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Journal of Neurochemistry

Cover image for Vol. 127 Issue 6

December 2013

Volume 127, Issue 6

Pages i–xiii, 733–893

  1. IN THIS ISSUE

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
      In this Issue (pages i–xiii)

      Version of Record online: 3 DEC 2013 | DOI: 10.1111/jnc.12525

  2. SHORT COMMUNICATION

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. Molecular Basis of Disease

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      Specific changes of sulfatide levels in individuals with pre-clinical Alzheimer's disease: an early event in disease pathogenesis (pages 733–738)

      Hua Cheng, Miao Wang, Jian-Liang Li, Nigel J. Cairns and Xianlin Han

      Version of Record online: 29 JUL 2013 | DOI: 10.1111/jnc.12368

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      To determine lipid changes at the stage of pre-clinical Alzheimer's disease (AD) (i.e., cognitively normal at death, but with AD neuropathology), we performed lipidomics analysis and found that sulfatide levels were significantly lower in subjects with pre-clinical AD compared to those without AD neuropathology. The results suggest that sulfatide loss is among the earliest events of AD development.

  3. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. Gene Regulation & Genetics

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      Alternative polyadenylation and miR-34 family members regulate tau expression (pages 739–749)

      John R. Dickson, Carla Kruse, Daniel R. Montagna, Bente Finsen and Michael S. Wolfe

      Version of Record online: 18 SEP 2013 | DOI: 10.1111/jnc.12437

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      mRNA 3'-untranslated regions (3'-UTR) often regulate transcript stability or translation. Despite the centrality of the tau protein in Alzheimer's and other neurodegenerative diseases, the human tau 3'-UTR has been little studied. This report identifies regions of the tau 3'-UTR that influence expression and shows that microRNA (miR)-34a targets this 3'-UTR to lower expression, which is considered an important therapeutic goal.

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      Genetic variation at the delta-sarcoglycan (SGCD) locus elevates heritable sympathetic nerve activity in human twin pairs (pages 750–761)

      C. Makena Hightower, Kuixing Zhang, José P. Miramontes-González, Fangwen Rao, Zhiyun Wei, Andrew J. Schork, Caroline M. Nievergelt, Nilima Biswas, Manjula Mahata, Nina Elkelis, Laurent Taupenot, Mats Stridsberg, Michael G. Ziegler and Daniel T. O'Connor

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12346

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      We propose the following to describe effects of human delta-sarcoglycan (SGCD) variation on sympathetic and cardio-metabolic traits. SGCD variation alters expression, major allele A to minor allele G, augmenting sympathochromaffin norepinephrine (NE) and CHGB release. Increased plasma NE negatively impacts systemic vascular compliance, while mobilizing free fatty acids. Common variation gives rise to phenotypic consequences and without apparent myocardial involvement.

    3. Signal Transduction & Synaptic Transmission

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      Long-term nicotine treatment down-regulates α6β2* nicotinic receptor expression and function in nucleus accumbens (pages 762–771)

      Xiomara A. Perez, J.Michael McIntosh and Maryka Quik

      Version of Record online: 13 OCT 2013 | DOI: 10.1111/jnc.12442

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      Long-term nicotine treatment decreases dopamine (DA) transmission in the mesolimbic dopaminergic system. Our data suggest this may involve a decrease in α6β2* nicotinic receptor expression and function. These changes may play a key role in nicotine reward and dependence.

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      c-Jun N-terminal kinase regulates mGluR-dependent expression of post-synaptic FMRP target proteins (pages 772–781)

      Travis L. Schmit, James A. Dowell, Margaret E. Maes and Michael Wilhelm

      Version of Record online: 24 OCT 2013 | DOI: 10.1111/jnc.12453

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      Expression of many FMRP target proteins is enhanced in FXS. Here, we evaluated the role of JNKs in FXS. We found that JNK signaling is activated upon mGluR stimulation in wild-type neurons. Conversely, JNK activity is basally elevated in fmr1 knockout. Inhibiting JNK reduced the expression of FMRP target proteins and driving JNK activity increased the expression of these proteins.

    5. Bioenergetics & Metabolism

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      Probenecid potentiates MPTP/MPP+ toxicity by interference with cellular energy metabolism (pages 782–792)

      Daniel Alvarez-Fischer, Carmen Noelker, Anne Grünewald, Franca Vulinović, Serge Guerreiro, Julia Fuchs, Lixia Lu, Anne Lombès, Etienne C. Hirsch, Wolfgang H. Oertel, Patrick P. Michel and Andreas Hartmann

      Version of Record online: 8 JUL 2013 | DOI: 10.1111/jnc.12343

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      We showed in the present study that probenecid lowers the intra-cellular ATP production by interfering with the cellular metabolism (black and green arrows). We excluded an altered MPP+ uptake via dopamine transporter (DAT) (blue arrow) or a disturbed glycolysis pathway as cause of the potentiated MPP+ toxicity and showed an indirect reduction in the Complex I activity. We therefore hypothesize (red dotted lines) that probenecid acts either by altering substrate oxidation downstream of pyruvate or by influencing the citric acid cycle. We showed that deleterious effects of probenecid can be reversed by extra-cellular ATP (red arrows).

  4. THIS ARTICLE HAS BEEN RETRACTED

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
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      Retracted: Superoxide-dependent uptake of vitamin C in human glioma cells (pages 793–804)

      Federico S. Rodríguez, Katterine A. Salazar, Nery A. Jara, María A García-Robles, Fernando Pérez, Luciano E. Ferrada, Fernando Martínez and Francisco J. Nualart

      Version of Record online: 19 AUG 2013 | DOI: 10.1111/jnc.12365

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      This study strongly suggests that the Bystander effect, that is, glioma cell interaction with oxidant-producing microglia, could be an important mechanism for glioma vitamin C loading in the absence of functional sodium-vitamin C cotransporter 2 (SVCT2) expression. The high cellular vitamin C load in glioma cells results from a high uptake of extracellular dehydroascorbic acid (DHA) generated by neighboring microglia. This Bystander effect may explain the high antioxidative potential observed in high-grade gliomas, considering that high-grade gliomas may be the only neoplasm where oxidant-producing microglia can almost equal the number of tumor cells.

      Corrected by:

      Retraction: Retraction

      Vol. 133, Issue 6, 935, Version of Record online: 27 MAY 2015

  5. ORIGINAL ARTICLES

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. Brain Development & Cell Differentiation

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      Purine metabolism during neuronal differentiation: the relevance of purine synthesis and recycling (pages 805–818)

      Martin Göttle, Heike Burhenne, Diane Sutcliffe and H. A. Jinnah

      Version of Record online: 18 AUG 2013 | DOI: 10.1111/jnc.12366

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      Differentiation of dopaminergic PC6-3 cells is accompanied by increased purine pools and energy state. The lack of a functional purine recycling pathway causes purine limitation in both undifferentiated and differentiated cells, as well as profound loss of dopamine content. The results imply an unknown mechanism by which intracellular purine levels regulate dopamine levels.

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      The notch signaling pathway: its role in focal CNS demyelination and apotransferrin-induced remyelination (pages 819–836)

      Evangelina Aparicio, Patricia Mathieu, Milagros Pereira Luppi, María Florencia Almeira Gubiani and Ana María Adamo

      Version of Record online: 18 OCT 2013 | DOI: 10.1111/jnc.12440

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      Evidence of the participation of Notch signaling in the demyelination/remyelination process will help further understand demyelinating disorders such as Multiple Sclerosis and the use of aTf should be taken into consideration as a possible therapeutic intervention.

    3. Molecular Basis of Disease

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      Dopaminergic neurotoxicity of S-ethyl N,N-dipropylthiocarbamate (EPTC), molinate, and S-methyl-N,N-diethylthiocarbamate (MeDETC) in Caenorhabditis elegans (pages 837–851)

      Samuel W. Caito, William M. Valentine and Michael Aschner

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/jnc.12349

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      A correlation exists between pesticide use and Parkinson's disease. We investigated the ability of thiocarbamate pesticides to induce dopaminergic neurodegeneration in Caenorhabditis elegans. Treatment with thiocarbamates led to selective loss of dopaminergic cell morphology, and decreased dopamine content and dopaminergic-dependent behavior. Our data suggest that thiocarbamate pesticides may be environmental risk factors for Parkinson's disease.

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      Age-dependent alterations of the kynurenine pathway in the YAC128 mouse model of Huntington disease (pages 852–867)

      Gelareh Mazarei, David P. Budac, Ge Lu, Hans Adomat, Emma S. Tomlinson Guns, Thomas Möller and Blair R. Leavitt

      Version of Record online: 14 JUL 2013 | DOI: 10.1111/jnc.12350

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      We propose that induction of indoleamine 2,3 dioxygenase (Ido1) expression and activity in the striatum by mutant huntingtin (mHTT) plays a central role in the observed imbalance of downstream kynurenine (Kyn) pathway metabolites. This imbalance, and altered transport of kynurenine pathway metabolites through the blood brain barrier (BBB) from blood to CNS, may result in increased sensitivity of striatal neurons to glutamate toxicity in Huntington disease.

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      Retinitis Pigmentosa: over-expression of anti-ageing protein Klotho in degenerating photoreceptors (pages 868–879)

      Pietro Farinelli, Blanca Arango-Gonzalez, Jakob Völkl, Ioana Alesutan, Florian Lang, Eberhart Zrenner, François Paquet-Durand and Per A.R. Ekström

      Version of Record online: 22 JUL 2013 | DOI: 10.1111/jnc.12353

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      Retinitis Pigmentosa (RP) involves a hereditary degeneration of photoreceptors. Here, we demonstrate an over-expression of the anti-ageing protein Klotho in several rodent Retinitis Pigmentosa models. The over-expression of the protein is also shown to be linked to the degeneration of photoreceptors. In summary, our work suggests Klotho as a novel player in the retina, with a clear connection to photoreceptor cell death as well as with an influence on retinal organization.

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      Critical role of calpain in spinal cord degeneration in Parkinson's disease (pages 880–890)

      Supriti Samantaray, Varduhi H. Knaryan, Donald C. Shields and Naren L. Banik

      Version of Record online: 20 AUG 2013 | DOI: 10.1111/jnc.12374

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      We proposed calpain over-activation and calpain-calpastatin dysregulation driving in a cascade of inflammatory responses (microglial activation and T cell infiltration) and degenerative pathways culminating in axonal degeneration and neuronal death in spinal cord of Parkinson's disease patients. This may be one of the crucial mechanisms in the degenerative process.

  6. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. IN THIS ISSUE
    3. SHORT COMMUNICATION
    4. ORIGINAL ARTICLES
    5. THIS ARTICLE HAS BEEN RETRACTED
    6. ORIGINAL ARTICLES
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content

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