Journal of Neurochemistry

Cover image for Vol. 143 Issue 2

Early View (Online Version of Record published before inclusion in an issue)

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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  1. Original Articles

    1. Role of the GM1 ganglioside oligosaccharide portion in the TrkA-dependent neurite sprouting in neuroblastoma cells

      Elena Chiricozzi, Diego Yuri Pomè, Margherita Maggioni, Erika Di Biase, Chiara Parravicini, Luca Palazzolo, Nicoletta Loberto, Ivano Eberini and Sandro Sonnino

      Version of Record online: 13 SEP 2017 | DOI: 10.1111/jnc.14146

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      GM1 ganglioside (II3Neu5Ac-Gg4Cer) is known to promote neurite formation in neuroblastoma cells like N2a cells by activating TrkA-MAPK pathway. This study shows that GM1 modulates TrkA activity by stabilizing the TrkA-NGF complex with its oligosaccharide portion. The complex induces the TrkA phosphorylation and MAPK-pathway activation, triggering the differentiation signaling. These findings provide a new view for the role of the oligosaccharide chain of gangliosides in plasma membrane signaling.

    2. Enhanced motivation to alcohol in transgenic mice expressing human α-synuclein

      Carola Rotermund, Gustavo K. Reolon, Sarah Leixner, Cindy Boden, Ainhoa Bilbao and Philipp J. Kahle

      Version of Record online: 12 SEP 2017 | DOI: 10.1111/jnc.14151

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      α-Synuclein (αSYN) is known for its implication with Parkinson's disease. Moreover, αSYN is becoming recognized for an involvement in alcoholism, both in animal models and human patients. We tested whether transgenic over-expression of αSYN in mice would affect responses to ethanol. Indeed, αSYN transgenic mice had a higher motivation for ethanol. Also, ethanol injections caused higher induction of pCREB in brain regions involved in alcohol addictive behavior. This study lends further support to the linkage of αSYN to alcoholism.

  2. Reviews

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      Dementia risk and prevention by targeting modifiable vascular risk factors

      Sana Tariq and Philip A. Barber

      Version of Record online: 6 SEP 2017 | DOI: 10.1111/jnc.14132

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      Vascular risk factors through their interaction with genetic susceptibility and the environment result in vessel wall damage, which leads to chronic hypoperfusion and may exacerbate the accumulation of Aβ. Together these processes cause neuronal dysfunction leading to atrophy, which manifests subclinically or clinically by stroke and small vessel disease on one side, and AD or cerebral amyloid angiopathy on the other. Older persons are most susceptible to AD, VaD or mixed dementia. We propose a multidimensional approach to optimize the opportunity for prevention by focusing on modifying vascular risk factors.

  3. Original Articles

    1. Brain endothelial cells induce astrocytic expression of the glutamate transporter GLT-1 by a Notch-dependent mechanism

      Meredith L. Lee, Zila Martinez-Lozada, Elizabeth N. Krizman and Michael B. Robinson

      Version of Record online: 5 SEP 2017 | DOI: 10.1111/jnc.14135

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      Signaling from endothelial cells has been shown to affect astrocyte specification and maturation. We show that co-culturing astrocytes with endothelial cells increases expression of the glial glutamate transporter GLT-1 as well as expression of a transcriptional reporter in a contact-dependent mechanism. This increase is dependent on Notch signaling, as inhibition of the Notch pathway by treatment with a γ-secretase inhibitor or knock-down of RBPJ prevents the endothelia-induced increase in GLT-1.

    2. Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia

      Yelena Gulchina, Song-Jun Xu, Melissa A. Snyder, Felice Elefant and Wen-Jun Gao

      Version of Record online: 5 SEP 2017 | DOI: 10.1111/jnc.14101

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      Glutamate hypofunction has been a prominent hypothesis in schizophrenia pathology; however, when and how NMDAR dysfunction occurs is unknown. We report that NMDAR hypofunction is a feature of early postnatal development. Epigenetic hyper-repression of the Grin2b promoter and subsequent loss of NR2B protein and synaptic NMDAR hypofunction weakens plPFC function. This may underlie early cognitive impairments in schizophrenia.

      Read the Editorial Highlight for this article on doi: 10.1111/jnc.14133.

  4. Editorial Highlights

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      The methylazoxymethanol acetate rat model: molecular and epigenetic effect in the developing prefrontal cortex : An Editorial Highlight for ‘Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia’ on doi: 10.1111/jnc.14101

      Xiyu Zhu, Felipe V. Gomes and Anthony A. Grace

      Version of Record online: 5 SEP 2017 | DOI: 10.1111/jnc.14133

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      This Editorial highlights an article by Gulchina and colleagues in the current issue of the Journal of Neurochemistry, in which the authors describe molecular and epigenetic changes in the developing prefrontal cortex of the rats exposed to methylazoxymethanol acetate (MAM). They found an NMDAR hypofunction present in the prefrontal cortex of juvenile MAM rats which was associated with abnormal epigenetic regulation of the Grin2b gene. These changes may be related to early cognitive impairments observed in MAM rats and schizophrenia patients.

  5. Reviews

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      Rho-associated protein kinases as therapeutic targets for both vascular and parenchymal pathologies in Alzheimer's disease

      Aaron Y. Lai and JoAnne McLaurin

      Version of Record online: 29 AUG 2017 | DOI: 10.1111/jnc.14130

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      We reviewed evidence that supports using inhibitors of ROCKs to treat Alzheimer Disease (AD). The multifaceted AD pathologies on both sides of the blood–brain barrier can be ameliorated by inhibition of ROCKs providing a potentially viable therapeutic strategy.

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      Prevention of cognitive impairment: scientific guidance and windows of opportunity

      Philip B. Gorelick

      Version of Record online: 16 AUG 2017 | DOI: 10.1111/jnc.14113

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      Worldwide, dementia prevalence is expected to triple over the next 30 years. Strategies to prevent or slow cognitive decline in older persons have not been successful. More recently, however, we have begun to think more broadly about the antecedents of the dementias of later life and have begun to recognize the importance of modifiable cardiovascular risk factors and the occurrence of coexistent stroke, a preventable condition, in patients with Alzheimer's disease. In this opinion-piece I review United States-based guidance statements for maintenance of cognitive vitality, recent clinical trials to prevent cognitive impairment, and potential gaps in relation to clinical strategies to prevent cognitive impairment. The graphic depicts steps to be taken to preserve cognitive vitality in line with recommendations from the Institute of Medicine report.

      This article is part of the Special Issue “Vascular Dementia”

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      Re-imagining Alzheimer's disease – the diminishing importance of amyloid and a glimpse of what lies ahead

      Kai-Hei Tse and Karl Herrup

      Version of Record online: 21 JUN 2017 | DOI: 10.1111/jnc.14079

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      The Alzheimer's field can seem like the blind men of the legend trying to describe an elephant by the first part they touch. The amyloid plaque has been inevitably the first part recognized by the newcomers to the Alzheimer's field. Nevertheless, looking at the longitudinal changes of the human brain, there are other age-associated pathologies prior to amyloid depositions that can equally cause age-related dementia. Indeed, a more holistic approach is needed to understand Alzheimer's. Here we offer three possibilities, namely DNA damage, cell cycle dysregulation and myelin degradation, as the examples of how amyloid-independent mechanisms could cause age-associated dementia.

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      Is sporadic Alzheimer′s disease a developmental disorder?

      Thomas Arendt, Jens Stieler and Uwe Ueberham

      Version of Record online: 28 MAY 2017 | DOI: 10.1111/jnc.14036

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      Alzheimer′s disease (AD) is a neurodegenerative disorder of higher age that specifically occurs in human. Here, we summarize recent evidence, that the evolutionary and developmental dimensions of brain structure and function provide the key to our understanding of AD.

      This article is part of a series “Beyond Amyloid”.

    5. You have full text access to this OnlineOpen article
      Brain aging and neurodegeneration: from a mitochondrial point of view

      Amandine Grimm and Anne Eckert

      Version of Record online: 14 MAY 2017 | DOI: 10.1111/jnc.14037

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      We aim to look at brain aging processes from a “mitocentric” point of view by asking: What happens to brain mitochondrial bioenergetics / dynamics during aging? Why are neurons so sensitive to the age-related mitochondrial impairments? Are there sex differences in the age-induced mitochondrial dysfunction? A better understanding of mitochondrial physiology may help identify therapeutic targets against neurodegeneration.

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      Microtubule dynamics and the neurodegenerative triad of Alzheimer's disease: The hidden connection

      Roland Brandt and Lidia Bakota

      Version of Record online: 19 APR 2017 | DOI: 10.1111/jnc.14011

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      Microtubule abnormalities are a common feature in several neurodegenerative diseases. Here, we describe how changes in microtubule dynamics are involved in the different aspects of the neurodegenerative triad of Alzheimer's disease. We discuss evidence that microtubule dynamics is (mis)regulated in a distinct manner in different neuronal compartments. Modulation of microtubule dynamics could be of potential benefit, but needs to be precisely controlled in a cell and compartment-specific manner to avoid harmful side effects.


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