Journal of Neurochemistry

Cover image for Vol. 129 Issue 3

Edited By: Jörg Schulz

Impact Factor: 3.973

ISI Journal Citation Reports © Ranking: 2012: 71/252 (Neurosciences); 83/290 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. Evidence for an angiotensin-(1-7) neuropeptidase expressed in the brain medulla and CSF of sheep

    Allyson C. Marshall, Nancy T. Pirro, James C. Rose, Debra I. Diz and Mark C. Chappell

    Article first published online: 19 APR 2014 | DOI: 10.1111/jnc.12720

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    Angiotensin-(1-7) actions are mediated by the AT7/Mas receptor and include reduced blood pressure, decreased oxidative stress, enhanced baroreflex sensitivity, and increased nitric oxide (NO). Ang-(1-7) is directly formed from Ang I by neprilysin (NEP). We identify a new pathway for Ang-(1-7) metabolism in the brain distinct from angiotensin-converting enzyme-dependent hydrolysis. The Ang-(1-7) endopeptidase (A7-EP) degrades the peptide to Ang-(1-4) and may influence central Ang-(1-7) tone.

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    Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects

    Robert Vassar, Peer-Hendrik Kuhn, Christian Haass, Matthew E. Kennedy, Lawrence Rajendran, Philip C. Wong and Stefan F. Lichtenthaler

    Article first published online: 19 APR 2014 | DOI: 10.1111/jnc.12715

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    The protease BACE1 is a major drug target in Alzheimer disease. Together with its homolog BACE2, both proteases have an increasing number of functions within and outside of the nervous system. This review highlights recent progress in understanding cell biology, substrates, and functions of BACE proteases and discusses the therapeutic options and potential mechanism-based liabilities, in particular for BACE inhibitors in Alzheimer disease.

  3. HIV-1 protein Tat produces biphasic changes in NMDA-evoked increases in intracellular Ca2+ concentration via activation of Src kinase and nitric oxide signaling pathways

    Kelly A. Krogh, Nicole Wydeven, Kevin Wickman and Stanley A. Thayer

    Article first published online: 19 APR 2014 | DOI: 10.1111/jnc.12724

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    HIV-associated neurocognitive disorders (HAND) afflict about half of HIV-infected patients. HIV-infected cells shed viral proteins, such as the transactivator of transcription (Tat), which can cause neurotoxicity by over activation of NMDA receptors (NMDARs). We show that HIV-1 Tat evoked biphasic changes in NMDA-evoked [Ca2+]i responses. Initially, Tat potentiated NMDA-evoked responses following LRP-mediated activation of Src kinase. Subsequently, Tat-induced NMDAR potentiation adapted by activation of a NOS/sGC/PKG pathway that attenuated NMDA-evoked increases in [Ca2+]i. Adaptation may be a novel neuroprotective mechanism to prevent excessive Ca2+ influx. Solid and dashed arrows represent direct and potentially indirect connections, respectively.

  4. Impairments of long-term depression induction and motor coordination precede Aβ accumulation in the cerebellum of APPswe/PS1dE9 double transgenic mice

    Yuki Kuwabara, Masato Ishizeki, Naoto Watamura, Junya Toba, Aya Yoshii, Takafumi Inoue and Toshio Ohshima

    Article first published online: 19 APR 2014 | DOI: 10.1111/jnc.12728

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    APPswe/PS1d9E mice, a commonly used Alzheimer's mouse model, have Aβ plaques in the cerebellum after 8 months old. We show that soluble Aβ impairs LTD induction in the cerebellar slice. APPswe/PS1d9E mice demonstrate defects of motor coordination and LTD induction in the cerebellum at the pre-Aβ accumulation period.

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