2,395 results match your criteria Journal of Neuroinflammation [Journal]


Icariin attenuates neuroinflammation and exerts dopamine neuroprotection via an Nrf2-dependent manner.

J Neuroinflammation 2019 Apr 22;16(1):92. Epub 2019 Apr 22.

Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.

Background: Oxidative stress and neuroinflammation are considered the major central events in the process of Parkinson's disease (PD). Nrf2 is a key regulator of endogenous defense systems. New finds have contacted activation of Nrf2 signaling with anti-inflammatory activities. Read More

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http://dx.doi.org/10.1186/s12974-019-1472-xDOI Listing
April 2019
1 Read

HLA and killer cell immunoglobulin-like receptor (KIRs) genotyping in patients with acute ischemic stroke.

J Neuroinflammation 2019 Apr 17;16(1):88. Epub 2019 Apr 17.

Internal Medicine and Stroke Care Ward, Department of Health Promotion Sciences, Maternal and Infant Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, P.zza delle Cliniche n.2, 90127, Palermo, Italy.

Introduction: In humans, a major component of natural killer (NK) and T cell target recognition depends on the surveillance of human leukocyte antigen (HLA) class I molecules by killer immunoglobulin-like receptors (KIRs).

Aims: To implement the knowledge about the immunological genetic background of acute ischemic stroke susceptibility in relation to the frequency of the KIR genes and HLA alleles.

Methods: Subjects with acute ischemic stroke and subjects without stroke were genotyped for the presence of KIR genes and of the three major KIR ligand groups, HLA-C1, HLA-C2, and HLA-Bw4, both HLA-B and HLA-A loci. Read More

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http://dx.doi.org/10.1186/s12974-019-1469-5DOI Listing

Role of inflammation in depression relapse.

J Neuroinflammation 2019 Apr 17;16(1):90. Epub 2019 Apr 17.

Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, 06030, USA.

Major depressive disorder (MDD) is a leading cause of disability worldwide. After the first episode, patients with remitted MDD have a 60% chance of experiencing a second episode. Consideration of therapy continuation should be viewed in terms of the balance between the adverse effects of medication and the need to prevent a possible relapse. Read More

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http://dx.doi.org/10.1186/s12974-019-1475-7DOI Listing

Role of NADPH oxidase-2 in the progression of the inflammatory response secondary to striatum excitotoxic damage.

J Neuroinflammation 2019 Apr 17;16(1):91. Epub 2019 Apr 17.

Instituto de Fisiología Celular, División de Neurociencias, Universidad Nacional Autónoma de México (UNAM), Apartado Postal 70-253, 04510, Ciudad de México, Mexico.

Background: During excitotoxic damage, neuronal death results from the increase in intracellular calcium, the induction of oxidative stress, and a subsequent inflammatory response. NADPH oxidases (NOX) are relevant sources of reactive oxygen species (ROS) during excitotoxic damage. NADPH oxidase-2 (NOX-2) has been particularly related to neuronal damage and death, as well as to the resolution of the subsequent inflammatory response. Read More

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http://dx.doi.org/10.1186/s12974-019-1478-4DOI Listing

Targeting prokineticin system counteracts hypersensitivity, neuroinflammation, and tissue damage in a mouse model of bortezomib-induced peripheral neuropathy.

J Neuroinflammation 2019 Apr 17;16(1):89. Epub 2019 Apr 17.

Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, via Vanvitelli, 32, 20129, Milan, Italy.

Background: Neuropathy is a dose-limiting side effect of many chemotherapeutics, including bortezomib. The mechanisms underlying this condition are not fully elucidated even if a contribution of neuroinflammation was suggested. Here, we investigated the role of a chemokine family, the prokineticins (PKs), in the development of bortezomib-induced peripheral neuropathy (BIPN), and we used a PK receptor antagonist to counteract the development and progression of the pathology. Read More

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http://dx.doi.org/10.1186/s12974-019-1461-0DOI Listing

Ultrastructural evidence of microglial heterogeneity in Alzheimer's disease amyloid pathology.

J Neuroinflammation 2019 Apr 16;16(1):87. Epub 2019 Apr 16.

Axe neurosciences, Centre de recherche du CHU de Québec-Université Laval, 2705, boulevard Laurier, T2-50, Quebec, QC, G1V 4G2, Canada.

Background: Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by the deposition of extracellular fibrillar amyloid β (fΑβ) and the intracellular accumulation of neurofibrillary tangles. As AD progresses, Aβ drives a robust and prolonged inflammatory response via its recognition by microglia, the brain's immune cells. Microglial reactivity to fAβ plaques may impair their normal surveillance duties, facilitating synaptic loss and neuronal death, as well as cognitive decline in AD. Read More

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http://dx.doi.org/10.1186/s12974-019-1473-9DOI Listing
April 2019
1 Read

Dysregulation of sonic hedgehog pathway and pericytes in the brain after lentiviral infection.

J Neuroinflammation 2019 Apr 13;16(1):86. Epub 2019 Apr 13.

Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, 700 W. Olney Road, Lewis Hall 3174, Norfolk, VA, 23501, USA.

Background: Impairment of the blood-brain barrier (BBB) has been associated with cognitive decline in many CNS diseases, including HIV-associated neurocognitive disorders (HAND). Recent research suggests an important role for the Sonic hedgehog (Shh) signaling pathway in the maintenance of BBB integrity under both physiological and pathological conditions.

Methods: In the present study, we sought to examine the expression of Shh and its downstream effectors in relation to brain pericytes and BBB integrity in HIV-infected humans and rhesus macaques infected with simian immunodeficiency virus (SIV), an animal model of HIV infection and CNS disease. Read More

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http://dx.doi.org/10.1186/s12974-019-1463-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461821PMC
April 2019
1 Read

Activation of GPR40 produces mechanical antiallodynia via the spinal glial interleukin-10/β-endorphin pathway.

J Neuroinflammation 2019 Apr 13;16(1):84. Epub 2019 Apr 13.

King's Lab, Shanghai Jiao Tong University School of Pharmacy, 800 Dongchuan Road, Shanghai, 200240, China.

Background: The G protein-coupled receptor 40 (GPR40), broadly expressed in various tissues such as the spinal cord, exerts multiple physiological functions including pain regulation. This study aimed to elucidate the mechanisms underlying GPR40 activation-induced antinociception in neuropathic pain, particularly related to the spinal glial expression of IL-10 and subsequent β-endorphin.

Methods: Spinal nerve ligation-induced neuropathic pain model was used in this study. Read More

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http://dx.doi.org/10.1186/s12974-019-1457-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461825PMC

Macrophage migration inhibitory factor facilitates prostaglandin E production of astrocytes to tune inflammatory milieu following spinal cord injury.

J Neuroinflammation 2019 Apr 13;16(1):85. Epub 2019 Apr 13.

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong, 226001, People's Republic of China.

Background: Astrocytes have been shown to produce several pro- and anti-inflammatory cytokines to maintain homeostasis of microenvironment in response to vast array of CNS insults. Some inflammation-related cytokines are responsible for regulating such cell events. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that can be inducibly expressed in the lesioned spinal cord. Read More

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http://dx.doi.org/10.1186/s12974-019-1468-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461812PMC

TNFα inhibitors as targets for protective therapies in MSA: a viewpoint.

J Neuroinflammation 2019 Apr 11;16(1):80. Epub 2019 Apr 11.

Division of Clinical Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstraße 35, A-6020, Innsbruck, Austria.

Multiple system atrophy (MSA) is a unique and fatal α-synucleinopathy associated with oligodendroglial inclusions and secondary neurodegeneration affecting striatum, substantia nigra, pons, and cerebellum. The pathogenesis remains elusive; however, there is emerging evidence suggesting a prominent role of neuroinflammation. Here, we critically review the relationship between αS and microglial activation depending on its aggregation state and its role in neuroinflammation to explore the potential of TNFα inhibitors as a treatment strategy for MSA and other neurodegenerative diseases. Read More

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http://dx.doi.org/10.1186/s12974-019-1477-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458780PMC
April 2019
5.408 Impact Factor

Inhibition of apoptosis signal-regulating kinase by paeoniflorin attenuates neuroinflammation and ameliorates neuropathic pain.

J Neuroinflammation 2019 Apr 11;16(1):83. Epub 2019 Apr 11.

Department of Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.

Background: Neuropathic pain is a serious clinical problem that needs to be solved urgently. ASK1 is an upstream protein of p38 and JNK which plays important roles in neuroinflammation during the induction and maintenance of chronic pain. Therefore, inhibition of ASK1 may be a novel therapeutic approach for neuropathic pain. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1476-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458750PMC
April 2019
4 Reads

GPR34 in spinal microglia exacerbates neuropathic pain in mice.

J Neuroinflammation 2019 Apr 11;16(1):82. Epub 2019 Apr 11.

Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, 65, Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Background: Neuropathic pain is caused by sensory nerve injury, but effective treatments are currently lacking. Microglia are activated in the spinal dorsal horn after sensory nerve injury and contribute to neuropathic pain. Accordingly, molecules expressed by these cells are considered potential targets for therapeutic strategies. Read More

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http://dx.doi.org/10.1186/s12974-019-1458-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458787PMC

A novel small molecular NLRP3 inflammasome inhibitor alleviates neuroinflammatory response following traumatic brain injury.

J Neuroinflammation 2019 Apr 11;16(1):81. Epub 2019 Apr 11.

Department of Anatomy and Neurobiology, School of Medicine, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, 23298-0709, USA.

Background: Neuroinflammation is an essential player in many neurological diseases including traumatic brain injury (TBI). Recent studies have identified that inflammasome complexes are responsible for inflammatory responses in many pathological conditions. Inflammasomes are intracellular multiprotein complexes which regulate the innate immune response, activation of caspase-1, production of pro-inflammatory cytokines IL-1β and IL-18, and induction of cell death (pyroptosis). Read More

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http://dx.doi.org/10.1186/s12974-019-1471-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458637PMC
April 2019
1 Read

Microglial NLRP3 inflammasome activation mediates IL-1β release and contributes to central sensitization in a recurrent nitroglycerin-induced migraine model.

J Neuroinflammation 2019 Apr 10;16(1):78. Epub 2019 Apr 10.

Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, 1st You Yi Road, Yu Zhong District, Chongqing, 400016, People's Republic of China.

Background: Central sensitization is an important mechanism of chronic migraine (CM) and is related to the inflammatory response of microglia. The NOD-like receptor protein 3 (NLRP3) inflammasome may regulate the inflammatory process of microglia in several neurological diseases, but its role in CM is largely unknown. Therefore, the aim of this study was to identify the precise role of microglial NLRP3 in CM. Read More

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http://dx.doi.org/10.1186/s12974-019-1459-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456991PMC
April 2019
1 Read

Myosin1f-mediated neutrophil migration contributes to acute neuroinflammation and brain injury after stroke in mice.

J Neuroinflammation 2019 Apr 10;16(1):77. Epub 2019 Apr 10.

Department of Neurosurgery, Stanford University School of Medicine, 1201 Welch Road, MSLS Building, Room P306, Stanford, CA, 94305, USA.

Background: During the acute stroke phase, neutrophils from the peripheral blood are first to arrive in the ischemic brain, which then attracts other immune cells that exacerbate neuroinflammation in the ischemic tissue. Myosin1f was reported to specifically mediate neutrophil migration in the peripheral tissues, but whether it plays a critical role in the neuroinflammatory response after ischemic stroke remains unknown. In this study, we aim to test the hypothesis that myosin1f-mediated neutrophil migration is critical in acute neuroinflammation induced by ischemic stroke. Read More

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http://dx.doi.org/10.1186/s12974-019-1465-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456973PMC
April 2019
3 Reads

Transiently proliferating perivascular microglia harbor M1 type and precede cerebrovascular changes in a chronic hypertension model.

J Neuroinflammation 2019 Apr 10;16(1):79. Epub 2019 Apr 10.

Department of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho Kamigyo-ku, Kyoto, 602-8566, Japan.

Background: Microglia play crucial roles in the maintenance of brain homeostasis. Activated microglia show a biphasic influence, promoting beneficial repair and causing harmful damage via M2 and M1 microglia, respectively. It is well-known that microglia are initially activated to the M2 state and subsequently switch to the M1 state, called M2-to-M1 class switching in acute ischemic models. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1467-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456949PMC
April 2019
3 Reads

The role of microglia in viral encephalitis: a review.

J Neuroinflammation 2019 Apr 9;16(1):76. Epub 2019 Apr 9.

Department of Neurology, The First Affiliated Hospital, Harbin Medical University, 23 You Zheng Street, Harbin, 150001, Heilong Jiang Province, People's Republic of China.

Viral encephalitis is still very prominent around the world, and traditional antiviral therapies still have shortcomings. Some patients cannot get effective relief or suffer from serious sequelae. At present, people are studying the role of the innate immune system in viral encephalitis. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1443-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454758PMC
April 2019
4 Reads

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

J Neuroinflammation 2019 Apr 8;16(1):75. Epub 2019 Apr 8.

Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, 210008, China.

Background: Activation of microglial cells plays an important role in neuroinflammation after ischemic stroke. Inhibiting the activation of microglial cells has been suggested as a potential therapeutic approach in the treatment of ischemic stroke.

Methods: Oxygen-glucose deprivation in primary microglial cells and transient middle cerebral artery occlusion (MCAO) in C57BL/6 mice were used as the in vitro and in vivo ischemic stroke models. Read More

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http://dx.doi.org/10.1186/s12974-019-1464-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6452518PMC
April 2019
2 Reads

Anti-CNTN1 IgG3 induces acute conduction block and motor deficits in a passive transfer rat model.

J Neuroinflammation 2019 Apr 5;16(1):73. Epub 2019 Apr 5.

Department of Neurology, University Hospital Würzburg, Josef-Schneider-Str. 11, 97080, Würzburg, Germany.

Background: Autoantibodies against the paranodal protein contactin-1 have recently been described in patients with severe acute-onset autoimmune neuropathies and mainly belong to the IgG4 subclass that does not activate complement. IgG3 anti-contactin-1 autoantibodies are rare, but have been detected during the acute onset of disease in some cases. There is evidence that anti-contactin-1 prevents adhesive interaction, and chronic exposure to anti-contactin-1 IgG4 leads to structural changes at the nodes accompanied by neuropathic symptoms. Read More

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http://dx.doi.org/10.1186/s12974-019-1462-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6450014PMC
April 2019
1 Read
5.408 Impact Factor

Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease.

J Neuroinflammation 2019 Apr 5;16(1):74. Epub 2019 Apr 5.

Department of Neuroscience, Del Monte Institute for Neuroscience, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 603, Rochester, NY, 14642, USA.

Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD). Neuritic plaques composed of amyloid β and neurofibrillary tangle-laden neurons are surrounded by reactive astrocytes and microglia. Exposure of microglia, the resident myeloid cell of the CNS, to amyloid β causes these cells to acquire an inflammatory phenotype. Read More

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http://dx.doi.org/10.1186/s12974-019-1453-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449993PMC
April 2019
1 Read

Highly glycosylated CD147 promotes hemorrhagic transformation after rt-PA treatment in diabetes: a novel therapeutic target?

J Neuroinflammation 2019 Apr 5;16(1):72. Epub 2019 Apr 5.

Department of Neurology, Huashan Hospital, Fudan University, No.12 Middle Wulumuqi Road, Shanghai, 200040, China.

Background: Diabetes is known to be a main risk factor of post-stroke hemorrhagic transformation following recombinant tissue plasminogen activator (rt-PA) therapy. However, the mechanism through which diabetes exacerbates hemorrhagic transformation is insufficiently understood. We aimed to verify that CD147, the extracellular matrix metalloproteinase (MMP) inducer, played a vital role in the progress. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1460-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449915PMC
April 2019
5 Reads

HIV-1 Tat enhances purinergic P2Y4 receptor signaling to mediate inflammatory cytokine production and neuronal damage via PI3K/Akt and ERK MAPK pathways.

J Neuroinflammation 2019 Apr 4;16(1):71. Epub 2019 Apr 4.

Xuzhou Key Laboratory of Neurobiology, Department of Neurobiology and Anatomy, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.

Background: HIV-associated neurocognitive disorders (HANDs) afflict more than half of HIV-1-positive individuals. The transactivator of transcription (Tat) produced by HIV virus elicits inflammatory process and is a major neurotoxic mediator that induce neuron damage during HAND pathogenesis. Activated astrocytes are important cells involved in neuroinflammation and neuronal damage. Read More

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http://dx.doi.org/10.1186/s12974-019-1466-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449963PMC
April 2019
11 Reads
5.408 Impact Factor

Correction to: Expansion and activation of distinct central memory T lymphocyte subsets in complex regional pain syndrome.

J Neuroinflammation 2019 Apr 3;16(1):70. Epub 2019 Apr 3.

Discipline of Anatomy & Histology, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Room E513, Anderson Stuart Building, Sydney, NSW, 2006, Australia.

Following publication of the original article [1], the authors reported an error in Figure 4 as the wrong figure was used. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1470-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446317PMC
April 2019
3 Reads

Elevated circulating TGFβ1 during acute liver failure activates TGFβR2 on cortical neurons and exacerbates neuroinflammation and hepatic encephalopathy in mice.

J Neuroinflammation 2019 Apr 2;16(1):69. Epub 2019 Apr 2.

Central Texas Veterans Health Care System, Temple, TX, USA.

Background: Acute liver failure resulting from drug-induced liver injury can lead to the development of neurological complications called hepatic encephalopathy (HE). Hepatic transforming growth factor beta 1 (TGFβ1) is upregulated due to liver failure in mice and inhibiting circulating TGFβ reduced HE progression. However, the specific contributions of TGFβ1 on brain cell populations and neuroinflammation during HE are not known. Read More

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http://dx.doi.org/10.1186/s12974-019-1455-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446280PMC
April 2019
2 Reads

Hyperactivation of proprioceptors induces microglia-mediated long-lasting pain in a rat model of chronic fatigue syndrome.

J Neuroinflammation 2019 Mar 30;16(1):67. Epub 2019 Mar 30.

Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, 65 Tsurumaicho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.

Background: Patients diagnosed with chronic fatigue syndrome (CFS) or fibromyalgia experience chronic pain. Concomitantly, the rat model of CFS exhibits microglial activation in the lumbar spinal cord and pain behavior without peripheral tissue damage and/or inflammation. The present study addressed the mechanism underlying the association between pain and chronic stress using this rat model. Read More

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http://dx.doi.org/10.1186/s12974-019-1456-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441145PMC
March 2019
2 Reads

Balance between innate versus adaptive immune system and the risk of dementia: a population-based cohort study.

J Neuroinflammation 2019 Mar 30;16(1):68. Epub 2019 Mar 30.

Department of Epidemiology, Erasmus MC - University Medical Center Rotterdam, PO Box 2040, 3000CA, Rotterdam, the Netherlands.

Background: Immunity has been suggested to be important in the pathogenesis of dementia. However, the contribution of innate versus adaptive immunity in the development of dementia is not clear. In this study, we aimed to investigate (1) the association between components of innate immunity (granulocytes and platelets) and adaptive immunity (lymphocytes) with risk of dementia and (2) the association between their derived ratios (granulocyte-to-lymphocyte ratio [GLR], platelet-to-lymphocyte ratio [PLR], and systemic immune-inflammation index [SII]), reflecting the balance between innate and adaptive immunity, with risk of dementia. Read More

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http://dx.doi.org/10.1186/s12974-019-1454-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441146PMC

Interleukin-10 inhibits interleukin-1β production and inflammasome activation of microglia in epileptic seizures.

J Neuroinflammation 2019 Mar 28;16(1):66. Epub 2019 Mar 28.

Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.

Background: Microglia are important for secreting chemical mediators of inflammatory responses in the central nervous system. Interleukin (IL)-10 and IL-1β secreted by glial cells support neuronal functions, but the related mechanisms remain vague. Our goal was to demonstrate the efficacy of IL-10 in suppressing IL-1β and in inflammasome activation in mice with epileptic seizure based on an epileptic-seizure mouse model. Read More

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http://dx.doi.org/10.1186/s12974-019-1452-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6437919PMC
March 2019
1 Read

Visualizing neuroinflammation with fluorescence and luminescent lanthanide-based in situ hybridization.

J Neuroinflammation 2019 Mar 21;16(1):65. Epub 2019 Mar 21.

Department of Molecular Sciences and ARC Centre of Excellence for Nanoscale Biophotonics, Macquarie University, North Ryde, NSW, 2109, Australia.

Background: Neurokine signaling via the release of neurally active cytokines arises from glial reactivity and is mechanistically implicated in central nervous system (CNS) pathologies such as chronic pain, trauma, neurodegenerative diseases, and complex psychiatric illnesses. Despite significant advancements in the methodologies used to conjugate, incorporate, and visualize fluorescent molecules, imaging of rare yet high potency events within the CNS is restricted by the low signal to noise ratio experienced within the CNS. The brain and spinal cord have high cellular autofluorescence, making the imaging of critical neurokine signaling and permissive transcriptional cellular events unreliable and difficult in many cases. Read More

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http://dx.doi.org/10.1186/s12974-019-1451-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6427895PMC

Systemic administration of orexin A ameliorates established experimental autoimmune encephalomyelitis by diminishing neuroinflammation.

J Neuroinflammation 2019 Mar 20;16(1):64. Epub 2019 Mar 20.

University of Rouen Normandy, INSERM U1234 PANTHER, Institute for Research and Innovation in Biomedicine (IRIB), Faculté de Médecine et Pharmacie, 22 Boulevard Gambetta, 76183, Rouen, France.

Background: Orexins (hypocretins, Hcrt) A and B are GPCR-binding hypothalamic neuropeptides known to regulate sleep/wake states and feeding behavior. A few studies have shown that orexin A exhibits anti-inflammatory and neuroprotective properties, suggesting that it might provide therapeutic effects in inflammatory and neurodegenerative diseases like multiple sclerosis (MS). In MS, encephalitogenic Th1 and Th17 cells trigger an inflammatory response in the CNS destroying the myelin sheath. Read More

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http://dx.doi.org/10.1186/s12974-019-1447-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425555PMC

Expansion and activation of distinct central memory T lymphocyte subsets in complex regional pain syndrome.

J Neuroinflammation 2019 Mar 18;16(1):63. Epub 2019 Mar 18.

Discipline of Anatomy & Histology, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Room E513, Anderson Stuart Building, Sydney, NSW, 2006, Australia.

Background: Complex regional pain syndrome (CRPS) is a debilitating condition where trauma to a limb results in devastating persistent pain that is disproportionate to the initial injury. The pathophysiology of CRPS remains unknown; however, accumulating evidence suggests it is an immunoneurological disorder, especially in light of evidence of auto-antibodies in ~ 30% of patients. Despite this, a systematic assessment of all circulating leukocyte populations in CRPS has never been performed. Read More

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http://dx.doi.org/10.1186/s12974-019-1449-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423749PMC
March 2019
3 Reads

Loss of NF-κB p50 function synergistically augments microglial priming in the middle-aged brain.

J Neuroinflammation 2019 Mar 12;16(1):60. Epub 2019 Mar 12.

Department of Anatomy and Cell Biology, The Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.

Background: While NF-κB p50 function is impaired in central nervous system disease, aging in non-CNS tissues, and response to reactive oxygen species, the role of NF-κB p50 in aging-associated microglial pro-inflammatory priming is poorly understood.

Methods: Male NF-κB p50 and NF-κB p50 mice at three different ages (1.5-3. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
Publisher Site
http://dx.doi.org/10.1186/s12974-019-1446-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419422PMC
March 2019
4 Reads

Urolithin A attenuates memory impairment and neuroinflammation in APP/PS1 mice.

J Neuroinflammation 2019 Mar 14;16(1):62. Epub 2019 Mar 14.

Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, 510260, China.

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by an abnormal accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and impaired neurogenesis. Urolithin A (UA), a gut-microbial metabolite of ellagic acid, has been reported to exert anti-inflammatory effects in the brain. However, it is unknown whether UA exerts its properties of anti-inflammation and neuronal protection in the APPswe/PS1ΔE9 (APP/PS1) mouse model of AD. Read More

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http://dx.doi.org/10.1186/s12974-019-1450-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417212PMC
March 2019
3 Reads

Microglia lacking a peroxisomal β-oxidation enzyme chronically alter their inflammatory profile without evoking neuronal and behavioral deficits.

J Neuroinflammation 2019 Mar 13;16(1):61. Epub 2019 Mar 13.

Department of Pharmaceutical and Pharmacological Sciences, Laboratory for Cell Metabolism, KU Leuven - University of Leuven, Campus Gasthuisberg O/N2, Herestraat 49, B-3000, Leuven, Belgium.

Background: Microglia play a central role in most neurological disorders, but the impact of microgliosis on brain environment and clinical functions is not fully understood. Mice lacking multifunctional protein-2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, develop a fatal disorder characterized by motor problems similar to the milder form of MFP2 deficiency in humans. The hallmark of disease in mice is the chronic proliferation of microglia in the brain, but molecular pathomechanisms that drive rapid clinical deterioration in human and mice remain unknown. Read More

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http://dx.doi.org/10.1186/s12974-019-1442-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417251PMC
March 2019
2 Reads

Cerebrospinal fluid biomarkers for predicting development of multiple sclerosis in acute optic neuritis: a population-based prospective cohort study.

J Neuroinflammation 2019 Mar 11;16(1):59. Epub 2019 Mar 11.

Department of Neurology, Slagelse Hospital, Slagelse, Denmark.

Background: Long-term outcome in multiple sclerosis (MS) depends on early treatment. In patients with acute optic neuritis (ON), an early inflammatory event, we investigated markers in cerebrospinal fluid (CSF), which may predict a diagnosis of MS.

Methods: Forty patients with acute ON were recruited in a prospective population-based cohort with median 29 months (range 19-41) of follow-up. Read More

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http://dx.doi.org/10.1186/s12974-019-1440-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6410527PMC

CD55 upregulation in astrocytes by statins as potential therapy for AQP4-IgG seropositive neuromyelitis optica.

J Neuroinflammation 2019 Mar 9;16(1):57. Epub 2019 Mar 9.

Departments of Medicine and Physiology, University of California, 1246 Health Sciences East Tower, 513 Parnassus Ave, San Francisco, CA, 94143-0521, USA.

Background: Neuromyelitis optica spectrum disorder (herein called NMO) is an inflammatory demyelinating disease that can be initiated by binding of immunoglobulin G autoantibodies (AQP4-IgG) to aquaporin-4 on astrocytes, causing complement-dependent cytotoxicity (CDC) and downstream inflammation. The increased NMO pathology in rodents deficient in complement regulator protein CD59 following passive transfer of AQP4-IgG has suggested the potential therapeutic utility of increasing the expression of complement regulator proteins.

Methods: A cell-based ELISA was developed to screen for pharmacological upregulators of endogenous CD55 and CD59 in a human astrocyte cell line. Read More

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http://dx.doi.org/10.1186/s12974-019-1448-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6408857PMC

Intrathecal triamcinolone acetonide exerts anti-inflammatory effects on Lewis rat experimental autoimmune neuritis and direct anti-oxidative effects on Schwann cells.

J Neuroinflammation 2019 Mar 9;16(1):58. Epub 2019 Mar 9.

Department of Neurology, St. Josef Hospital, Ruhr-University Bochum, Gudrunstr. 56, 44791, Bochum, Germany.

Background: Corticosteroids dominate in the treatment of chronic autoimmune neuropathies although long-term use is characterized by devastating side effects.

Methods: We introduce the intrathecal application of the synthetic steroid triamcinolone (TRIAM) as a novel therapeutic option in experimental autoimmune neuritis in Lewis rats RESULTS: After immunization with neuritogenic P2 peptide, we show a dose-dependent therapeutic effect of one intrathecal injection of 0.3 or 0. Read More

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http://dx.doi.org/10.1186/s12974-019-1445-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6408772PMC

Inflammatory, regulatory, and autophagy co-expression modules and hub genes underlie the peripheral immune response to human intracerebral hemorrhage.

J Neuroinflammation 2019 Mar 5;16(1):56. Epub 2019 Mar 5.

Department of Neurology, University of California Davis School of Medicine, Sacramento, CA, 95817, USA.

Background: Intracerebral hemorrhage (ICH) has a high morbidity and mortality. The peripheral immune system and cross-talk between peripheral blood and brain have been implicated in the ICH immune response. Thus, we delineated the gene networks associated with human ICH in the peripheral blood transcriptome. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1433-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399982PMC
March 2019
5 Reads

Murine astrocytes produce IL-24 and are susceptible to the immunosuppressive effects of this cytokine.

J Neuroinflammation 2019 Mar 2;16(1):55. Epub 2019 Mar 2.

Department of Biological Sciences, University of North Carolina at Charlotte, 9201 University City Blvd., Charlotte, NC, 28223, USA.

Background: Glia are key regulators of inflammatory responses within the central nervous system (CNS) following infection or trauma. We have previously demonstrated the ability of activated glia to rapidly produce pro-inflammatory mediators followed by a transition to an anti-inflammatory cytokine production profile that includes the immunosuppressive cytokine interleukin (IL)-10 and the closely related cytokine IL-19. IL-24, another member of the IL-10 family, has been studied in a number of inflammatory conditions in the periphery and is known to modulate immune cell activity. Read More

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http://dx.doi.org/10.1186/s12974-019-1444-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397747PMC
March 2019
1 Read

FTY720 controls disease severity and attenuates sciatic nerve damage in chronic experimental autoimmune neuritis.

J Neuroinflammation 2019 Mar 2;16(1):54. Epub 2019 Mar 2.

Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques, INSERM U1119/Université de Strasbourg, Faculté de Médecine, 11 rue Humann, 67085, Strasbourg, France.

Background: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune-mediated inflammatory disease of the peripheral nervous system characterized by a response directed against certain myelin proteins and for which therapies are limited. Previous studies have suggested a beneficial role of FTY720, a sphingosine 1-phosphate (S1P) receptor agonist, known to deplete lymphocytes from the peripheral blood by sequestering them into lymph nodes, in the treatment of experimental autoimmune neuritis (EAN). Therefore, we investigated whether FTY720 is also beneficial in chronic experimental autoimmune neuritis (c-EAN), a recently developed rat model mimicking human CIDP. Read More

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http://dx.doi.org/10.1186/s12974-019-1441-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397476PMC
March 2019
5 Reads

Amlexanox attenuates experimental autoimmune encephalomyelitis by inhibiting dendritic cell maturation and reprogramming effector and regulatory T cell responses.

J Neuroinflammation 2019 Mar 1;16(1):52. Epub 2019 Mar 1.

Department of Neurology, The Second Hospital of Hebei Medical University, Key Laboratory of Hebei Neurology, No. 215 Heping Road, Shijiazhuang, 050000, Hebei, China.

Background: Amlexanox (ALX), a TBK1 inhibitor, can modulate immune responses and has anti-inflammatory properties. To investigate its role in regulating the progression of experimental autoimmune encephalomyelitis (EAE), we studied the effect of ALX on the maturation of dendritic cells (DCs) and the responses of effector and regulatory T cells (Tregs).

Methods: In vitro, bone marrow-derived DCs (BMDCs) were cultured and treated with ALX. Read More

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http://dx.doi.org/10.1186/s12974-019-1438-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396467PMC
March 2019
2 Reads

Impact of microbiota on central nervous system and neurological diseases: the gut-brain axis.

J Neuroinflammation 2019 Mar 1;16(1):53. Epub 2019 Mar 1.

Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX, 77030, USA.

Development of central nervous system (CNS) is regulated by both intrinsic and peripheral signals. Previous studies have suggested that environmental factors affect neurological activities under both physiological and pathological conditions. Although there is anatomical separation, emerging evidence has indicated the existence of bidirectional interaction between gut microbiota, i. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1434-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397457PMC
March 2019
12 Reads

Myelinoclastic diffuse sclerosis (Schilder's disease) is immunologically distinct from multiple sclerosis: results from retrospective analysis of 92 lumbar punctures.

J Neuroinflammation 2019 Feb 28;16(1):51. Epub 2019 Feb 28.

Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.

Background: Myelinoclastic diffuse sclerosis (MDS; also termed Schilder's disease) is a rare inflammatory demyelinating disorder of the central nervous system characterised by demyelination of vast areas of the white matter. It is unclear whether MDS is a variant of multiple sclerosis (MS) or a disease entity in its own right.

Objective: To compare the cerebrospinal fluid (CSF) features of MDS with those of MS. Read More

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http://dx.doi.org/10.1186/s12974-019-1425-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396538PMC
February 2019
2 Reads

Genetic variability of inflammation and oxidative stress genes does not play a major role in the occurrence of adverse events of dopaminergic treatment in Parkinson's disease.

J Neuroinflammation 2019 Feb 27;16(1):50. Epub 2019 Feb 27.

Pharmacogenetics Laboratory, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000, Ljubljana, Slovenia.

Background: Inflammation and oxidative stress are recognized as important contributors to Parkinson's disease pathogenesis. As such, genetic variability in these pathways could have a role in susceptibility for the disease as well as in the treatment outcome. Dopaminergic treatment is effective in management of motor symptoms, but poses a risk for motor and non-motor adverse events. Read More

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http://dx.doi.org/10.1186/s12974-019-1439-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393982PMC
February 2019
2 Reads

Laquinimod, a prototypic quinoline-3-carboxamide and aryl hydrocarbon receptor agonist, utilizes a CD155-mediated natural killer/dendritic cell interaction to suppress CNS autoimmunity.

J Neuroinflammation 2019 Feb 26;16(1):49. Epub 2019 Feb 26.

Institute of Neuropathology, University Medical Center Göttingen, Göttingen, Germany.

Background: Quinoline-3-carboxamides, such as laquinimod, ameliorate CNS autoimmunity in patients and reduce tumor cell metastasis experimentally. Previous studies have focused on the immunomodulatory effect of laquinimod on myeloid cells. The data contained herein suggest that quinoline-3-carboxamides improve the immunomodulatory and anti-tumor effects of NK cells by upregulating the adhesion molecule DNAX accessory molecule-1 (DNAM-1). Read More

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http://dx.doi.org/10.1186/s12974-019-1437-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390632PMC
February 2019
3 Reads

Astrocytic ceramide as possible indicator of neuroinflammation.

J Neuroinflammation 2019 Feb 25;16(1):48. Epub 2019 Feb 25.

Department of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit Amsterdam, VU University Medical Center, PO Box 7057, 1007 MB, Amsterdam, the Netherlands.

Background: Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease dementia (PDD), and frontotemporal lobar dementia (FTLD) are characterized by progressive neuronal loss but differ in their underlying pathological mechanisms. However, neuroinflammation is commonly observed within these different forms of dementia. Recently, it has been suggested that an altered sphingolipid metabolism may contribute to the pathogenesis of a variety of neurodegenerative conditions. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1436-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388480PMC
February 2019
8 Reads

Glial activation and inflammation along the Alzheimer's disease continuum.

J Neuroinflammation 2019 Feb 21;16(1):46. Epub 2019 Feb 21.

Department of Neurology, Akershus University Hospital, P.B. 1000, N-1478, Lørenskog, Norway.

Background: Neuronal and glial cell interaction is essential for synaptic homeostasis and may be affected in Alzheimer's disease (AD). We measured cerebrospinal fluid (CSF) neuronal and glia markers along the AD continuum, to reveal putative protective or harmful stage-dependent patterns of activation.

Methods: We included healthy controls (n = 36) and Aβ-positive (Aβ+) cases (as defined by pathological CSF amyloid beta 1-42 (Aβ42)) with either subjective cognitive decline (SCD, n = 19), mild cognitive impairment (MCI, n = 39), or AD dementia (n = 27). Read More

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http://dx.doi.org/10.1186/s12974-019-1399-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6383268PMC
February 2019

Activation of retinoid X receptor by bexarotene attenuates neuroinflammation via PPARγ/SIRT6/FoxO3a pathway after subarachnoid hemorrhage in rats.

J Neuroinflammation 2019 Feb 21;16(1):47. Epub 2019 Feb 21.

Department of Physiology and Pharmacology, Loma Linda University, 11041 Campus St. Risley Hall, Loma Linda, CA, 92354, USA.

Background: Subarachnoid hemorrhage (SAH) is a life-threatening subtype of stroke with high mortality and disabilities. Retinoid X receptor (RXR) has been shown to be neuroprotective against ischemia/reperfusion injury. This study aimed to investigate the effects of the selective RXR agonist bexarotene on neuroinflammation in a rat model of SAH. Read More

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http://dx.doi.org/10.1186/s12974-019-1432-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6385420PMC
February 2019
1 Read

Therapeutic blockade of HMGB1 reduces early motor deficits, but not survival in the SOD1 mouse model of amyotrophic lateral sclerosis.

J Neuroinflammation 2019 Feb 19;16(1):45. Epub 2019 Feb 19.

Faculty of Medicine, School of Biomedical Sciences, The University of Queensland, St Lucia, Brisbane, QLD, 4072, Australia.

Background: Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing neurodegenerative disease without effective treatment. The receptor for advanced glycation end products (RAGE) and the toll-like receptor (TLR) system are major components of the innate immune system, which have been implicated in ALS pathology. Extracellularly released high-mobility group box 1 (HMGB1) is a pleiotropic danger-associated molecular pattern (DAMP), and is an endogenous ligand for both RAGE and TLR4. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1435-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6380064PMC
February 2019
5 Reads

CD200-CD200R1 inhibitory signaling prevents spontaneous bacterial infection and promotes resolution of neuroinflammation and recovery after stroke.

J Neuroinflammation 2019 Feb 18;16(1):40. Epub 2019 Feb 18.

Department of Neurology, McGovern Medical School, University of Texas Health Science Center, 6431 Fannin Street, Houston, TX, 77370, USA.

Background: Ischemic stroke results in a robust inflammatory response within the central nervous system. As the immune-inhibitory CD200-CD200 receptor 1 (CD200R1) signaling axis is a known regulator of immune homeostasis, we hypothesized that it may play a role in post-stroke immune suppression after stroke.

Methods: In this study, we investigated the role of CD200R1-mediated signaling in stroke using CD200 receptor 1-deficient mice. Read More

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http://dx.doi.org/10.1186/s12974-019-1426-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378746PMC
February 2019
3 Reads
5.408 Impact Factor

Chemokines and matrix metalloproteinases in cerebrospinal fluid of patients with central nervous system complications caused by varicella-zoster virus.

J Neuroinflammation 2019 Feb 18;16(1):42. Epub 2019 Feb 18.

Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Background: Varicella-zoster virus (VZV) is a common viral agent causing central nervous system (CNS) infections including encephalitis, meningitis, and Ramsay Hunt syndrome. Neurological complications occur frequently despite antiviral treatment. Matrix metalloproteinases (MMPs) and cytokines are involved in the neuroinflammatory response during CNS infection. Read More

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http://dx.doi.org/10.1186/s12974-019-1428-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378740PMC
February 2019
2 Reads