Journal of Neurochemistry

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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
    γ-Secretase in microglia – Implications for neurodegeneration and neuroinflammation

    Jochen Walter, Nadja Kemmerling, Patrick Wunderlich and Konstantin Glebov

    Accepted manuscript online: 23 SEP 2017 03:50AM EST | DOI: 10.1111/jnc.14224

  2. Activation of the NLRP3 inflammasome in microglia: The role of ceramide

    Hannah Scheiblich, Anna Schlütter, Douglas T. Golenbock, Eicke Latz, Pilar Martinez-Martinez and Michael T. Heneka

    Accepted manuscript online: 23 SEP 2017 03:50AM EST | DOI: 10.1111/jnc.14225

  3. Telomerase reverse transcriptase (TERT) - enhancer of zeste homolog 2 (EZH2) network regulates lipid metabolism and DNA damage responses in glioblastoma

    Fahim Ahmad, Shruti Patrick, Touseef Sheikh, Vikas Sharma, Pankaj Pathak, Prit Benny Malgulwar, Anupam Kumar, Shanker Datt Joshi, Chitra Sarkar and Ellora Sen

    Version of Record online: 22 SEP 2017 | DOI: 10.1111/jnc.14152

    Thumbnail image of graphical abstract

    Mutation in telomerase reverse transcriptase (TERT) promoter correlates with poor prognosis in glioblastoma (GBM). As elevated enhancer of zeste homolog 2 (EZH2) and fatty acid synthase (FASN) levels were accompanied by heightened microsatellite instability in TERT-mutant GBMs, their correlations were investigated. Genetic and pharmacological manipulation of TERT indicated the importance of TERT–EZH2 axis in regulating lipid metabolism and ataxia-telangiectasia-mutated (ATM) activation. This study provides better understanding of aberrant metabolic programming in GBM based on distinctive genetic alterations.

  4. 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.

  5. 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.