Journal of Neurochemistry

Cover image for Vol. 144 Issue 3

Edited By: Jörg Schulz

Impact Factor: 4.083

ISI Journal Citation Reports © Ranking: 2016: 66/259 (Neurosciences); 78/290 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

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    Animal models of Wilson disease

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  4. Microglia modulation through external vagus nerve stimulation in a murine model of Alzheimer's disease

    Robert Kaczmarczyk, Dario Tejera, Bruce J. Simon and Michael T. Heneka

    Version of Record online: 21 FEB 2018 | DOI: 10.1111/jnc.14284

    Thumbnail image of graphical abstract

    Microglia activation plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson's disease and in acute brain trauma, including stroke and traumatic brain injury. Non-invasive vagus nerve stimulation (nVNS) is able to revert the neuroinflammatory phenotype of microglia in a mouse model of AD. nVNS is thought to exert this effect by the release of norepinephrine and acetylcholine from the locus coeruleus and nucleus basalis of Meynert, respectively. nVNS may therefore provide a novel treatment paradigm for neurodegenerative diseases by inducing the neuroprotective action of microglia and suppressing the detrimental release of proinflammatory mediators.

  5. Sphingosine 1-phosphate receptors regulate TLR4-induced CXCL5 release from astrocytes and microglia

    Sinead A. O'Sullivan, Catherine O'Sullivan, Luke M. Healy, Kumlesh K. Dev and Graham K. Sheridan

    Version of Record online: 21 FEB 2018 | DOI: 10.1111/jnc.14313

    Thumbnail image of graphical abstract

    In addition to its immunomodulatory actions, the multiple sclerosis (MS) drug FTY720 binds to membrane sphingosine 1-phosphate (S1P) receptors and regulates the release of inflammatory mediators from glial cells in the central nervous system. In this study, we found that lipopolysaccharide (LPS) induced the release of chemokines, in particular C-X-C motif chemokine 5 (CXCL5), from astrocytes and microglia and that phosphorylated FTY720 (pFTY720) blocks this process. Our data suggest that LPS induces transactivation of glial S1P receptors, in a sphingosine kinase-dependent manner, resulting in chemokine synthesis and that pFTY720 interrupts this signalling cascade by causing intracellular accumulation of membrane S1P1R. Therefore, FTY720's therapeutic effects in MS may include modulation of neuroinflammation through direct regulation of S1PR signalling in astrocytes and microglia.

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