Journal of Neurochemistry
© International Society for Neurochemistry
Edited By: Jörg Schulz
Impact Factor: 4.244
ISI Journal Citation Reports © Ranking: 2013: 63/252 (Neurosciences); 74/291 (Biochemistry & Molecular Biology)
Online ISSN: 1471-4159
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Recently Published Articles
- Neuroprotective role of Nrf2 for retinal ganglion cells in ischemia-reperfusion
Zhenhua Xu, Hongkwan Cho, Matthew J. Hartsock, Katherine L. Mitchell, Junsong Gong, Lijuan Wu, Yanhong Wei, Shuang Wang, Rajesh K. Thimmulappa, Michael B. Sporn, Shyam Biswal, Derek S. Welsbie and Elia J. Duh
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13064
Oxidative stress is thought to be an important mediator of retinal ganglion cell death in ischemia-reperfusion injury. We found that the transcription factor NF-E2-related factor 2 (Nrf2), a major regulator of oxidative stress, is an important endogenous neuroprotective molecule in retinal ganglion cells in ischemia-reperfusion, exerting a cell-autonomous protective effect. The triterpenoid 2-Cyano-3,12-dioxooleana-1,9-dien-28-imidazolide (CDDO-Im) reduces neurodegeneration following ischemia-reperfusion in an Nrf2-dependent fashion. This suggests that Nrf2-activating drugs including triterpenoids could be a therapeutic strategy for retinal neuroprotection.
- You have free access to this contentEffect of α-synuclein on membrane permeability and synaptic transmission: a clue to neurodegeneration?
Alexei Surguchev and Andrei Surguchov
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13045
This is an Editorial highlighting the article “Extracellular α-synuclein alters synaptic transmission in rain neurons by perforating the neuronal plasma membrane” by Pacheco and coauthors, in this issue of Journal of Neurochemistry. The authors demonstrate, using a variety of techniques, that alpha-synuclein possesses neurotoxicity toward brain neuronal plasma membranes exposed directly to extracellular alpha-synuclein oligomers. Extracellular oligomeric α-synuclein rapidly associates to hippocampal membranes and induces pore formation in the hippocampal cells. This increases membrane conductance and calcium influx. Oligomeric α-synuclein also induces changes in synaptic current activity in hippocampal neurons. The authors’ findings support the pathogenic role of extracellular alpha-synuclein in the brain, and should provide a new strategy for the treatment of Parkinson's disease and other synucleinopathies, neurodegenerative diseases with aberrant accumulation of aggregated alpha-synuclein in neurons, nerve fibers or glial cells.
Read the full article‘Extracellular α-synuclein alters synaptic transmission in brain neurons by perforating the neuronal plasma’ on membrane doi: 10.1111/jnc.13060
- Caveolin-1 mediates tissue plasminogen activator-induced MMP-9 up-regulation in cultured brain microvascular endothelial cells
Xinchun Jin, Yanyun Sun, Ji Xu and Wenlan Liu
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13065
Thrombolysis with tissue plasminogen activator (tPA) increases matrix metalloproteinase-9 (MMP-9) activity in the ischemic brain, which exacerbates ischemic blood brain barrier (BBB) injury and increases the risk of symptomatic cerebral hemorrhage. Our results suggest a novel mechanism underlying this tPA-MMP 9 axis. In response to tPA treatment, caveolin-1 protein levels increased in endothelial cells, which mediate MMP-9 mRNA up-regulation and its secretion into extracellular space. Caveolin-1 may, however, not facilitate MMP-9 secretion in endothelial cells. Our data suggest caveolin-1 as a novel therapeutic target for protecting the BBB against ischemic damage. The schematic outlines tPA-induced MMP-9 upreguation.
- Protein kinase A directly phosphorylates metabotropic glutamate receptor 5 to modulate its function
Ken Uematsu, Myriam Heiman, Marina Zelenina, Júlio Padovan, Brian T. Chait, Anita Aperia, Akinori Nishi and Paul Greengard
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13038
We identified serine residue 870 (S870) in metabotropic glutamate receptor 5 (mGluR5) as a direct substrate for protein kinase A (PKA). The phosphorylation of this site regulates the ability of mGluR5 to induce extracellular signal-regulated kinase (ERK) phosphorylation and intracellular Ca2+ oscillations. This study provides a direct molecular mechanism by which PKA signaling interacts with glutamate neurotransmission.
- Regulation of RAGE splicing by hnRNP A1 and Tra2β-1 and its potential role in AD pathogenesis
Xiao-Yan Liu, Hong-Lei Li, Jia-Bin Su, Fei-Hong Ding, Jing-Jing Zhao, Fang Chai, Yuan-Xin Li, Shi-Cao Cui, Feng-Yan Sun, Zhi-Ying Wu, Ping Xu and Xian-Hua Chen
Article first published online: 2 MAR 2015 | DOI: 10.1111/jnc.13069
The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis. Mechanism for imbalanced expression of these two isoforms in AD brain remains elusive. We proposed here a hypothetic model to illustrate that impaired glucose metabolism in AD brain may increase the expression of splicing protein hnRNP A1 and reduce Tra2β-1, which cause the imbalanced expression of mRAGE and esRAGE.