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40
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Text
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URL Address
<a href="http://doi.org/10.1096/fj.201900567RR" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fj.201900567RR</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1679-1694
Issue
1
Volume
34
ISSN
8926638
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Update Year & Number
January 2020 Update
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
Department of Pharmaceutical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pharmacological inhibition of CSF1R by GW2580 reduces microglial proliferation and is protective against neuroinflammation and dopaminergic neurodegeneration.
Publisher
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FASEB Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-01
Subject
The topic of the resource
microglia; neuroprotection; Parkinson's disease; proliferation
Creator
An entity primarily responsible for making the resource
Neal Matthew L; Fleming Sheila M; Budge Kevin M; Boyle Alexa M; Kim Chunki; Alam Gelareh; Beier Eric E; Wu Long‐Jun; Richardson Jason R
Description
An account of the resource
Increased pro‐inflammatory cytokine levels and proliferation of activated microglia have been found in Parkinson's disease (PD) patients and animal models of PD, suggesting that targeting of the microglial inflammatory response may result in neuroprotection in PD. Microglial proliferation is regulated by many factors, but colony stimulating factor‐1 receptor (CSF1R) has emerged as a primary factor. Using data mining techniques on existing microarray data, we found that mRNA expression of the CSF1R ligand, CSF‐1, is increased in the brain of PD patients compared to controls. In two different neurotoxic mouse models of PD, acute MPTP and sub‐chronic LPS treatment, mRNA and protein levels of CSF1R and CSF‐1 were significantly increased. Treatment with the CSF1R inhibitor GW2580 significantly attenuated MPTP‐induced CSF1R activation and Iba1‐positive cell proliferation, without a reduction of the basal Iba1‐positive population in the substantia nigra. GW2580 treatment also significantly decreased mRNA levels of pro‐inflammatory factors, without alteration of anti‐inflammatory mediators, and significantly attenuated the MPTP‐induced loss of dopamine neurons and motor behavioral deficits. Importantly, these effects were observed in the absence of overt microglial depletion, suggesting that targeting CSF1R signaling may be a viable neuroprotective strategy in PD that disrupts pro‐inflammatory signaling, but maintains the beneficial effects of microglia. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1096/fj.201900567RR" target="_blank" rel="noreferrer noopener">10.1096/fj.201900567RR</a>
Format
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Journal Article
2020
Alam Gelareh
Beier Eric E
Boyle Alexa M
Budge Kevin M
Department of Pharmaceutical Sciences
Faseb Journal
Fleming Sheila M
January 2020 Update
Journal Article
Kim Chunki
Microglia
Neal Matthew L
NEOMED College of Pharmacy
Neuroprotection
Parkinson's disease
proliferation
Richardson Jason R
Wu Long‐Jun
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2017.08.009</a>
Pages
115–127
Volume
108
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Alternative microglial activation is associated with cessation of progressive dopamine neuron loss in mice systemically administered lipopolysaccharide.
Publisher
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Neurobiology of disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
Animals; Astrocytes/immunology/pathology; Cell Death/physiology; Corpus Striatum/immunology/pathology; Cytokines/metabolism; Disease Progression; Dopaminergic Neurons/*immunology/pathology; Inbred C57BL; Inflammation/pathology/physiopathology; Lipopolysaccharides/*toxicity; Male; Messenger/metabolism; Mice; Microglia/*immunology/pathology; Nerve Degeneration/*immunology/pathology; Neurodegenerative Diseases/immunology/pathology; Neuroimmunomodulation/physiology; Random Allocation; RNA; Time Factors
Creator
An entity primarily responsible for making the resource
Beier Eric E; Neal Matthew; Alam Gelerah; Edler Melissa; Wu Long-Jun; Richardson Jason R
Description
An account of the resource
Inflammation arising from central and/or peripheral sources contributes to the pathogenesis of multiple neurodegenerative diseases including Parkinson's disease (PD). Emerging data suggest that differential activation of glia could lead to the pathogenesis and progression of PD. Here, we sought to determine the relationship between lipopolysaccharide (LPS) treatment, loss of dopaminergic neurons and differential activation of glia. Using a model of repeated injections with LPS (1mg/kg, i.p. for 4days), we found that LPS induced a 34% loss of dopamine neurons in the substantia nigra 19days after initiation of treatment, but no further cell loss was observed at 36days. LPS induced a strong pro-inflammatory response with increased mRNA expression of pro-inflammatory markers, including tumor necrosis factor-alpha (4.8-fold), inducible nitric oxide synthase (2.0-fold), interleukin-1 beta (8.9-fold), interleukin-6 (10.7-fold), and robust glial activation were observed at 1day after final dose of LPS. These pro-inflammatory genes were then reduced at 19days after treatment, when there was a rise in the anti-inflammatory genes Ym1 (1.8-fold) and arginase-1 (2.6-fold). Additionally, 36days after the last LPS injection there was a significant increase in interleukin-10 (2.1-fold) expression. The qPCR data results were supported by protein data, including cytokine measurements, western blotting, and immunofluorescence in brain microglia. Taken together, these data demonstrate that progressive neurodegeneration in the substantia nigra following LPS is likely arrested by microglia shifting to an anti-inflammatory phenotype. Thus, strategies to promote resolution of neuroinflammation may be a promising avenue to slow the progressive loss of dopamine neurons in PD.
Identifier
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<a href="http://doi.org/10.1016/j.nbd.2017.08.009" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2017.08.009</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Alam Gelerah
Animals
Astrocytes/immunology/pathology
Beier Eric E
Cell Death/physiology
Corpus Striatum/immunology/pathology
Cytokines/metabolism
Department of Pharmaceutical Sciences
Disease Progression
Dopaminergic Neurons/*immunology/pathology
Edler Melissa
Inbred C57BL
Inflammation/pathology/physiopathology
Lipopolysaccharides/*toxicity
Male
Messenger/metabolism
Mice
Microglia/*immunology/pathology
Neal Matthew
NEOMED College of Pharmacy
Nerve Degeneration/*immunology/pathology
Neurobiology of disease
Neurodegenerative Diseases/immunology/pathology
Neuroimmunomodulation/physiology
Random Allocation
Richardson Jason R
RNA
Time Factors
Wu Long-Jun