Journal of neurochemistry
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Journal of neurochemistry · Apr 2017
Cerebrospinal fluid biomarkers as a measure of disease activity and treatment efficacy in relapsing-remitting multiple sclerosis.
Cerebrospinal fluid (CSF) biomarkers can reflect different aspects of the pathophysiology of relapsing-remitting multiple sclerosis (RRMS). Understanding the impact of different disease modifying therapies on the CSF biomarker profile may increase their implementation in clinical practice and their appropriateness for monitoring treatment efficacy. This study investigated the influence of first-line (interferon beta) and second-line (natalizumab) therapies on seven CSF biomarkers in RRMS and their correlation with clinical and radiological outcomes. ⋯ NFL and CHIT1 levels correlated with relapse status, and NFL and CXCL13 levels correlated with the formation of new magnetic resonance imaging lesions. Furthermore, we found an association between inflammatory and degenerative biomarkers. The results indicate that CSF levels of NFL, CXCL13, CHI3L1, and CHIT1 correlate with the clinical and/or radiological disease activity, providing additional dimensions in the assessment of treatment efficacy.
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Journal of neurochemistry · Mar 2017
EditorialExPPNing how acetylcholine improves gait in Parkinson's disease: An Editorial Highlight for 'Deletion of the Vesicular Acetylcholine Transporter from Pedunculopontine/laterodorsal tegmental neurons modifies gait'.
Read the highlighted article 'Deletion of the Vesicular Acetylcholine Transporter from Pedunculopontine/laterodorsal tegmental neurons modifies gait' on page 787.
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Journal of neurochemistry · Mar 2017
Transient receptor potential vanilloid type 4 channels mediate Na-K-Cl-co-transporter-induced brain edema after traumatic brain injury.
Na+ -K+ -2Cl- co-transporter (NKCC1) plays an important role in traumatic brain injury (TBI)-induced brain edema via the MAPK cascade. The transient receptor potential vanilloid type 4 (TRPV4) channel participates in neurogenic inflammation, pain transmission, and edema. In this study, we investigated the relationship between NKCC1 and TRPV4 and the related signaling pathways in TBI-induced brain edema and neuronal damage. ⋯ Administration of either the TRPV4 antagonist, RN1734, or NKCC1 antagonist, bumetanide, significantly attenuated TBI-induced brain edema through decreasing the phosphorylation of MEK, ERK, and Akt proteins. Bumetanide injection inhibited TRPV4 expression, which suggests NKCC1 activation is critical to TRPV4 activation. Our results showed that hippocampal NKCC1 activation increased TRPV4 expression after TBI and then induced severe brain edema and neuronal damage through activation of the MAPK cascade and Akt-related signaling pathway.
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Retraction: "Aging is associated with altered inflammatory, arachidonic acid cascade, and synaptic markers, influenced by epigenetic modifications, in the human frontal cortex" by Keleshian VL, Modi HR, Rapoport SI, Rao JS. The above article from Journal of Neurochemistry, published online on 17 February 2013 in Wiley Online Library (wileyonlinelibrary.com) and in volume 121, issue 1, pp. 63-73, has been retracted by agreement between the corresponding author Stanley Rapoport, the Journal's Editor-in-Chief, Jörg Schulz, and John Wiley & Sons Ltd. The Editorial Office was contacted by the author Stanley Rapoport with the request to retract this and a related publication (see below), informing the Editor-in-Chief that the National Institutes of Health (NIH) had found Dr. Jagadeesh S. ⋯ J. (2007) Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2. J. Neurochem. 102, 1918-1927.
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Retraction: "Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2" by Rao JS, Ertley RN, Rapoport SI, Bazinet RP, Lee HJ. The above article from Journal of Neurochemistry, published online on 13 April 2007 in Wiley Online Library (wileyonlinelibrary.com) and in volume 102, issue 6, pp. 1918-1927, has been retracted by agreement between the corresponding author Stanley Rapoport, co-author Richard Bazinet, the Journal's Editor-in-Chief Jörg Schulz, and John Wiley & Sons Ltd. The Editorial Office was contacted by the author Stanley Rapoport with the request to retract this and a related publication (see below), informing the Editor-in-Chief that the National Institutes of Health (NIH) had found Dr. Jagadeesh S. ⋯ J. (2007) Chronic NMDA administration to rats up-regulates frontal cortex cytosolic phospholipase A2 and its transcription factor, activator protein-2. J. Neurochem. 102, 1918-1927.