Journal of Neurochemistry

Cover image for Vol. 143 Issue 1

Edited By: Jörg Schulz

Impact Factor: 4.083

ISI Journal Citation Reports © Ranking: 2016: 65/258 (Neurosciences); 77/286 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. You have free access to this content
    Cerebral amyloid angiopathy as a cause of neurodegeneration

    Eric E. Smith

    Version of Record online: 21 SEP 2017 | DOI: 10.1111/jnc.14157

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    Sporadic, age-related cerebral amyloid angiopathy (CAA), caused by vascular Aβ deposition, is most commonly recognized clinically as a cause of hemorrhagic stroke. This review synthesizes emerging evidence that CAA is associated with cardinal features of neurodegeneration – atrophy and cognitive impairment – and highlights multiple pathomechanisms of brain injury that may cause cognitive impairment in this disease.

  2. Corticosterone and exogenous glucose alter blood glucose levels, neurotoxicity, and vascular toxicity produced by methamphetamine

    John F. Bowyer, Karen M. Tranter, Sumit Sarkar, Nysia I. George, Joseph P. Hanig, Kimberly A. Kelly, Lindsay T. Michalovicz, Diane B. Miller and James P. O'Callaghan

    Version of Record online: 21 SEP 2017 | DOI: 10.1111/jnc.14143

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    This study evaluated exogenous glucose and corticosterone pretreatment to methamphetamine on blood glucose levels and neural/vascular toxicity. Methamphetamine with saline, glucose, or corticosterone had significantly higher glucose levels. Methamphetamine+corticosterone and methamphetamine+glucose mortality rates were substantially higher than methamphetamine. Methamphetamine+corticosterone significantly increased neurodegeneration above other treatments. Neuroinflammation (microglial activation) was associated with degenerating neurons and largely surrounded vasculature after methamphetamine, an effect exacerbated by corticosterone pretreatment. Our findings implicate elevated glucose levels and hyperthermia in methamphetamine-induced neurotoxicity, neurovascular damage, and lethality.

  3. You have free access to this content
    Epigenetics and DNA methylomic profiling in Alzheimer's disease and other neurodegenerative diseases

    Janou A. Y. Roubroeks, Rebecca G. Smith, Daniel L. A. van den Hove and Katie Lunnon

    Version of Record online: 21 SEP 2017 | DOI: 10.1111/jnc.14148

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    Epigenetic mechanisms have been hypothesized to play a role in a number of different neurodegenerative diseases, such as Alzheimer's disease, Huntington's disease, Parkinson's disease and amyotrophic lateral sclerosis. In this review, we provide an overview of current studies performed in the field, with a focus on DNA methylation, before discussing the potential direction of future studies.

  4. Sigma-1 receptor ligands inhibit catecholamine secretion from adrenal chromaffin cells due to block of nicotinic acetylcholine receptors

    Rebecca L. Brindley, Mary Beth Bauer, Nolan D. Hartley, Kyle J. Horning and Kevin P.M. Currie

    Version of Record online: 19 SEP 2017 | DOI: 10.1111/jnc.14149

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    Sigma-1 receptors are intracellular chaperone proteins that can translocate to the plasma membrane to modulate various ion channels and cellular functions. We investigated the impact of several sigma-1 receptor ligands including fluvoxamine (a selective serotonin reuptake inhibitor) on catecholamine secretion from adrenal chromaffin cells. Our data suggest that sigma-1 receptors do not acutely regulate catecholamine secretion. Rather, sigma-1 receptor ligands inhibited secretion evoked by cholinergic stimulation because of direct block of Ca2+entry via nicotinic acetylcholine receptors.

  5. Transcriptional profiling of human neural precursors post alcohol exposure reveals impaired neurogenesis via dysregulation of ERK signaling and miR-145

    Lithin K. Louis, Renjitha Gopurappilly, Harshini Surendran, Sunit Dutta and Rajarshi Pal

    Version of Record online: 19 SEP 2017 | DOI: 10.1111/jnc.14155

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    Gestational alcohol exposure causes a range of neuropsychological disorders, but lack of relevant model poses serious limitations toward understanding such defects. Our data unveil that EtOH perturbs MAPK/ERK signaling accompanied by deregulation of miR-145 targeting the neural specifier Sox-2 causing compromised neuronal complexity resulting in abnormal neurogenesis. Employing molecular endpoints in humanized model, we show for the first time that acute alcohol exposure could lead to impaired brain development.

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