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

  1. You have free access to this content
    Mitochondrial function and autophagy: integrating proteotoxic, redox, and metabolic stress in Parkinson's disease

    Jianhua Zhang, Matilda Lillian Culp, Jason G. Craver and Victor Darley-Usmar

    Version of Record online: 14 FEB 2018 | DOI: 10.1111/jnc.14308

    Thumbnail image of graphical abstract

    This review provides highlights on recent observations regarding the multifacet impact of pathological proteins, endogenously produced reactive species, environmental toxins, and metabolism including glucose and fatty acid metabolism, on mitochondria – autophagy function, in the context of Parkinson's disease. The review also discusses future studies of designing targeted strategies to aid the treatment of Parkinson's disease.

  2. Palmitate-induced C/EBP homologous protein activation leads to NF-κB-mediated increase in BACE1 activity and amyloid beta genesis

    Gurdeep Marwarha, Jared Schommer, Jonah Lund, Trevor Schommer and Othman Ghribi

    Version of Record online: 14 FEB 2018 | DOI: 10.1111/jnc.14292

    Thumbnail image of graphical abstract

    The mechanisms that underlie the palmitate-enriched diet-induced increase in amyloid beta (Aβ) burden in the brain and subsequent increase in the risk of Alzheimer's disease are poorly comprehended. Herein, we show that palmitate-enriched diet causes C/EBP homologous protein (CHOP) activation resulting in an increase in NF-κB transcriptional activity mediated transactivation of the β-site APP cleaving enzyme 1 (BACE1) promoter. The ensuing increase in BACE1 protein levels and BACE1 enzymatic activity results in a significant increase in Aβ genesis and augmentation in the neurodegenerative cascade inherent in Alzheimer's disease.

  3. A dual role for Integrin α6β4 in modulating hereditary neuropathy with liability to pressure palsies

    Yannick Poitelon, Vittoria Matafora, Nicholas Silvestri, Desirée Zambroni, Claire McGarry, Nora Serghany, Thomas Rush, Domenica Vizzuso, Felipe A. Court, Angela Bachi, Lawrence Wrabetz and Maria Laura Feltri

    Version of Record online: 13 FEB 2018 | DOI: 10.1111/jnc.14295

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    Laminin receptor integrin α6β4 modulates peripheral myelin protein 22 (PMP22) neuropathy. In this study, we employed biochemical and genetic studies to shed light on the relationship between PMP22 and signaling from the Schwann cell extracellular matrix. We demonstrate that ablation of β4 integrin delays the progression of Hereditary Neuropathy with Pressure Palsy (HNPP), but also causes a reduction in the speed of action potential propagation in HNPP animals. These findings suggest that in HNPP, integrin α6β4 has opposing effects on two distinct pathomechanisms, i.e. the formation of tomacula and the propagation of action potentials.

  4. Stress-induced tRNA cleavage and tiRNA generation in rat neuronal PC12 cells

    Elkordy Alaa, Eikan Mishima, Kuniyasu Niizuma, Yasutoshi Akiyama, Miki Fujimura, Teiji Tominaga and Takaaki Abe

    Accepted manuscript online: 12 FEB 2018 09:35AM EST | DOI: 10.1111/jnc.14321

  5. You have full text access to this OnlineOpen article
    Bidirectional variation in glutamate efflux in the medial prefrontal cortex induced by selective positive and negative allosteric mGluR5 modulators

    Sarah N. Isherwood, Trevor W. Robbins, Jeffrey W. Dalley and Anton Pekcec

    Version of Record online: 12 FEB 2018 | DOI: 10.1111/jnc.14290

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    NMDA-receptor-dependent abnormal prefrontal glutamatergic signalling is linked to neuropsychiatric disorders. Although NMDA receptors interact with mGluR5, the consequence on glutamate efflux remains unknown. We demonstrate that mGluR5-positive allosteric modulation (PAM) increased prefrontal glutamate efflux and potentiated the effect of NMDA receptor antagonism, whereas negative allosteric modulation (NAM) decreased this measure. These agents may correct glutamatergic abnormalities clinically.

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