuss different immune mechanisms as well as factors released or exposed by myelinating glia in disease conditions. The spectrum of inflammatory mediators varies with different myelin disorders and has a major impact on the beneficial or detrimental role of immune cells in keeping nervous system integrity.


Corresponding author: Benoit Barrette, Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Hermann-Rein Strasse 3, Goettingen, D-37075, Germany, e-mail:

About the authors

Benoit Barrette

Benoit Barrette finished his PhD in 2008 at the CHUL research center (Quebec city, Canada) under the supervision of Steve Lacroix, professor at the department of Neurosciences (Université Laval). He studied Schwann cell neuroinflammatory molecular triggers released during wallerian degeneration and could demonstrate that inflammatory response is required to support the axonal regeneration after a peripheral nerve injury. He joined the Klaus-Armin Nave’s laboratory as a post-doc to work with the first mouse model in which inflammatory demyelination and lymphocyte infiltration is caused by a primary oligodendrocyte defect impairing the peroxisome biogenesis. By using this model, his task is to decipher the role played by the different lymphocyte populations and the innate immune response in the neuropathology’s progression.

Klaus-Armin Nave

Klaus-Armin Nave is director of the Department of Neurogenetics at the Max-Planck-Institute of Experimental Medicine in Goettingen, Germany. He obtained his PhD from U.C. San Diego and completed a post-doctoral fellowship at the Salk Institute. His research focus is on mechanisms of myelination and mouse models of human myelin diseases. His specific interest is the role of oligodendrocytes in maintaining axonal integrity, a function that is independent of myelination.

Julia M. Edgar

Julia Edgar is a lecturer in the Institute of Infection, Immunity and Inflammation at the University of Glasgow and associate member of the Department of Neurogenetics at the Max Planck Institute of Experimental Medicine in Goettingen, Germany. She obtained her PhD from the University of Edinburgh in 1999 and undertook her post-doctoral training in the laboratory of Ian Griffiths at the University of Glasgow. She is interested in how disorders of the central nervous system myelin sheath affect axonal health and in particular, how the oligodendrocyte exerts axonal protection.

We thank Dr. Rudolf Martini for many helpful discussions and Dr. Stefan Nessler for comments on the manuscript. B.B. was supported by a postdoctoral fellowship from the Multiple Sclerosis Society of Canada and the Deutsche Forschungsgemeinschaft (SFB/TR43). J.M.E. was supported by an ERC Advanced Grant to K.A.N.

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Received: 2013-7-10
Accepted: 2013-8-15
Published Online: 2013-08-16
Published in Print: 2013-12-01

©2013 by Walter de Gruyter Berlin Boston

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