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Journal of Neurochemistry

Cover image for Vol. 129 Issue 6

June 2014

Volume 129, Issue 6

Pages i–viii, 895–1038

  1. Issue Cover

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      Issue Cover (June 2014)

      Version of Record online: 11 JUN 2014 | DOI: 10.1111/jnc.12564

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      Front cover: Primary astrocytes were purified and induced to express mutant human TDP-43. Immunofluorescent staining revealed that mutant human TDP-43 (hTDP43) was robustly expressed in purified astrocytes. Purified astrocytes were plated on 6-well plates and deprived of Dox on day 2 after plating. J. Neurochem. 2014, vol. 129 (6), pp. 932–939.

      Read the full article on doi: 10.1111/jnc.12660

  2. Issue Information

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      Issue Information (pages i–ii)

      Version of Record online: 11 JUN 2014 | DOI: 10.1111/jnc.12565

  3. IN THIS ISSUE

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      In this Issue (pages iii–viii)

      Version of Record online: 11 JUN 2014 | DOI: 10.1111/jnc.12566

  4. EDITORIAL HIGHLIGHT

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      LRRK2: dropping (kinase) inhibitions and seeking an (immune) response (pages 895–897)

      Adamantios Mamais and Mark R. Cookson

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12691

      Read the full articleInterferon-γinduces leucine-rich repeat kinase LRRK2 via extracellular signal-regulated kinase ERK5 in macrophages’ on page 980.

  5. REVIEW ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      Protective and toxic roles of dopamine in Parkinson's disease (pages 898–915)

      Juan Segura-Aguilar, Irmgard Paris, Patricia Muñoz, Emanuele Ferrari, Luigi Zecca and Fabio A. Zucca

      Version of Record online: 18 MAR 2014 | DOI: 10.1111/jnc.12686

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      Dopamine oxidation to dopamine o-quinone, aminochrome and 5,6-indolequinone plays an important role in neurodegeneration in Parkinson's disease since they induce mitochondria and protein degradation dysfunction; formation of neurotoxic alpha synuclein protofibrils and oxidative stress. However, the cells have a protective system against dopamine oxidation composed by dopamine uptake mediated by Vesicular monoaminergic transporter-2 (VMAT-2), neuromelanin formation, two-electron reduction and GSH-conjugation mediated by Glutathione S-transferase M2-2 (GSTM2).

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      Animal models of sports-related head injury: bridging the gap between pre-clinical research and clinical reality (pages 916–931)

      Mariana Angoa-Pérez, Michael J. Kane, Denise I. Briggs, Nieves Herrera-Mundo, David C. Viano and Donald M. Kuhn

      Version of Record online: 19 MAR 2014 | DOI: 10.1111/jnc.12690

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      Sports-related head injury (SRHI) has emerged as a significant public health issue as athletes can develop psychiatric and neurodegenerative disorders later in life. Animal models have always been an integral part of the study of human TBI but few existing methods are valid for studying SRHI. In this review, we propose criteria for effective animal models of SRHI. Movement of the head upon impact is judged to be of primary importance in leading to concussion and persistent CNS dysfunction.

  6. ORIGINAL ARTICLES

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
    1. Gene Regulation & Genetics

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      Profiling the genes affected by pathogenic TDP-43 in astrocytes (pages 932–939)

      Cao Huang, Bo Huang, Fangfang Bi, Linda H. Yan, Jianbin Tong, Jufang Huang, Xu-Gang Xia and Hongxia Zhou

      Version of Record online: 9 FEB 2014 | DOI: 10.1111/jnc.12660

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      Restricted expression of pathogenic TDP-43 in astrocytes causes non-cell-autonomous motor neuron death in transgenic rats. As revealed by microarray assay, pathogenic TDP-43 in astrocytes preferentially altered expression of the genes encoding secretory proteins. Whereas neurotrophic genes were down-regulated, neurotoxic genes were up-regulated. Therefore, TDP-43 pathogenesis is associated with simultaneous induction of neurotoxic genes and repression of neurotrophic genes in astrocytes.

      Cover Image for this issue: doi: 10.1111/jnc.12564.

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      2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice (pages 940–954)

      Eva-Verena Schaible, Julia Windschügl, Wiesia Bobkiewicz, Yordan Kaburov, Larissa Dangel, Tobias Krämer, Changsheng Huang, Anne Sebastiani, Clara Luh, Christian Werner, Kristin Engelhard, Serge C. Thal and Michael K.E. Schäfer

      Version of Record online: 2 APR 2014 | DOI: 10.1111/jnc.12708

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      We examined neuroprotective effects of 2-methoxyestradiol (2ME2) and the hypoxia-inducible factor 1-α (HIF-1α) response following traumatic brain injury in mice. Early 2ME2 administration reduced the secondary brain damage and neuronal HIF-1α probably involving ubiquitin proteasome system-mediated degradation. The up-regulation of neuropathological HIF-1α target genes and pro-apoptotic BNIP3 protein was attenuated. We propose that the inhibition of a maladaptive HIF-1α response may contribute to 2ME2-mediated neuroprotection.

    3. Brain Development & Cell Differentiation

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      Divergent developmental expression and function of the proton-coupled oligopeptide transporters PepT2 and PhT1 in regional brain slices of mouse and rat (pages 955–965)

      Yongjun Hu, Yehua Xie, Richard F. Keep and David E. Smith

      Version of Record online: 20 MAR 2014 | DOI: 10.1111/jnc.12687

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      Developmental gene and protein expression of peptide transporters was evaluated in various regions of rodent brain, along with age-dependent uptake of dipeptide. We found marked changes in protein expression and functional activity of PhT1 and PepT2, the former predominating in adult and the latter in neonate. These developmental changes may markedly impact the neural activity of endogenous and exogenous peptides/mimetics.

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      Matrix metalloproteinase 2 and membrane type 1 matrix metalloproteinase co-regulate axonal outgrowth of mouse retinal ganglion cells (pages 966–979)

      Djoere Gaublomme, Tom Buyens, Lies De Groef, Michelle Stakenborg, Els Janssens, Signe Ingvarsen, Astrid Porse, Niels Behrendt and Lieve Moons

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12703

      Thumbnail image of graphical abstract

      Axonal regeneration in the central nervous system is lacking in adult mammals, thereby impeding recovery from injury to the nervous system. Matrix metalloproteinases (MMPs) constitute a family of zinc-dependent proteases that were sporadically reported to influence axon outgrowth. Inhibition of specific MMPs reduced neurite outgrowth from mouse retinal explants. Our data indicate MMP-2 and MT1-MMP as promising axonal outgrowth-promoting molecules and show a possible link between MMP-2 and β1-integrin in axon outgrowth.

    5. Neuroinflammation & Neuroimmunology

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      Interferon-γ induces leucine-rich repeat kinase LRRK2 via extracellular signal-regulated kinase ERK5 in macrophages (pages 980–987)

      Martin Kuss, Eleni Adamopoulou and Philipp J. Kahle

      Version of Record online: 24 FEB 2014 | DOI: 10.1111/jnc.12668

      Thumbnail image of graphical abstract

      Leucine-rich repeat kinase 2 (LRRK2) is a major risk factor for the development of Parkinson's disease (PD). However, the role of LRRK2 in the affected neurons remains enigmatic. Recently, LRRK2 has been reported to be strongly expressed in the immune system. Here, we demonstrate that LRRK2 is induced by Interferon gamma via extracellular signal-regulated kinase 5 (ERK5) in macrophages, thus providing new insights in LRRK2 and ERK5 biology.

      Read the Editorial Highlight for this article on page 895.

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      Interferon regulatory factor 8 protects against cerebral ischaemic-reperfusion injury (pages 988–1001)

      Mei Xiang, Lang Wang, Sen Guo, Yan-Yun Lu, Hao Lei, Ding-Sheng Jiang, Yan Zhang, Yi Liu, Yan Zhou, Xiao-Dong Zhang and Hongliang Li

      Version of Record online: 13 MAR 2014 | DOI: 10.1111/jnc.12682

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      In the present study, we found that the transcriptional factor IRF8 plays a protective role in the cerebral ischaemic-reperfusion injury by attenuating neuronal apoptosis, oxidative stress and inflammation. Besides the known function of IRF8 in regulating the inflammatory gene expression, we first demonstrated that IRF8 can directly modulate apoptosis and oxidative stress by controlling the relative genes expression.

    7. Molecular Basis of Disease

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      Altered brain protein expression profiles are associated with molecular neurological dysfunction in the PKU mouse model (pages 1002–1012)

      Esther Imperlini, Stefania Orrù, Claudia Corbo, Aurora Daniele and Francesco Salvatore

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12683

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      We identified a set of proteins whose expression is affected by hyperphenylalaninemia. We think that phenylketonuria (PKU) brain dysfunction also depends on reduced Syn2 and Dpysl2 levels, increased Glu2/3 and NR1 levels, and decreased Pkm, Ckb, Pgam1 and Eno1 levels. These findings finally confirm that alteration in synaptic function, in transmission and in energy metabolism underlie brain damage provoked by hyperphenylalaninemias.

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      CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegeneration (pages 1013–1023)

      Jan Liman, Sebastian Deeg, Aaron Voigt, Hannes Voßfeldt, Christoph P. Dohm, André Karch, Jochen Weishaupt, Jörg B. Schulz, Mathias Bähr and Pawel Kermer

      Version of Record online: 24 MAR 2014 | DOI: 10.1111/jnc.12684

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      We propose that increased caspase-dependent cleavage of mutated Ataxin-3, because of missing CDK5 shielding, leads to aggregation and cell death. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. We think that CDK5 functions as a shield against cleavage-induced toxification and thereby is an interesting target for therapeutic intervention in polyQ disease in general.

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      Inhibition of striatal-enriched tyrosine phosphatase 61 in the dorsomedial striatum is sufficient to increased ethanol consumption (pages 1024–1034)

      Emmanuel Darcq, Sami Ben Hamida, Su Wu, Khanky Phamluong, Viktor Kharazia, Jian Xu, Paul Lombroso and Dorit Ron

      Version of Record online: 27 MAR 2014 | DOI: 10.1111/jnc.12701

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      We show that ethanol-mediated inhibition of STEP61 in the DMS leads to Fyn activation and GluN2B phosphorylation. (a) Under basal conditions, active STEP61 inhibits Fyn activity and dephosphorylates GluN2B. (b) Ethanol leads to the phosphorylation of STEP61 on a specific inhibitory site. The inhibition of STEP61 activity contributes to the activation of Fyn in response to ethanol, which, in turn, phosphorylates GluN2B. These molecular adaptations in the DMS promote ethanol drinking.

  7. RETRACTION

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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  8. CORRIGENDUM

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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      Corrigendum (page 1036)

      Version of Record online: 28 APR 2014 | DOI: 10.1111/jnc.12689

      This article corrects:
  9. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. Issue Cover
    3. Issue Information
    4. IN THIS ISSUE
    5. EDITORIAL HIGHLIGHT
    6. REVIEW ARTICLES
    7. ORIGINAL ARTICLES
    8. RETRACTION
    9. CORRIGENDUM
    10. ACKNOWLEDGEMENT OF REVIEWERS
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