2,342 results match your criteria Journal of Neuroinflammation [Journal]


Combined utility of white blood cell count and blood glucose for predicting in-hospital outcomes in acute ischemic stroke.

J Neuroinflammation 2019 Feb 14;16(1):37. Epub 2019 Feb 14.

Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, No.1055, Sanxiang Road, Suzhou, 215004, Jiangsu, China.

Background: High white blood cell (WBC) count and high blood glucose level are risk factors for mortality and pneumonia after acute ischemic stroke (AIS). We investigated the combined effect of high WBC count and high blood glucose level on hospital admission and in-hospital mortality and pneumonia in acute AIS patients.

Methods: A total of 3124 AIS patients enrolled from December 2013 to May 2014 across 22 hospitals in Suzhou city were included in the present study. Read More

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http://dx.doi.org/10.1186/s12974-019-1422-7DOI Listing
February 2019

Responses of perivascular macrophages to circulating lipopolysaccharides in the subfornical organ with special reference to endotoxin tolerance.

J Neuroinflammation 2019 Feb 14;16(1):39. Epub 2019 Feb 14.

Department of Anatomy and Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634-8521, Japan.

Background: Circulating endotoxins including lipopolysaccharides (LPS) cause brain responses such as fever and decrease of food and water intake, while pre-injection of endotoxins attenuates these responses. This phenomenon is called endotoxin tolerance, but the mechanisms underlying it remain unclear. The subfornical organ (SFO) rapidly produces proinflammatory cytokines including interleukin-1β (IL-1β) in response to peripherally injected LPS, and repeated LPS injection attenuates IL-1β production in the SFO, indicating that the SFO is involved in endotoxin tolerance. Read More

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http://dx.doi.org/10.1186/s12974-019-1431-6DOI Listing
February 2019

More than just inflammation: Ureaplasma species induce apoptosis in human brain microvascular endothelial cells.

J Neuroinflammation 2019 Feb 14;16(1):38. Epub 2019 Feb 14.

University Children's Hospital, University of Wuerzburg, Josef-Schneider-Str. 2, 97080, Wuerzburg, Germany.

Background: Ureaplasma species (spp.) are commonly regarded as low-virulent commensals but may cause invasive diseases in immunocompromised adults and in neonates, including neonatal meningitis. The interactions of Ureaplasma spp. Read More

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http://dx.doi.org/10.1186/s12974-019-1413-8DOI Listing
February 2019

Therapeutic hypercapnia reduces blood-brain barrier damage possibly via protein kinase Cε in rats with lateral fluid percussion injury.

J Neuroinflammation 2019 Feb 13;16(1):36. Epub 2019 Feb 13.

Department of Anesthesiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Background: This study investigated whether therapeutic hypercapnia (TH) ameliorated blood-brain barrier (BBB) damage and improved the neurologic outcome in a rat model of lateral fluid percussion injury (FPI), and explored the possible underlying mechanism.

Methods: Rats underwent lateral FPI and received inhalation of 30%O-70%N or 30%O-N plus CO to maintain arterial blood CO tension (PaCO) between 80 and 100 mmHg for 3 h. To further explore the possible mechanisms for the protective effects of TH, a PKC inhibitor staurosporine or PKCαβ inhibitor GÖ6976 was administered via intracerebral ventricular injection. Read More

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http://dx.doi.org/10.1186/s12974-019-1427-2DOI Listing
February 2019

Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects against Aβ toxicity via attenuating Aβ-induced endoplasmic reticulum stress.

J Neuroinflammation 2019 Feb 13;16(1):35. Epub 2019 Feb 13.

School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.

Background: Extracellular accumulation of amyloid β-peptide (Aβ) is one of pathological hallmarks of Alzheimer's disease (AD) and contributes to the neuronal loss. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER) stress-inducible neurotrophic factor. Many groups, including ours, have proved that MANF rescues neuronal loss in several neurological disorders, such as Parkinson's disease and cerebral ischemia. Read More

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http://dx.doi.org/10.1186/s12974-019-1429-0DOI Listing
February 2019

Correction to: The atypical RhoGTPase RhoE/Rnd3 is a key molecule to acquire a neuroprotective phenotype in microglia.

J Neuroinflammation 2019 Feb 12;16(1):31. Epub 2019 Feb 12.

Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Avd. Conocimiento 17, PTS Granada, 18016, Granada, Spain.

In the version of this article that was originally published [1]; some information in the "Author's contributions" section was omitted. Read More

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http://dx.doi.org/10.1186/s12974-019-1416-5DOI Listing
February 2019

Correlation of alteration of HLA-F expression and clinical characterization in 593 brain glioma samples.

J Neuroinflammation 2019 Feb 12;16(1):33. Epub 2019 Feb 12.

Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, No. 6 Tiantan Xili, Dongcheng District, Beijing, 100050, China.

Background: Human gliomas are highly fatal tumors with a significant feature of immune suppression. The association of the immune system in gliomas is gradually revealed, and immunotherapy is expected to improve the survival of glioma patients. In-depth understanding of the immune microenvironment of gliomas and their associated immunotherapy was increased exponentially in recent years. Read More

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http://dx.doi.org/10.1186/s12974-019-1418-3DOI Listing
February 2019

AMPK activation attenuates inflammatory pain through inhibiting NF-κB activation and IL-1β expression.

J Neuroinflammation 2019 Feb 12;16(1):34. Epub 2019 Feb 12.

Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, Hubei, People's Republic of China.

Background: Chronic pain is a major clinical problem with limited treatment options. Previous studies have demonstrated that activation of adenosine monophosphate-activated protein kinase (AMPK) can attenuate neuropathic pain. Inflammation/immune response at the site of complete Freund's adjuvant (CFA) injection is known to be a critical trigger of the pathological changes that produce inflammatory pain. Read More

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http://dx.doi.org/10.1186/s12974-019-1411-xDOI Listing
February 2019

Annexin A1-derived peptide Ac in a pilocarpine-induced status epilepticus model: anti-inflammatory and neuroprotective effects.

J Neuroinflammation 2019 Feb 12;16(1):32. Epub 2019 Feb 12.

Department of Morphology and Genetics, Federal University of São Paulo (UNIFESP), São Paulo, SP, 04023-900, Brazil.

Background: The inflammatory process has been described as a crucial mechanism in the pathophysiology of temporal lobe epilepsy. The anti-inflammatory protein annexin A1 (ANXA1) represents an interesting target in the regulation of neuroinflammation through the inhibition of leukocyte transmigration and the release of proinflammatory mediators. In this study, the role of the ANXA1-derived peptide Ac in an experimental model of status epilepticus (SE) was evaluated. Read More

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http://dx.doi.org/10.1186/s12974-019-1414-7DOI Listing
February 2019

Neuroinflammation and fractalkine signaling in Alzheimer's disease.

J Neuroinflammation 2019 Feb 11;16(1):30. Epub 2019 Feb 11.

Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, 12901 Bruce B Downs Bvld, Tampa, FL, 33612, USA.

Alzheimer's disease (AD) is a progressive, neurodegenerative disorder, and the most common form of dementia. As the understanding of AD has progressed, it is now believed that AD is an amyloid-initiated tauopathy with neuroinflammation serving as the link between amyloid deposition, tau pathology, and neurodegeneration. As microglia are the main immune effectors in the central nervous system, they have been the focus of attention in studies investigating the neuroinflammatory component of AD. Read More

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http://dx.doi.org/10.1186/s12974-019-1412-9DOI Listing
February 2019

TNF-α/STAT3 pathway epigenetically upregulates Nav1.6 expression in DRG and contributes to neuropathic pain induced by L5-VRT.

J Neuroinflammation 2019 Feb 8;16(1):29. Epub 2019 Feb 8.

Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Rehabilitation Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, China.

Background: Studies showed that upregulation of Nav1.6 increased the neuronal excitability and participated in neuropathic pain in the dorsal root ganglion (DRG). However, the molecular mechanisms underlying Nav1. Read More

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http://dx.doi.org/10.1186/s12974-019-1421-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368780PMC
February 2019

Semaphorin4A causes loss of mature oligodendrocytes and demyelination in vivo.

J Neuroinflammation 2019 Feb 8;16(1):28. Epub 2019 Feb 8.

Department of Neurosurgery, Penn State University College of Medicine, 500 University Drive, Hershey, PA, 17033, USA.

Background: Inappropriate contact between the immune system and the central nervous system is thought to be a cause of demyelination. We previously reported the ability of the class IV semaphorin, Semaphorin4A (Sema4A), to induce apoptosis in human oligodendrocytes; however, these results have yet to be translated to an in vivo setting. Importantly, HIV-associated neurocognitive disorder remains a significant complication for patients on combined anti-retroviral therapy, with white matter damage seen on MRI. Read More

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http://dx.doi.org/10.1186/s12974-019-1420-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368782PMC
February 2019

The role of microglial inflammasome activation in pyroptotic cell death following penetrating traumatic brain injury.

J Neuroinflammation 2019 Feb 8;16(1):27. Epub 2019 Feb 8.

Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, Florida, USA.

Background: Traumatic brain injury remains a significant cause of death and disability in the USA. Currently, there are no effective therapies to mitigate disability except for surgical interventions necessitating a need for continued research into uncovering novel therapeutic targets. In a recent study, we used a rodent model of penetrating traumatic brain injury known as penetrating ballistic-like brain injury (PBBI) to examine the role of innate immunity in post-traumatic secondary injury mechanisms. Read More

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http://dx.doi.org/10.1186/s12974-019-1423-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6367831PMC
February 2019

Co-inhibition of PGF and VEGF blocks their expression in mononuclear phagocytes and limits neovascularization and leakage in the murine retina.

J Neuroinflammation 2019 Feb 7;16(1):26. Epub 2019 Feb 7.

Laboratory for Experimental Immunology of the Eye, Department of Ophthalmology, University of Cologne, Faculty of Medicine and University Hospital Cologne, 50931, Cologne, Germany.

Background: Age-related macular degeneration (AMD) is a leading cause of visual impairment in the elderly. The neovascular (wet) form of AMD can be treated with intravitreal injections of different anti-vascular endothelial growth factor (VEGF) agents. Placental growth factor (PGF) is another member of the VEGF family of cytokines with pro-angiogenic and pro-inflammatory effects. Read More

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http://dx.doi.org/10.1186/s12974-019-1419-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6366121PMC
February 2019
1 Read

Non-myeloablative busulfan chimeric mouse models are less pro-inflammatory than head-shielded irradiation for studying immune cell interactions in brain tumours.

J Neuroinflammation 2019 Feb 5;16(1):25. Epub 2019 Feb 5.

Stem Cell and Neurotherapies Laboratory, Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.

Background: Chimeric mouse models generated via adoptive bone marrow transfer are the foundation for immune cell tracking in neuroinflammation. Chimeras that exhibit low chimerism levels, blood-brain barrier disruption and pro-inflammatory effects prior to the progression of the pathological phenotype, make it difficult to distinguish the role of immune cells in neuroinflammatory conditions. Head-shielded irradiation overcomes many of the issues described and replaces the recipient bone marrow system with donor haematopoietic cells expressing a reporter gene or different pan-leukocyte antigen, whilst leaving the blood-brain barrier intact. Read More

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http://dx.doi.org/10.1186/s12974-019-1410-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362590PMC
February 2019

Neuroprotective effect of Apelin 13 on ischemic stroke by activating AMPK/GSK-3β/Nrf2 signaling.

J Neuroinflammation 2019 Feb 1;16(1):24. Epub 2019 Feb 1.

Department of Pharmacy, Xijing Hospital, Air Force Medical University, No. 127, Changle West Road, Xi'an, 710032, Shaanxi, China.

Background: Previous studies had showed that Apelin 13 could protect against apoptosis induced by ischemic/reperfusion (I/R). However, the mechanisms whereby Apelin 13 protected brain I/R remained to be elucidated. The present study was designed to determine whether Apelin 13 provided protection through AMPK/GSK-3β/Nrf2 pathway. Read More

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http://dx.doi.org/10.1186/s12974-019-1406-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357442PMC
February 2019
1 Read

Oligodendrocyte-specific ATF4 inactivation does not influence the development of EAE.

J Neuroinflammation 2019 Feb 1;16(1):23. Epub 2019 Feb 1.

Department of Neuroscience, University of Minnesota, Minneapolis, MN, 55455, USA.

Background: Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory demyelinating and neurodegenerative diseases of the CNS. Although recent studies suggest the neuroprotective effects of oligodendrocytes in neurodegenerative diseases, it remains unknown whether oligodendrocyte death induced by inflammatory attacks contributes to neurodegeneration in MS and EAE. Upon endoplasmic reticulum (ER) stress, activation of pancreatic ER kinase (PERK) promotes cell survival through induction of activating transcription factor 4 (ATF4) by phosphorylating eukaryotic translation initiation factor 2α (eIF2α). Read More

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http://dx.doi.org/10.1186/s12974-019-1415-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357515PMC
February 2019
1 Read

The TRPC6 inhibitor, larixyl acetate, is effective in protecting against traumatic brain injury-induced systemic endothelial dysfunction.

J Neuroinflammation 2019 Jan 31;16(1):21. Epub 2019 Jan 31.

Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.

Background: The incidence of traumatic brain injuries (TBIs) is on the rise in the USA. Concussions, or mild TBIs without skull fracture, account for about 75% of all TBIs. Mild TBIs (mTBIs) lead to memory and cognitive deficits, headaches, intraocular pressure rises, axonal degeneration, neuroinflammation, and an array of cerebrovascular dysfunctions, including increased vascular permeability and decreased cerebral blood flow. Read More

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http://dx.doi.org/10.1186/s12974-019-1407-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6354413PMC
January 2019
1 Read

CSF1R antagonism limits local restimulation of antiviral CD8 T cells during viral encephalitis.

J Neuroinflammation 2019 Jan 31;16(1):22. Epub 2019 Jan 31.

Department of Internal Medicine, Division of Infectious Diseases, Washington University School of Medicine, Saint Louis, MO, 63110, USA.

Background: Microglia are resident macrophages of the central nervous system (CNS) locally maintained through colony-stimulating factor 1 receptor (CSF1R) signaling. Microglial depletion via CSF1R inactivation improves cognition in mouse models of neuroinflammation, but limits virologic control in the CNS of mouse models of neurotropic infections by unknown mechanisms. We hypothesize that CSF1R plays a critical role in myeloid cell responses that restrict viral replication and locally restimulate recruited antiviral T cells within the CNS. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-019-1397-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6354430PMC
January 2019
5 Reads

The spleen may be an important target of stem cell therapy for stroke.

J Neuroinflammation 2019 Jan 30;16(1):20. Epub 2019 Jan 30.

Xiangtan Central Hospital, Clinical Practice Base of Central South University, Xiangtan, 411100, China.

Stroke is the most common cerebrovascular disease, the second leading cause of death behind heart disease and is a major cause of long-term disability worldwide. Currently, systemic immunomodulatory therapy based on intravenous cells is attracting attention. The immune response to acute stroke is a major factor in cerebral ischaemia (CI) pathobiology and outcomes. Read More

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http://dx.doi.org/10.1186/s12974-019-1400-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352449PMC
January 2019
2 Reads

Cerebrovascular manifestations of herpes simplex virus infection of the central nervous system: a systematic review.

J Neuroinflammation 2019 Jan 29;16(1):19. Epub 2019 Jan 29.

Department of Neurology, Christian Doppler Medical Center, Paracelsus Medical University, Ignaz-Harrer-Str. 79, 5020, Salzburg, Austria.

Background: Intracerebral hemorrhage and ischemic stroke are increasingly recognized complications of central nervous system (CNS) infection by herpes simplex virus (HSV).

Aim Of The Study: To analyze clinical, imaging, and laboratory findings and outcomes of cerebrovascular manifestations of HSV infection.

Methods: Systematic literature review from January 2000 to July 2018. Read More

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http://dx.doi.org/10.1186/s12974-019-1409-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352343PMC
January 2019
1 Read

JNK signalling mediates aspects of maternal immune activation: importance of maternal genotype in relation to schizophrenia risk.

J Neuroinflammation 2019 Jan 28;16(1):18. Epub 2019 Jan 28.

Institute of Neuroscience and Psychology, West Medical Building, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK.

Background: Important insight into the mechanisms through which gene-environmental interactions cause schizophrenia can be achieved through preclinical studies combining prenatal immune stimuli with disease-related genetic risk modifications. Accumulating evidence associates JNK signalling molecules, including MKK7/MAP2K7, with genetic risk. We tested the hypothesis that Map2k7 gene haploinsufficiency in mice would alter the prenatal immune response to the viral mimetic polyriboinosinic-polyribocytidylic acid (polyI:C), specifically investigating the impact of maternal versus foetal genetic variants. Read More

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http://dx.doi.org/10.1186/s12974-019-1408-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6350402PMC
January 2019

Evidence of a distinct peripheral inflammatory profile in sport-related concussion.

J Neuroinflammation 2019 Jan 26;16(1):17. Epub 2019 Jan 26.

Faculty of Kinesiology & Physical Education, University of Toronto, Toronto, ON, Canada.

Background: Inflammation is considered a hallmark of concussion pathophysiology in experimental models, yet is understudied in human injury. Despite the growing use of blood biomarkers in concussion, inflammatory biomarkers have not been well characterized. Furthermore, it is unclear if the systemic inflammatory response to concussion differs from that of musculoskeletal injury. Read More

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http://dx.doi.org/10.1186/s12974-019-1402-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347801PMC
January 2019
2 Reads

A novel neurotherapeutic for multiple sclerosis, ischemic injury, methamphetamine addiction, and traumatic brain injury.

J Neuroinflammation 2019 Jan 23;16(1):14. Epub 2019 Jan 23.

Neuroimmunology Research, R&D-31, VA Portland Health Care System, 3710 SW U.S. Veterans Hospital Rd., Portland, OR, 97239, USA.

Neurovascular, autoimmune, and traumatic injuries of the central nervous system (CNS) all have in common an initial acute inflammatory response mediated by influx across the blood-brain barrier of activated mononuclear cells followed by chronic and often progressive disability. Although some anti-inflammatory therapies can reduce cellular infiltration into the initial lesions, there are essentially no effective treatments for the progressive phase. We here review the successful treatment of animal models for four separate neuroinflammatory and neurodegenerative CNS conditions using a single partial MHC class II construct called DRa1-hMOG-35-55 or its newest iteration, DRa1(L50Q)-hMOG-35-55 (DRhQ) that can be administered without a need for class II tissue type matching due to the conserved DRα1 moiety of the drug. Read More

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http://dx.doi.org/10.1186/s12974-018-1393-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6346590PMC
January 2019
2 Reads

Cerebrospinal fluid levels of glial marker YKL-40 strongly associated with axonal injury in HIV infection.

J Neuroinflammation 2019 Jan 24;16(1):16. Epub 2019 Jan 24.

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

Background: HIV-1 infects the central nervous system (CNS) shortly after transmission. This leads to a chronic intrathecal immune activation. YKL-40, a biomarker that mainly reflects activation of astroglial cells, has not been thoroughly investigated in relation to HIV. Read More

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http://dx.doi.org/10.1186/s12974-019-1404-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345016PMC
January 2019

Blood-brain barrier permeability and physical exercise.

J Neuroinflammation 2019 Jan 24;16(1):15. Epub 2019 Jan 24.

Department of Human Physiology, Faculty of Health Sciences, Medical University of Gdansk, Tuwima Str. 15, 80-210, Gdansk, Poland.

In this narrative review, a theoretical framework on the crosstalk between physical exercise and blood-brain barrier (BBB) permeability is presented. We discuss the influence of physical activity on the factors affecting BBB permeability such as systemic inflammation, the brain renin-angiotensin and noradrenergic systems, central autonomic function and the kynurenine pathway. The positive role of exercise in multiple sclerosis and Alzheimer's disease is described. Read More

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http://dx.doi.org/10.1186/s12974-019-1403-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345022PMC
January 2019

Cerebrospinal fluid CXLC13 indicates disease course in neuroinfection: an observational study.

J Neuroinflammation 2019 Jan 19;16(1):13. Epub 2019 Jan 19.

Department of Neurology, Christian-Doppler-Klinik, Paracelsus Medical University, Salzburg, Austria.

Background: The chemokine CXCL13 is an intensively investigated biomarker in Lyme neuroborreliosis (LNB). Its role in other neuroinfections is increasingly recognized but less clear.

Objective: To determine the significance of CXCL13 in established central nervous system (CNS) infections other than LNB by matching cerebrospinal fluid (CSF) CXCL13 elevations with severity of the disease course. Read More

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http://dx.doi.org/10.1186/s12974-019-1405-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6339696PMC
January 2019
3 Reads

Loss of Par1b/MARK2 primes microglia during brain development and enhances their sensitivity to injury.

J Neuroinflammation 2019 Jan 17;16(1):11. Epub 2019 Jan 17.

Department of Neuroscience and Cell Biology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ, 08854, USA.

Background: Microglia, the resident immune cells of the brain, exhibit various morphologies that correlate with their functions under physiological and pathological conditions. In conditions such as aging and stress, microglia priming occurs, which leads to altered morphology and lower threshold for activation upon further insult. However, the molecular mechanisms that lead to microglia priming are unclear. Read More

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http://dx.doi.org/10.1186/s12974-018-1390-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335724PMC
January 2019

Transplantation of neural precursors generated from spinal progenitor cells reduces inflammation in spinal cord injury via NF-κB pathway inhibition.

J Neuroinflammation 2019 Jan 17;16(1):12. Epub 2019 Jan 17.

New York Medical College, Valhalla, NY, 10595, USA.

Background: Traumatic spinal cord injury (SCI) triggers a chain of events that is accompanied by an inflammatory reaction leading to necrotic cell death at the core of the injury site, which is restricted by astrogliosis and apoptotic cell death in the surrounding areas. Activation of nuclear factor-κB (NF-κB) signaling pathway has been shown to be associated with inflammatory response induced by SCI. Here, we elucidate the pattern of activation of NF-κB in the pathology of SCI in rats and investigate the effect of transplantation of spinal neural precursors (SPC-01) on its activity and related astrogliosis. Read More

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http://dx.doi.org/10.1186/s12974-019-1394-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335809PMC
January 2019

Cathepsin C promotes microglia M1 polarization and aggravates neuroinflammation via activation of Ca-dependent PKC/p38MAPK/NF-κB pathway.

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

Department of Anatomy, Dalian Medical University, West Section No.9, South Road, Lvshun, Dalian, 116044, Liaoning, China.

Background: Microglia-derived lysosomal cathepsins are important inflammatory mediators to trigger signaling pathways in inflammation-related cascades. Our previous study showed that the expression of cathepsin C (CatC) in the brain is induced predominantly in activated microglia in neuroinflammation. Moreover, CatC can induce chemokine production in brain inflammatory processes. Read More

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http://dx.doi.org/10.1186/s12974-019-1398-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335804PMC
January 2019
1 Read

The phagocytic state of brain myeloid cells after ischemia revealed by superresolution structured illumination microscopy.

J Neuroinflammation 2019 Jan 16;16(1). Epub 2019 Jan 16.

Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via G. La Masa 19, 20156, Milan, Italy.

Background: Phagocytosis is a key function of myeloid cells and is highly involved in brain ischemic injury. It has been scarcely studied in vivo, thus preventing a deep knowledge of the processes occurring in the ischemic environment. Structured illumination microscopy (SIM) is a superresolution technique which helps study phagocytosis, a process involving the recruitment of vesicles sized below the resolution limits of standard confocal microscopy. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
Publisher Site
http://dx.doi.org/10.1186/s12974-019-1401-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335825PMC
January 2019
4 Reads

Mesenchymal stem cells alleviate the early brain injury of subarachnoid hemorrhage partly by suppression of Notch1-dependent neuroinflammation: involvement of Botch.

J Neuroinflammation 2019 Jan 15;16(1). Epub 2019 Jan 15.

Department of Neurosurgery, Zhujiang Hospital, Southern Medical University, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Guangzhou, 510282, China.

Background: Activated microglia-mediated neuroinflammation has been regarded as an underlying key player in the pathogenesis of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI). The therapeutic potential of bone marrow mesenchymal stem cells (BMSCs) transplantation has been demonstrated in several brain injury models and is thought to involve modulation of the inflammatory response. The present study investigated the salutary effects of BMSCs on EBI after SAH and the potential mechanism mediated by Notch1 signaling pathway inhibition. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
Publisher Site
http://dx.doi.org/10.1186/s12974-019-1396-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334441PMC
January 2019
8 Reads

CSF inflammatory markers differ in gram-positive versus gram-negative shunt infections.

J Neuroinflammation 2019 Jan 9;16(1). Epub 2019 Jan 9.

Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

Background: Cerebrospinal fluid (CSF) shunt placement is frequently complicated by bacterial infection. Shunt infection diagnosis relies on bacterial culture of CSF which can often produce false-negative results. Negative cultures present a conundrum for physicians as they are left to rely on other CSF indices, which can be unremarkable. Read More

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http://dx.doi.org/10.1186/s12974-019-1395-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325818PMC
January 2019

Early treatment with minocycline following stroke in rats improves functional recovery and differentially modifies responses of peri-infarct microglia and astrocytes.

J Neuroinflammation 2019 Jan 9;16(1). Epub 2019 Jan 9.

Centre for Neuroscience, College of Medicine and Public Health, Flinders University, GPO Box 2100, Adelaide, SA, 5001, Australia.

Background: Altered neuronal connectivity in peri-infarct tissue is an important contributor to both the spontaneous recovery of neurological function that commonly develops after stroke and improvements in recovery that have been induced by experimental treatments in animal models. Microglia and astrocytes are primary determinants of the environment in peri-infarct tissue and hence strongly influence the potential for neuronal plasticity. However, the specific roles of these cells and the timing of critical changes in their function are not well understood. Read More

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http://dx.doi.org/10.1186/s12974-018-1379-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325745PMC
January 2019
1 Read

Neuropathology in intrauterine growth restricted newborn piglets is associated with glial activation and proinflammatory status in the brain.

J Neuroinflammation 2019 Jan 8;16(1). Epub 2019 Jan 8.

UQ Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Herston, QLD, 4029, Australia.

Background: The fetal brain is particularly vulnerable to intrauterine growth restriction (IUGR) conditions evidenced by neuronal and white matter abnormalities and altered neurodevelopment in the IUGR infant. To further our understanding of neurodevelopment in the newborn IUGR brain, clinically relevant models of IUGR are required. This information is critical for the design and implementation of successful therapeutic interventions to reduce aberrant brain development in the IUGR newborn. Read More

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http://dx.doi.org/10.1186/s12974-018-1392-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323795PMC
January 2019

Long-term characterization of activated microglia/macrophages facilitating the development of experimental brain metastasis through intravital microscopic imaging.

J Neuroinflammation 2019 Jan 7;16(1). Epub 2019 Jan 7.

Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics-Huazhong University of Science and Technology, Room G304, Wuhan, 430074, Hubei, China.

Background: Microglia/macrophages (M/Ms) with multiple functions derived from distinct activation states are key surveillants maintaining brain homeostasis. However, their activation status and role during the brain metastasis of malignant tumors have been poorly characterized.

Methods: Heterozygous CX3CR1-GFP transgenic mice were used to visualize the dynamic changes of M/Ms during the development of experimental brain metastasis through long-term intravital imaging equipped with redesigned bilateral cranial windows. Read More

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http://dx.doi.org/10.1186/s12974-018-1389-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323850PMC
January 2019
1 Read

Transplantation of mesenchymal stem cells genetically engineered to overexpress interleukin-10 promotes alternative inflammatory response in rat model of traumatic brain injury.

J Neuroinflammation 2019 Jan 5;16(1). Epub 2019 Jan 5.

Field Neurosciences Institute of Laboratory for Restorative Neurology, Central Michigan University, Mt. Pleasant, MI, 48859, USA.

Background: Traumatic brain injury (TBI) is a major cause for long-term disability, yet the treatments available that improve outcomes after TBI limited. Neuroinflammatory responses are key contributors to determining patient outcomes after TBI. Transplantation of mesenchymal stem cells (MSCs), which release trophic and pro-repair cytokines, represents an effective strategy to reduce inflammation after TBI. Read More

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http://dx.doi.org/10.1186/s12974-018-1383-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320578PMC
January 2019
1 Read

Peripheral adaptive immunity of the triple transgenic mouse model of Alzheimer's disease.

J Neuroinflammation 2019 Jan 5;16(1). Epub 2019 Jan 5.

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.

Background: Immunologic abnormalities have been described in peripheral blood and central nervous system of patients suffering from Alzheimer's disease (AD), yet their role in the pathogenesis still remains poorly defined.

Aim And Methods: We used the triple transgenic mouse model (3xTg-AD) to reproduce Aβ (amyloid plaques) and tau (neurofibrillary tangles) neuropathologies. We analyzed important features of the adaptive immune system in serum, primary (bone marrow) as well as secondary (spleen) lymphoid organs of 12-month-old 3xTg-AD mice using flow cytometry and ELISPOT. Read More

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http://dx.doi.org/10.1186/s12974-018-1380-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320637PMC
January 2019

Crosstalk between NFκB-dependent astrocytic CXCL1 and neuron CXCR2 plays a role in descending pain facilitation.

J Neuroinflammation 2019 Jan 3;16(1). Epub 2019 Jan 3.

Department of Anesthesiology and Pain Research center, The First Affiliated Hospital of Jiaxing University, Jiaxing, 314001, China.

Background: Despite accumulating evidence on the role of glial cells and their associated chemicals in mechanisms of pain, few studies have addressed the potential role of chemokines in the descending facilitation of chronic pain. We aimed to study the hypothesis that CXCL1/CXCR2 axis in the periaqueductal gray (PAG), a co-restructure of the descending nociceptive system, is involved in descending pain facilitation.

Methods: Intramedullary injection of Walker 256 mammary gland carcinoma cells of adult female Sprague Dawley rats was used to establish a bone cancer pain (BCP) model. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
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http://dx.doi.org/10.1186/s12974-018-1391-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317220PMC
January 2019
3 Reads

A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke.

J Neuroinflammation 2018 Dec 20;15(1):348. Epub 2018 Dec 20.

Department of Neurology, The Second Xiangya Hospital, Central South University, Renmin Road 139#, Changsha, 410011, Hunan, China.

Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood-brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. Read More

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http://dx.doi.org/10.1186/s12974-018-1387-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302517PMC
December 2018

Fluoxetine attenuates neuroinflammation in early brain injury after subarachnoid hemorrhage: a possible role for the regulation of TLR4/MyD88/NF-κB signaling pathway.

J Neuroinflammation 2018 Dec 20;15(1):347. Epub 2018 Dec 20.

Department of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.

Background: Neuroinflammation is closely associated with functional outcome in subarachnoid hemorrhage (SAH) patients. Our recent study demonstrated that fluoxetine inhibited NLRP3 inflammasome activation and attenuated necrotic cell death in early brain injury after SAH, while the effects and potential mechanisms of fluoxetine on neuroinflammation after SAH have not been well-studied yet.

Methods: One hundred and fifty-three male SD rats were subjected to the endovascular perforation model of SAH. Read More

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http://dx.doi.org/10.1186/s12974-018-1388-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302437PMC
December 2018
3 Reads
5.408 Impact Factor

Sequential alteration of microglia and astrocytes in the rat thalamus following spinal nerve ligation.

J Neuroinflammation 2018 Dec 20;15(1):349. Epub 2018 Dec 20.

Bordeaux University, Bordeaux, France.

Background: Spinal reactive astrocytes and microglia are known to participate to the initiation and maintenance of neuropathic pain. However, whether reactive astrocytes and microglia in thalamic nuclei that process sensory-discriminative aspects of pain play a role in pain behavior remains poorly investigated. Therefore, the present study evaluated whether the presence of reactive glia (hypertrophy, increased number and upregulation of glial markers) in the ventral posterolateral thalamic nucleus (VPL) correlates with pain symptoms, 14 and 28 days after unilateral L5/L6 spinal nerve ligation (SNL) in rats. Read More

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http://dx.doi.org/10.1186/s12974-018-1378-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302506PMC
December 2018

Imaging glial activation in patients with post-treatment Lyme disease symptoms: a pilot study using [C]DPA-713 PET.

J Neuroinflammation 2018 Dec 19;15(1):346. Epub 2018 Dec 19.

Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

The pathophysiology of post-treatment Lyme disease syndrome (PTLDS) may be linked to overactive immunity including aberrant activity of the brain's resident immune cells, microglia. Here we used [C]DPA-713 and positron emission tomography to quantify the 18 kDa translocator protein, a marker of activated microglia or reactive astrocytes, in the brains of patients with post-treatment Lyme disease symptoms of any duration compared to healthy controls. Genotyping for the TSPO rs6971 polymorphism was completed, and individuals with the rare, low affinity binding genotype were excluded. Read More

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http://dx.doi.org/10.1186/s12974-018-1381-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6299943PMC
December 2018
1 Read

A mathematical model of neuroinflammation in severe clinical traumatic brain injury.

J Neuroinflammation 2018 Dec 18;15(1):345. Epub 2018 Dec 18.

Department of Mathematics, University of Pittsburgh, 301 Thackeray Hall, Pittsburgh, PA, 15260, USA.

Background: Understanding the interdependencies among inflammatory mediators of tissue damage following traumatic brain injury (TBI) is essential in providing effective, patient-specific care. Activated microglia and elevated concentrations of inflammatory signaling molecules reflect the complex cascades associated with acute neuroinflammation and are predictive of recovery after TBI. However, clinical TBI studies to date have not focused on modeling the dynamic temporal patterns of simultaneously evolving inflammatory mediators, which has potential in guiding the design of future immunomodulation intervention studies. Read More

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http://dx.doi.org/10.1186/s12974-018-1384-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6299616PMC
December 2018
1 Read
5.408 Impact Factor

Monocyte infiltration rather than microglia proliferation dominates the early immune response to rapid photoreceptor degeneration.

J Neuroinflammation 2018 Dec 15;15(1):344. Epub 2018 Dec 15.

Department of Cell Biology and Human Anatomy, University of California, Davis, 1 Shields Avenue, Davis, CA, 95616, USA.

Background: Activation of resident microglia accompanies every known form of neurodegeneration, but the involvement of peripheral monocytes that extravasate and rapidly transform into microglia-like macrophages within the central nervous system during degeneration is far less clear.

Methods: Using a combination of in vivo ocular imaging, flow cytometry, and immunohistochemistry, we investigated the response of infiltrating cells in a light-inducible mouse model of photoreceptor degeneration.

Results: Within 24 h, resident microglia became activated and began migrating to the site of degeneration. Read More

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http://dx.doi.org/10.1186/s12974-018-1365-4DOI Listing
December 2018

The atypical RhoGTPase RhoE/Rnd3 is a key molecule to acquire a neuroprotective phenotype in microglia.

J Neuroinflammation 2018 Dec 15;15(1):343. Epub 2018 Dec 15.

Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Avd. Conocimiento 17, PTS Granada, 18016, Granada, Spain.

Background: Over-activated microglia play a central role during neuroinflammation, leading to neuronal cell death and neurodegeneration. Reversion of over-activated to neuroprotective microglia phenotype could regenerate a healthy CNS-supporting microglia environment. Our aim was to identify a dataset of intracellular molecules in primary microglia that play a role in the transition of microglia to a ramified, neuroprotective phenotype. Read More

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http://dx.doi.org/10.1186/s12974-018-1386-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6295018PMC
December 2018
1 Read

Methamphetamine neurotoxicity, microglia, and neuroinflammation.

J Neuroinflammation 2018 Dec 12;15(1):341. Epub 2018 Dec 12.

Department of Neuroscience, University of Florida College of Medicine and McKnight Brain Institute, JHM Health Science Center, PO Box 100244, Gainesville, FL, 32610, USA.

Methamphetamine (METH) is an illicit psychostimulant that is subject to abuse worldwide. While the modulatory effects of METH on dopamine neurotransmission and its neurotoxicity in the central nervous system are well studied, METH's effects on modulating microglial neuroimmune functions and on eliciting neuroinflammation to affect dopaminergic neurotoxicity has attracted considerable attention in recent years. The current review illuminates METH-induced neurotoxicity from a neuropathological perspective by summarizing studies reporting microglial activation after METH administration in rodents. Read More

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https://jneuroinflammation.biomedcentral.com/articles/10.118
Publisher Site
http://dx.doi.org/10.1186/s12974-018-1385-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292109PMC
December 2018
6 Reads

Circulating levels of IL-1 family cytokines and receptors in Alzheimer's disease: new markers of disease progression?

J Neuroinflammation 2018 Dec 12;15(1):342. Epub 2018 Dec 12.

Centre for Research and Training in Medicine for Aging, Department of Medicine and Health Sciences "Vincenzo Tiberio", University of Molise, Località Tappino, 86100, Campobasso, Italy.

Background: Although the mechanisms underlying AD neurodegeneration are not fully understood, it is now recognised that inflammation could play a crucial role in the initiation and progression of AD neurodegeneration. A neuro-inflammatory network, based on the anomalous activation of microglial cells, includes the production of a number of inflammatory cytokines both locally and systemically. These may serve as diagnostic markers or therapeutic targets for AD neurodegeneration. Read More

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http://dx.doi.org/10.1186/s12974-018-1376-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292179PMC
December 2018
1 Read

Colony-stimulating factor 1 receptor inhibition prevents disruption of the blood-retina barrier during chronic inflammation.

J Neuroinflammation 2018 Dec 12;15(1):340. Epub 2018 Dec 12.

Department of Ophthalmology, Inselspital, Bern University Hospital, and University of Bern, CH-3010, Bern, Switzerland.

Background: Microglia-associated inflammation is closely related to the pathogenesis of various retinal diseases such as uveitis and diabetic retinopathy, which are associated with increased vascular permeability. In this study, we investigated the effect of systemic lipopolysaccharide (LPS) exposure to activation and proliferation of retinal microglia /macrophages.

Methods: Balb/c and Cx3cr1 mice were challenged with LPS (1 mg/kg) daily for four consecutive days. Read More

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http://dx.doi.org/10.1186/s12974-018-1373-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292111PMC
December 2018

Bidirectional gut-brain-microbiota axis as a potential link between inflammatory bowel disease and ischemic stroke.

J Neuroinflammation 2018 Dec 11;15(1):339. Epub 2018 Dec 11.

Department of Anesthesiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310000, Zhejiang, China.

Emerging evidence suggests that gut-brain-microbiota axis (GBMAx) may play a pivotal role linking gastrointestinal and neuronal disease. In this review, we summarize the latest advances in studies of GBMAx in inflammatory bowel disease (IBD) and ischemic stroke. A more thorough understanding of the GBMAx could advance our knowledge about the pathophysiology of IBD and ischemic stroke and help to identify novel therapeutic targets via modulation of the GBMAx. Read More

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http://dx.doi.org/10.1186/s12974-018-1382-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6290529PMC
December 2018
5 Reads
5.408 Impact Factor