1
40
4
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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.2020.104956" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2020.104956</a>
Pages
104956
Volume
142
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.nbd.2020.104956" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.nbd.2020.104956</a>
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Update Year & Number
July 2020 List
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
Microglia depletion rapidly and reversibly alters amyloid pathology by modification of plaque compaction and morphologies.
Publisher
An entity responsible for making the resource available
Neurobiology of Disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-05
Subject
The topic of the resource
Microglia; Inflammation; Neuroprotection; AD; Barrier; CSF1R; Plaques
Creator
An entity primarily responsible for making the resource
Casali BT; MacPherson KP; Reed-Geaghan EG; Landreth GE
Description
An account of the resource
Alzheimer's disease (AD) is a prominent neurodegenerative disorder characterized by deposition of β-amyloid (Aβ)-containing extracellular plaques, accompanied by a microglial-mediated inflammatory response, that leads to cognitive decline. Microglia perform many disease-modifying functions such as phagocytosis of plaques, plaque compaction, and modulation of inflammation through the secretion of cytokines. Microglia are reliant upon colony-stimulating factor receptor-1 (CSF1R) activation for survival. In AD mouse models, chronic targeted depletion of microglia via CSF1R antagonism attenuates plaque formation in early disease but fails to alter plaque burden in late disease. It is unclear if acute depletion of microglia during the peak period of plaque deposition will alter disease pathogenesis, and if so, whether these effects are reversible upon microglial repopulation. To test this, we administered the CSF1R antagonist PLX5622 to the 5XFAD mouse model of AD at four months of age for approximately one month. In a subset of mice, the drug treatment was discontinued, and the mice were fed a control diet for an additional month. We evaluated plaque burden and composition, microgliosis, inflammatory marker expression, and neuritic dystrophy. In 5XFAD animals, CSF1R blockade for 28 days depleted microglia across brain regions by over 50%, suppressed microgliosis, and reduced plaque burden. In microglial-depleted AD animals, neuritic dystrophy was enhanced, and increased diffuse-like plaques and fewer compact-like plaques were observed. Removal of PLX5622 elicited microglial repopulation and subsequent plaque remodeling, resulting in more compact plaques predominating microglia-repopulated regions. We found that microglia limit diffuse plaques by maintaining compact-like plaque properties, thereby blocking the progression of neuritic dystrophy. Microglial repopulation reverses these effects. Collectively, we show that microglia are neuroprotective through maintenance of plaque compaction and morphologies during peak disease progression.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.nbd.2020.104956" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2020.104956</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
AD
barrier
Casali BT
CSF1R
Department of Pharmaceutical Sciences
Inflammation
journalArticle
July 2020 List
Landreth GE
MacPherson KP
Microglia
NEOMED College of Pharmacy
Neurobiology of disease
Neuroprotection
Plaques
Reed-Geaghan EG
-
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/10.1038/srep03274" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/srep03274</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
6-6
Volume
3
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Cysteinyl Leukotrienes Regulate Endothelial Cell Inflammatory And Proliferative Signals Through Cyslt(2) And Cyslt(1) Receptors
Publisher
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Scientific Reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-11
Subject
The topic of the resource
atherosclerosis; barrier; dysfunction; expression; gamma; intestinal epithelial-cells; ischemia-reperfusion injury; migration; pathway; Science & Technology - Other Topics; thrombin
Creator
An entity primarily responsible for making the resource
Duah E; Adapala R K; Al-Azzam N; Kondeti V; Gombedza F; Thodeti C K; Paruchuri S
Identifier
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<a href="http://doi.org/10.1038/srep03274" target="_blank" rel="noreferrer noopener">10.1038/srep03274</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
Adapala R K
Al-Azzam N
Atherosclerosis
barrier
Duah E
dysfunction
expression
gamma
Gombedza F
intestinal epithelial-cells
ischemia-reperfusion injury
Kondeti V
migration
Paruchuri S
pathway
Science & Technology - Other Topics
Scientific reports
Thodeti C K
Thrombin
-
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.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2012.10.029</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
133-139
Volume
1489
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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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Ngp1-01, A Multi-targeted Polycyclic Cage Amine, Attenuates Brain Endothelial Cell Death In Iron Overload Conditions
Publisher
An entity responsible for making the resource available
Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-12
Subject
The topic of the resource
activator; barrier; calcium channels; channels provide; intracerebral hemorrhage; Iron-overload; neurodegeneration; neurodegenerative disorders; neuroprotection; Neurosciences & Neurology; Nimodipine; parkinsons-disease; permeability; rat-brain; toxicity; transport; Vascular endothelial cells; Voltage-gated calcium channel
Creator
An entity primarily responsible for making the resource
Lockman J A; Geldenhuys W J; Jones-Higgins M R; Patrick J D; Allen D D; Van der Schyf C J
Description
An account of the resource
Development and progression of neurodegenerative disorders have, amongst other potential causes, been attributed to a disruption of iron regulatory mechanisms and iron accumulation. Excess extracellular iron may enter cells via nontraditional routes such as voltage-gated calcium channels and N-methyl-D-aspartate (NMDA) receptors leading to intracellular oxidative damage and ultimately mitochondrial failure. Nimodipine, an L-type calcium channel blocker has been shown to reduce iron-induced toxicity in neuronal and brain endothelial cells. Our current study investigates NGP1-01, a multimodal drug acting as an antagonist at both the NMDA receptor and the L-type calcium channel. Our previous studies support NGP1-01. as a promising neuroprotective agent in diseases involving calcium-related excitotoxicity. We demonstrate here that NGP1-01 (1 and 10 mu M) pretreatment abrogates the effects of iron overload in brain endothelial cells protecting cellular viability. Both concentrations of NGP1-01 were found to attenuate iron-induced reduction in cellular viability to a similar extent, and were statistically significant. To further verify the mechanism, the L-type calcium channel agonist FPL 64176 was administered to promote iron uptake. Addition of NGP1-01 dose-dependently reduced FPL 64176 stimulated uptake of iron. These data support further evaluation of NGP1-01 as a neuroprotective agent, not only in diseases associated with excitotoxicity, but also in those of iron overload. (C) 2012 Elsevier B.V. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2012.10.029</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
activator
Allen D D
barrier
Brain research
Calcium Channels
channels provide
Geldenhuys W J
intracerebral hemorrhage
Iron-overload
Jones-Higgins M R
Journal Article or Conference Abstract Publication
Lockman J A
Neurodegeneration
neurodegenerative disorders
Neuroprotection
Neurosciences & Neurology
nimodipine
parkinsons-disease
Patrick J D
Permeability
rat-brain
toxicity
transport
Van der Schyf C J
Vascular endothelial cells
Voltage-gated calcium channel
-
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/10.1124/jpet.109.157776" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/jpet.109.157776</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
371-379
Issue
2
Volume
332
Search for Full-text
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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
Nicotine Exacerbates Brain Edema during In Vitro and In Vivo Focal Ischemic Conditions
Publisher
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Journal of Pharmacology and Experimental Therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-02
Subject
The topic of the resource
acetylcholine-receptor subtypes; barrier; cigarette-smoking; exposure; middle cerebral-artery; occlusion; permeability; Pharmacology & Pharmacy; rat; risk; stroke; water
Creator
An entity primarily responsible for making the resource
Paulson J R; Yang T Z; Selvaraj P K; Mdzinarishvili A; Van der Schyf C J; Klein J; Bickel U; Abbruscato T J
Description
An account of the resource
We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na+, K+, 2Cl(-) cotransporter (NKCC) during in vitro hypoxia-aglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke. Oxygen glucose deprivation (OGD) was studied in rat hippocampal slices with short-term or long-term exposure to nicotine and cigarette smoke constituents. During short-term exposure, the presence of nicotine at a concentration mimicking heavy smokers increased water content of hippocampal slices during OGD. Furthermore, long-term 1-week administration of nicotine increased water content in hippocampal slices that could be attenuated with nicotine acetylcholine receptor (nAChR) antagonists, suggesting nicotine increase edema during OGD via nAChRs. A second model of focal ischemia, middle cerebral artery occlusion, showed an increase of infarct size during short-term exposure to nicotine and an increase of edema during both short-term and long-term administration of nicotine, compared with saline controls. These findings support the paradigm that nicotine products not only increase the incidence of stroke but also have the potential to worsen stroke outcome by increased edema formation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/jpet.109.157776" target="_blank" rel="noreferrer noopener">10.1124/jpet.109.157776</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2010
Abbruscato T J
acetylcholine-receptor subtypes
barrier
Bickel U
cigarette-smoking
exposure
Journal Article
Journal of Pharmacology and Experimental Therapeutics
Klein J
Mdzinarishvili A
middle cerebral-artery
occlusion
Paulson J R
Permeability
Pharmacology & Pharmacy
rat
Risk
Selvaraj P K
stroke
Van der Schyf C J
Water
Yang T Z