Journal of Neurochemistry

Cover image for Vol. 139 Issue 5

Edited By: Jörg Schulz

Impact Factor: 3.842

ISI Journal Citation Reports © Ranking: 2015: 71/256 (Neurosciences); 83/289 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. Fabp1 gene ablation inhibits high-fat diet-induced increase in brain endocannabinoids

    Gregory G. Martin, Danilo Landrock, Sarah Chung, Lawrence J. Dangott, Drew R. Seeger, Eric J. Murphy, Mikhail Y. Golovko, Ann B. Kier and Friedhelm Schroeder

    Version of Record online: 29 NOV 2016 | DOI: 10.1111/jnc.13890

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    Fatty acid binding protein-1 (FABP-1) is not detectable in brain but is highly expressed in liver. FABP-1 null (LKO) male mice on control, but not high-fat, diet had increased brain levels of arachidonic acid-containing endocannabinoids (AEA, 2-AG), correlating with increased free and total arachidonic acid in brain and serum; however, this dietary phenomenon was not observed in female LKO.

  2. You have full text access to this OnlineOpen article
    Rifampicin attenuates experimental autoimmune encephalomyelitis by inhibiting pathogenic Th17 cells responses

    Ke Ma, Xi Chen, Jia-Cheng Chen, Ying Wang, Xi-meng Zhang, Fan Huang, Jun-Jiong Zheng, Xiong Chen, Wei Yu, Ke-Ling Cheng, Yan-Qing Feng and Huai-yu Gu

    Version of Record online: 29 NOV 2016 | DOI: 10.1111/jnc.13871

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    Rifampicin, a broad-spectrum antibiotic, has neuroprotective, immunosuppressive, and anti-inflammatory properties. However, the effect of rifampicin on autoimmune disorders of the nervous system is not clear. In this study, we investigated whether rifampicin was beneficial to myelin oligodendrocyte glycoprotein peptide (MOG33–35)-induced experimental autoimmune encephalomyelitis (EAE) mice, the well-established animal model of multiple sclerosis (MS). We discovered that rifampicin is effective for attenuating the clinical severity of EAE. Our findings may be helpful for developing the therapeutic and preventive strategies for MS.

  3. Cerebrospinal fluid biomarkers as a measure of disease activity and treatment efficacy in relapsing-remitting multiple sclerosis

    Lenka Novakova, Markus Axelsson, Mohsen Khademi, Henrik Zetterberg, Kaj Blennow, Clas Malmeström, Fredrik Piehl, Tomas Olsson and Jan Lycke

    Version of Record online: 29 NOV 2016 | DOI: 10.1111/jnc.13881

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    CSF biomarkers reflect different aspects of the pathophysiology of multiple sclerosis. The present study investigated the influence of interferon beta and natalizumab on seven biomarkers and their correlation with clinical and radiological outcomes. The results indicate that CSF levels of neurofilament light protein (NFL), C-X-C motif chemokine 13 (CXCL13), chitinase-3-like protein 1 (CHI3L1), and chitotriosidase (CHIT1) correlate with the clinical and/or radiological disease activity, providing additional dimensions in the assessment of treatment efficacy.

  4. Role of a heterotrimeric G-protein, Gi2, in the corticogenesis: possible involvement in periventricular nodular heterotopia and intellectual disability

    Nanako Hamada, Yutaka Negishi, Makoto Mizuno, Fuyuki Miya, Ayako Hattori, Nobuhiko Okamoto, Mitsuhiro Kato, Tatsuhiko Tsunoda, Mami Yamasaki, Yonehiro Kanemura, Kenjiro Kosaki, Hidenori Tabata, Shinji Saitoh and Koh-ichi Nagata

    Version of Record online: 29 NOV 2016 | DOI: 10.1111/jnc.13878

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    We propose the role of a heterotrimeric G-protein, Gi2, in the brain development. We then identified a de novo heterozygous missense mutation of the α-subunit, GNAI2, in a patient with periventricular nodular heterotopia and intellectual disability. Although pathophysiological significance of this mutation remains to be clarified, gene abnormalities of GNAI2 might be involved in the pathogenesis of neurodevelopmental disorders.

  5. Pasireotide prevents nuclear factor of activated T cells nuclear translocation and acts as a protective agent in aminoglycoside-induced auditory hair cell loss

    Daniel Bodmer, Adrijana Perkovic, Marijana Sekulic-Jablanovic, Matthew B. Wright and Vesna Petkovic

    Version of Record online: 29 NOV 2016 | DOI: 10.1111/jnc.13880

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    Aminoglycosides such as gentamicin trigger a calcium ion influx (Ca2+) that activates pro-apoptotic signaling cascades in auditory hair cells (HCs). Pasireotide inhibits Ca2+ channel activity, preventing the accumulation of cellular Ca2+ provoked by gentamicin, thereby preventing the downstream events that culminate in nuclear factor of activated T cells (NFAT) activation. The cell-permeable peptide 11R-VIVIT interrupts the same pathway by binding to Calcineurin (CaN), selectively blocking its ability to activate NFAT. Our discovery of the protective effects of pasireotide and 11R-VIVIT, together with the characterization of their mechanism of action, suggests how we can rapidly reformulate a well-known drug for entry into clinical trials as a potential new therapy for hearing loss.

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