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Journal of Neuroinflammation

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https://www.readbyqxmd.com/read/28222766/increased-cortical-lesion-load-and-intrathecal-inflammation-is-associated-with-oligoclonal-bands-in-multiple-sclerosis-patients-a-combined-csf-and-mri-study
#1
Gabriele Farina, Roberta Magliozzi, Marco Pitteri, Richard Reynolds, Stefania Rossi, Alberto Gajofatto, Maria Donata Benedetti, Francesco Facchiano, Salvatore Monaco, Massimiliano Calabrese
BACKGROUND: Although IgG oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) are a frequent phenomenon in multiple sclerosis (MS) patients, their relationship with grey matter lesions, intrathecal/meningeal inflammation and clinical evolution has not been clarified yet. The aim of our study was to assess the relationship between the OCBs, the inflammatory/neurodegenerative CSF profile at diagnosis, the cortical lesion load and the clinical evolution after 10 years. METHODS: This is a 10-year observational, cross-sectional study based on a combined MRI, cognitive and CSF profiling of the examined patients...
February 21, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28219441/microglia-p2y6-receptor-is-related-to-parkinson-s-disease-through-neuroinflammatory-process
#2
Xiaodong Yang, Yue Lou, Guidong Liu, Xueping Wang, Yiwei Qian, Jianqing Ding, Shengdi Chen, Qin Xiao
BACKGROUND: Microglia in the central nervous system (CNS) were reported to play crucial role in neurodegeneration. Previous studies showed that P2Y6 receptor (P2Y6R) mainly contributed to microglia activation and phagocytosis in CNS. However, the level of P2Y6R in Parkinson's disease (PD) patients is unclear. Therefore, we measured the level of P2Y6R in PD patients and speculated whether it could be a potential biomarker for PD. Given on the basis that P2Y6R was higher in PD patients, we further explored the mechanisms underlying P2Y6R in the pathogenesis of PD...
February 20, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28219400/alleviation-of-secondary-brain-injury-posttraumatic-inflammation-and-brain-edema-formation-by-inhibition-of-factor-xiia
#3
Sarah Hopp, Marc W Nolte, Christian Stetter, Christoph Kleinschnitz, Anna-Leena Sirén, Christiane Albert-Weissenberger
BACKGROUND: Traumatic brain injury (TBI) is a devastating neurological condition and a frequent cause of permanent disability. Posttraumatic inflammation and brain edema formation, two pathological key events contributing to secondary brain injury, are mediated by the contact-kinin system. Activation of this pathway in the plasma is triggered by activated factor XII. Hence, we set out to study in detail the influence of activated factor XII on the abovementioned pathophysiological features of TBI...
February 20, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28202084/aprepitant-limits-in-vivo-neuroinflammatory-responses-in-a-rhesus-model-of-lyme-neuroborreliosis
#4
Alejandra N Martinez, Amanda R Burmeister, Geeta Ramesh, Lara Doyle-Meyers, Ian Marriott, Mario T Philipp
BACKGROUND: Substance P (SP) is produced at high levels in the central nervous system (CNS), and its target receptor, neurokinin 1 receptor (NK-1R), is expressed by glia and leukocytes. This tachykinin functions to exacerbate inflammatory responses at peripheral sites. Moreover, SP/NK-1R interactions have recently been associated with severe neuroinflammation and neuronal damage. We have previously demonstrated that NK-1R antagonists can limit neuroinflammatory damage in a mouse model of bacterial meningitis...
February 15, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28196545/roles-of-programmed-death-protein-1-programmed-death-ligand-1-in-secondary-brain-injury-after-intracerebral-hemorrhage-in-rats-selective-modulation-of-microglia-polarization-to-anti-inflammatory-phenotype
#5
Jie Wu, Liang Sun, Haiying Li, Haitao Shen, Weiwei Zhai, Zhengquan Yu, Gang Chen
BACKGROUND: Microglia and its polarization play critical roles in intracerebral hemorrhage-induced secondary brain injury. Programmed death protein 1/programmed death-ligand 1 has been reported to regulate neuroimmune cell functions. Signal transducers and activators of transcription 1 participate in microglia polarization, and programmed death protein 1/programmed death-ligand 1 could regulate the activation of signal transducers and activators of transcription 1. We herein show the critical role of programmed death protein 1/programmed death-ligand 1 in the polarization of microglia during intracerebral hemorrhage-induced secondary brain injury in rat models...
February 14, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28196519/erratum-to-sdf1-in-the-dorsal-corticospinal-tract-promotes-cxcr4-cell-migration-after-spinal-cord-injury
#6
Vicki M Tysseling, Divakar S Mithal, Vibhu Sahni, Derin Birch, Hosung Jung, Richard J Miller, John A Kessler
No abstract text is available yet for this article.
February 14, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28187742/regulatory-role-of-cytosolic-phospholipase-a2-alpha-in-the-induction-of-cd40-in-microglia
#7
Yafa Fetfet Malada-Edelstein, Nurit Hadad, Rachel Levy
BACKGROUND: The aberrant expression of CD40, a co-stimulatory receptor found on the antigen-presenting cells, is involved in the pathogenesis of various degenerative diseases. Our previous study demonstrated that the reduction of cytosolic phospholipase A2 alpha (cPLA2α) protein overexpression and activation in the spinal cord of a mouse model of ALS, hmSOD1 G93A, inhibited CD40 upregulation in microglia. The present study was designed to determine whether cPLA2α has a direct, participatory role in the molecular events leading to CD40 induction...
February 10, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28187734/the-potential-neuroprotective-role-of-a-histone-deacetylase-inhibitor-sodium-butyrate-after-neonatal-hypoxia-ischemia
#8
Joanna Jaworska, Malgorzata Ziemka-Nalecz, Joanna Sypecka, Teresa Zalewska
BACKGROUND: Histone deacetylase inhibitor (HDACi), sodium butyrate (SB), has been shown to be neuroprotective in adult brain injury models. Potential explanation for the inhibitor action involves among others reduced inflammation. We therefore anticipated that SB will provide a suitable option for brain injury in immature animals. The aim of our study was to test the hypothesis that one of the mechanisms of protection afforded by SB after neonatal hypoxia-ischemia is associated with anti-inflammatory action...
February 10, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28183352/combined-effect-of-bcg-vaccination-and-enriched-environment-promote-neurogenesis-and-spatial-cognition-via-a-shift-in-meningeal-macrophage-m2-polarization
#9
Fangfang Qi, Zejie Zuo, Junhua Yang, Saisai Hu, Yang Yang, Qunfang Yuan, Juntao Zou, Kaihua Guo, Zhibin Yao
BACKGROUND: The spatial learning abilities of developing mice benefit from extrinsic cues, such as an enriched environment, with concomitant enhancement in cognitive functions. Interestingly, such enhancements can be further increased through intrinsic Bacillus Calmette-Guérin (BCG) vaccination. RESULTS: Here, we first report that combined neonatal BCG vaccination and exposure to an enriched environment (Enr) induced combined neurobeneficial effects, including hippocampal long-term potentiation, and increased neurogenesis and spatial learning and memory, in mice exposed to the Enr and vaccinated with BCG relative to those in the Enr that did not receive BCG vaccination...
February 10, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28173836/complex-regulation-of-neutrophil-derived-mmp-9-secretion-in-central-nervous-system-tuberculosis
#10
Catherine W M Ong, Przemyslaw J Pabisiak, Sara Brilha, Poonam Singh, Federico Roncaroli, Paul T Elkington, Jon S Friedland
BACKGROUND: Central nervous system tuberculosis (CNS-TB) may be fatal even with treatment. Neutrophils are the key mediators of TB immunopathology, and raised CSF matrix metalloproteinase-9 (MMP-9) which correlates to neutrophil count in CNS-TB is associated with neurological deficit and death. The mechanisms by which neutrophils drive TB-associated CNS matrix destruction are not clearly defined. METHODS: Human brain biopsies with histologically proven CNS-TB were stained for neutrophils, neutrophil elastase, and MMP-9...
February 7, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28166793/cytotoxic-t-cells-modulate-inflammation-and-endogenous-opioid-analgesia-in-chronic-arthritis
#11
Uta Baddack-Werncke, Melanie Busch-Dienstfertig, Sara González-Rodríguez, Santhosh Chandar Maddila, Jenny Grobe, Martin Lipp, Christoph Stein, Gerd Müller
BACKGROUND: This study examined the development of chronic pain, a cardinal symptom of rheumatoid arthritis (RA), in mice with antigen- and collagen-induced arthritis (ACIA). Since the role of CD8(+) T cells in arthritis is controversial, we investigated the consequences of CD8-depletion on arthritis development and opioid modulation of pain in this novel model of chronic autoimmune arthritis. METHODS: Disease severity in control and CD8-depleted animals was determined by histological assessment of knee-joint sections and measurement of autoantibody formation...
February 6, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28153028/il-1%C3%AE-impairs-retrograde-flow-of-bdnf-signaling-by-attenuating-endosome-trafficking
#12
Anthony J Carlos, Liqi Tong, G Aleph Prieto, Carl W Cotman
BACKGROUND: Pro-inflammatory cytokines accumulate in the brain with age and Alzheimer's disease and can impair neuron health and cognitive function. Brain-derived neurotrophic factor (BDNF) is a key neurotrophin that supports neuron health, function, and synaptic plasticity. The pro-inflammatory cytokine interleukin-1β (IL-1β) impairs BDNF signaling but whether it affects BDNF signaling endosome trafficking has not been studied. METHODS: This study uses an in vitro approach in primary hippocampal neurons to evaluate the effect of IL-1β on BDNF signaling endosome trafficking...
February 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28153013/effects-of-dexamethasone-and-meloxicam-on-borrelia-burgdorferi-induced-inflammation-in-glial-and-neuronal-cells-of-the-central-nervous-system
#13
Geeta Ramesh, Alejandra N Martinez, Dale S Martin, Mario T Philipp
BACKGROUND: Lyme neuroborreliosis (LNB), caused by the spirochete Borrelia burgdorferi (Bb), affects both the central and peripheral nervous systems. Previously, we reported that in a model of acute LNB in rhesus monkeys, treatment with the anti-inflammatory drug dexamethasone significantly reduced both pleocytosis and levels of cerebrospinal fluid (CSF) immune mediators that were induced by Bb. Dexamethasone also inhibited the formation of inflammatory, neurodegenerative, and demyelinating lesions in the brain and spinal cord of these animals...
February 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28148307/intrathecal-th17-and-b-cell-associated-cytokine-and-chemokine-responses-in-relation-to-clinical-outcome-in-lyme-neuroborreliosis-a-large-retrospective-study
#14
Paula Gyllemark, Pia Forsberg, Jan Ernerudh, Anna J Henningsson
BACKGROUND: B cell immunity, including the chemokine CXCL13, has an established role in Lyme neuroborreliosis, and also, T helper (Th) 17 immunity, including IL-17A, has recently been implicated. METHODS: We analysed a set of cytokines and chemokines associated with B cell and Th17 immunity in cerebrospinal fluid and serum from clinically well-characterized patients with definite Lyme neuroborreliosis (group 1, n = 49), defined by both cerebrospinal fluid pleocytosis and Borrelia-specific antibodies in cerebrospinal fluid and from two groups with possible Lyme neuroborreliosis, showing either pleocytosis (group 2, n = 14) or Borrelia-specific antibodies in cerebrospinal fluid (group 3, n = 14)...
February 1, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28143556/aging-and-amyloid-%C3%AE-oligomers-enhance-tlr4-expression-lps-induced-ca-2-responses-and-neuron-cell-death-in-cultured-rat-hippocampal-neurons
#15
María Calvo-Rodríguez, Carmen de la Fuente, Mónica García-Durillo, Carmen García-Rodríguez, Carlos Villalobos, Lucía Núñez
BACKGROUND: Toll-like receptors (TLRs) are transmembrane pattern-recognition receptors of the innate immune system recognizing diverse pathogen-derived and tissue damage-related ligands. It has been suggested that TLR signaling contributes to the pathogenesis of age-related, neurodegenerative diseases, including Alzheimer's disease (AD). AD is associated to oligomers of the amyloid β peptide (Aβo) that cause intracellular Ca(2+) dishomeostasis and neuron cell death in rat hippocampal neurons...
January 31, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28143498/neuroprotective-effects-of-intrastriatal-injection-of-rapamycin-in-a-mouse-model-of-excitotoxicity-induced-by-quinolinic-acid
#16
Soraya Wilke Saliba, Erica Leandro Marciano Vieira, Rebeca Priscila de Melo Santos, Eduardo Candelario-Jalil, Bernd L Fiebich, Luciene Bruno Vieira, Antonio Lucio Teixeira, Antonio Carlos Pinheiro de Oliveira
BACKGROUND: The mammalian target of rapamycin (mTOR) is a kinase involved in a variety of physiological and pathological functions. However, the exact role of mTOR in excitotoxicity is poorly understood. Here, we investigated the effects of mTOR inhibition with rapamycin against neurodegeneration, and motor impairment, as well as inflammatory profile caused by an excitotoxic stimulus. METHODS: A single and unilateral striatal injection of quinolinic acid (QA) was used to induce excitotoxicity in mice...
January 31, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28143489/obesity-and-neuroinflammatory-phenotype-in-mice-lacking-endothelial-megalin
#17
Fernando Bartolome, Desiree Antequera, Eva Tavares, Consuelo Pascual, Rosario Maldonado, Antoni Camins, Eva Carro
BACKGROUND: The multiligand receptor megalin controls the brain uptake of a number of ligands, including insulin and leptin. Despite the role of megalin in the transport of these metabolically relevant hormones, the role of megalin at the blood-brain-barrier (BBB) has not yet been explored in the context of metabolic regulation. METHODS: Here we investigate the role of brain endothelial megalin in energy metabolism and leptin signaling using an endothelial cell-specific megalin deficient (EMD) mouse model...
January 31, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28122624/hiv-induces-expression-of-complement-component-c3-in-astrocytes-by-nf-%C3%AE%C2%BAb-dependent-activation-of-interleukin-6-synthesis
#18
Jadwiga Nitkiewicz, Alejandra Borjabad, Susan Morgello, Jacinta Murray, Wei Chao, Luni Emdad, Paul B Fisher, Mary Jane Potash, David J Volsky
BACKGROUND: Abnormal activation of the complement system contributes to some central nervous system diseases but the role of complement in HIV-associated neurocognitive disorder (HAND) is unclear. METHODS: We used real-time PCR and immunohistochemistry to detect complement expression in postmortem brain tissue from HAND patients and controls. To further investigate the basis for viral induction of gene expression in the brain, we studied the effect of HIV on C3 expression by astrocytes, innate immune effector cells, and targets of HIV...
January 26, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28118842/microglial-derived-mirna-let-7-and-hmgb1-contribute-to-ethanol-induced-neurotoxicity-via-tlr7
#19
Leon G Coleman, Jian Zou, Fulton T Crews
BACKGROUND: Toll-like receptor (TLR) signaling is emerging as an important component of neurodegeneration. TLR7 senses viral RNA and certain endogenous miRNAs to initiate innate immune responses leading to neurodegeneration. Alcoholism is associated with hippocampal degeneration, with preclinical studies linking ethanol-induced neurodegeneration with central innate immune induction and TLR activation. The endogenous miRNA let-7b binds TLR7 to cause neurodegeneration. METHODS: TLR7 and other immune markers were assessed in postmortem human hippocampal tissue that was obtained from the New South Wales Tissue Bank...
January 25, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28115020/cerebral-ischemic-damage-in-diabetes-an-inflammatory-perspective
#20
REVIEW
Vibha Shukla, Akhalesh Kumar Shakya, Miguel A Perez-Pinzon, Kunjan R Dave
Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality and disabilities. Diabetes involves chronic inflammation manifested by reactive oxygen species generation, expression of proinflammatory cytokines, and activation/expression of other inflammatory mediators...
January 23, 2017: Journal of Neuroinflammation
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