1
40
11
-
Hyperlink
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URL
https://doi.org/10.1186/s13073-022-01022-0
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Title
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PLCG2 is associated with the inflammatory response and is induced by amyloid plaques in Alzheimer's disease
Creator
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Andy P Tsai
Chuanpeng Dong
Peter Bor-Chian Lin
Evan J Messenger
Brad T Casali
Miguel Moutinho
Yunlong Liu
Adrian L Oblak
Bruce T Lamb
Gary E Landreth
Stephanie J Bissel
Kwangsik Nho
Date
A point or period of time associated with an event in the lifecycle of the resource
2022
Description
An account of the resource
Background: Alzheimer's disease (AD) is characterized by robust microgliosis and phenotypic changes that accompany disease pathogenesis. Accumulating evidence from genetic studies suggests the importance of phospholipase C γ 2 (PLCG2) in late-onset AD (LOAD) pathophysiology. However, the role of PLCG2 in AD is still poorly understood.
Methods: Using bulk RNA-Seq (N=1249) data from the Accelerating Medicines Partnership-Alzheimer's Disease Consortium (AMP-AD), we investigated whether PLCG2 expression increased in the brains of LOAD patients. We also evaluated the relationship between PLCG2 expression levels, amyloid plaque density, and expression levels of microglia specific markers (AIF1 and TMEM119). Finally, we investigated the longitudinal changes of PLCG2 expression in the 5xFAD mouse model of AD. To further understand the role of PLCG2 in different signaling pathways, differential gene expression and co-expression network analyses were performed using bulk RNA-Seq and microglial single-cell RNA-Seq data. To substantiate the human analyses, we performed differential gene expression analysis on wild-type (WT) and inactivated Plcg2 mice and used immunostaining to determine if the differentially expressed genes/pathways were altered by microglial cell coverage or morphology.
Results: We observed significant upregulation of PLCG2 expression in three brain regions of LOAD patients and significant positive correlation of PLCG2 expression with amyloid plaque density. These findings in the human brain were validated in the 5xFAD amyloid mouse model, which showed disease progression-dependent increases in Plcg2 expression associated with amyloid pathology. Of note, increased Plcg2 expression levels in 5xFAD mice were abolished by reducing microglia. Furthermore, using bulk RNA-Seq data, we performed differential expression analysis by comparing cognitively normal older adults (CN) with 75th percentile (high) and 25th percentile (low) PLCG2 gene expression levels to identify pathways related to inflammation and the inflammatory response. The findings in the human brain were validated by differential expression analyses between WT and plcg2 inactivated mice. PLCG2 co-expression network analysis of microglial single-cell RNA-Seq data identified pathways related to the inflammatory response including regulation of I-kappaB/NF-kappa B signaling and response to lipopolysaccharide.
Conclusions: Our results provide further evidence that PLCG2 plays an important role in AD pathophysiology and may be a potential target for microglia-targeted AD therapies.
Source
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Genome Med
. 2022 Feb 18;14(1):17. doi: 10.1186/s13073-022-01022-0.
Language
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English
2022
Alzheimer’s disease
Co-expression network analysis
inflammatory response
Microglia
PLCG2
Single-cell RNA-Seq analysis.
-
Hyperlink
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URL
https://doi.org/10.3390/antiox11050888
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Title
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Ocular Hypertension Results in Hypoxia within Glia and Neurons throughout the Visual Projection
Creator
An entity primarily responsible for making the resource
Assraa Hassan Jassim
Nana Yaa Nsiah
Denise M Inman
Date
A point or period of time associated with an event in the lifecycle of the resource
2022
Description
An account of the resource
The magnitude and duration of hypoxia after ocular hypertension (OHT) has been a matter of debate due to the lack of tools to accurately report hypoxia. In this study, we established a topography of hypoxia in the visual pathway by inducing OHT in mice that express a fusion protein comprised of the oxygen-dependent degradation (ODD) domain of HIF-1α and a tamoxifen-inducible Cre recombinase (CreERT2) driven by a ubiquitous CAG promoter. After tamoxifen administration, tdTomato expression would be driven in cells that contain stabilized HIF-1α. Intraocular pressure (IOP) and visual evoked potential (VEP) were measured after OHT at 3, 14, and 28 days (d) to evaluate hypoxia induction. Immunolabeling of hypoxic cell types in the retina and optic nerve (ON) was performed, as well as retinal ganglion cell (RGC) and axon number quantification at each time point (6 h, 3 d, 14 d, 28 d). IOP elevation and VEP decrease were detected 3 d after OHT, which preceded RGC soma and axon loss at 14 and 28 d after OHT. Hypoxia was detected primarily in Müller glia in the retina, and microglia and astrocytes in the ON and optic nerve head (ONH). Hypoxia-induced factor (HIF-α) regulates the expression of glucose transporters 1 and 3 (GLUT1, 3) to support neuronal metabolic demand. Significant increases in GLUT1 and 3 proteins were observed in the retina and ON after OHT. Interestingly, neurons and endothelial cells within the superior colliculus in the brain also experienced hypoxia after OHT as determined by tdTomato expression. The highest intensity labeling for hypoxia was detected in the ONH. Initiation of OHT resulted in significant hypoxia that did not immediately resolve, with low-level hypoxia apparent out to 14 and 28 d, suggesting that continued hypoxia contributes to glaucoma progression. Restricted hypoxia in retinal neurons after OHT suggests a hypoxia management role for glia.
Source
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Antioxidants (Basel)
. 2022 Apr 29;11(5):888. doi: 10.3390/antiox11050888.
Language
A language of the resource
English
2022
Astrocytes
Glaucoma
hypoxia
Microglia
Müller glia
Retinal Ganglion Cells
-
Text
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URL Address
<a href="http://doi.org/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1310-6</a>
Pages
278–278
Issue
1
Volume
15
Dublin Core
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Title
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Genetically enhancing the expression of chemokine domain of CX3CL1 fails to prevent tau pathology in mouse models of tauopathy.
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Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-09
Subject
The topic of the resource
Alzheimer's disease; Animal; Animals; Antigens; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Metabolism; Cells – Pathology; Chemokine CX3CL1/*genetics/metabolism; Cognition Disorders – Etiology; Cognition Disorders/etiology; CX3CL1; CX3CR1; Cytokines; Cytokines – Metabolism; Cytokines/metabolism; Differentiation/genetics/metabolism; Disease Models; Gene Expression Regulation/drug effects/*genetics; Genes; Genes – Drug Effects; Learning; Lipopolysaccharides; Lipopolysaccharides/toxicity; Maze Learning; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia; Microglia/drug effects/*metabolism/pathology; Models; Mutation; Mutation/genetics; Nerve Tissue Proteins; Nerve Tissue Proteins – Metabolism; Neurodegenerative Diseases; Neurodegenerative Diseases – Complications; Neurodegenerative Diseases – Pathology; Neuroinflammation; Surface; Surface – Metabolism; Tau; tau Proteins/genetics/metabolism; Tauopathies; Tauopathies/complications/genetics/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Bemiller Shane M; Maphis Nicole M; Formica Shane V; Wilson Gina N; Miller Crystal M; Xu Guixiang; Kokiko-Cochran Olga N; Kim Ki-Wook; Jung Steffen; Cannon Judy L; Crish Samuel D; Cardona Astrid E; Lamb Bruce T; Bhaskar Kiran
Description
An account of the resource
BACKGROUND: Fractalkine (CX3CL1) and its receptor (CX3CR1) play an important role in regulating microglial function. We have previously shown that Cx3cr1 deficiency exacerbated tau pathology and led to cognitive impairment. However, it is still unclear if the chemokine domain of the ligand CX3CL1 is essential in regulating neuronal tau pathology. METHODS: We used transgenic mice lacking endogenous Cx3cl1 (Cx3cl1(-/-)) and expressing only obligatory soluble form (with only chemokine domain) and lacking the mucin stalk of CX3CL1 (referred to as Cx3cl1(105Delta) mice) to assess tau pathology and behavioral function in both lipopolysaccharide (LPS) and genetic (hTau) mouse models of tauopathy. RESULTS: First, increased basal tau levels accompanied microglial activation in Cx3cl1(105Delta) mice compared to control groups. Second, increased CD45(+) and F4/80(+) neuroinflammation and tau phosphorylation were observed in LPS, hTau/Cx3cl1(-/-), and hTau/Cx3cl1(105Delta) mouse models of tau pathology, which correlated with impaired spatial learning. Finally, microglial cell surface expression of CX3CR1 was reduced in Cx3cl1(105Delta) mice, suggesting enhanced fractalkine receptor internalization (mimicking Cx3cr1 deletion), which likely contributes to the elevated tau pathology. CONCLUSIONS: Collectively, our data suggest that overexpression of only chemokine domain of CX3CL1 does not protect against tau pathology.
Identifier
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<a href="http://doi.org/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1310-6</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).
2018
Alzheimer's disease
Animal
Animals
Antigens
Bemiller Shane M
Bhaskar Kiran
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cannon Judy L
Cardona Astrid E
Cells – Drug Effects
Cells – Metabolism
Cells – Pathology
Chemokine CX3CL1/*genetics/metabolism
Cognition Disorders – Etiology
Cognition Disorders/etiology
Crish Samuel D
CX3CL1
CX3CR1
Cytokines
Cytokines – Metabolism
Cytokines/metabolism
Department of Pharmaceutical Sciences
Differentiation/genetics/metabolism
Disease Models
Formica Shane V
Gene Expression Regulation/drug effects/*genetics
Genes
Genes – Drug Effects
Journal of neuroinflammation
Jung Steffen
Kim Ki-Wook
Kokiko-Cochran Olga N
Lamb Bruce T
Learning
Lipopolysaccharides
Lipopolysaccharides/toxicity
Maphis Nicole M
Maze Learning
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia
Microglia/drug effects/*metabolism/pathology
Miller Crystal M
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Nerve Tissue Proteins
Nerve Tissue Proteins – Metabolism
Neurodegenerative Diseases
Neurodegenerative Diseases – Complications
Neurodegenerative Diseases – Pathology
Neuroinflammation
Surface
Surface – Metabolism
Tau
tau Proteins/genetics/metabolism
Tauopathies
Tauopathies/complications/genetics/*pathology
Transgenic
Wilson Gina N
Xu Guixiang
-
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/10.1007/s12035-020-01921-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s12035-020-01921-6</a>
ISSN
1559-1182 0893-7648
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1007/s12035-020-01921-6" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s12035-020-01921-6</a>
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Update Year & Number
June 2020 Update II
NEOMED College
NEOMED College of Medicine
NEOMED College of Pharmacy
NEOMED Department
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
Dublin Core
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Title
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Transgenic Overexpression of GPNMB Protects Against MPTP-Induced Neurodegeneration.
Publisher
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Molecular neurobiology
Date
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2020
2020-05-20
Subject
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GPNMB; Microglia; MPTP; Neuroinflammation; Neuroprotective; Parkinson's disease
Creator
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Budge Kevin; Neal Matthew L; Richardson Jason R; Safadi Fayez F
Description
An account of the resource
Parkinson's disease (PD) is a progressive neurodegenerative disease highlighted by a marked loss of dopaminergic cell loss and motor disturbances. Currently, there are no drugs that slow the progression of the disease. A myriad of factors have been implicated in the pathogenesis and progression of PD including neuroinflammation. Although anti-inflammatory agents are being evaluated as potential disease-modifying therapies for PD, none has proven effective to date, suggesting that new and novel targets are needed. Glycoprotein nonmetastatic melanoma protein B (GPNMB) is a transmembrane glycoprotein that has recently been shown to reduce inflammation in astrocytes and to be increased in post-mortem PD brain samples. Here we show that transgenic overexpression of GPNMB protects against dopaminergic neurodegeneration in a
Identifier
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<a href="http://doi.org/10.1007/s12035-020-01921-6" target="_blank" rel="noreferrer noopener">10.1007/s12035-020-01921-6</a>
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journalArticle
2020
Budge Kevin
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
GPNMB
journalArticle
June 2020 Update II
Microglia
Molecular neurobiology
MPTP
Neal Matthew L
NEOMED College of Medicine
NEOMED College of Pharmacy
Neuroinflammation
Neuroprotective
Parkinson's disease
Richardson Jason R
Safadi Fayez F
-
Text
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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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Update Year & Number
July 2020 List
NEOMED College
NEOMED College of Pharmacy
NEOMED Department
Department of Pharmaceutical Sciences
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Title
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Microglia depletion rapidly and reversibly alters amyloid pathology by modification of plaque compaction and morphologies.
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Neurobiology of Disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-05
Subject
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Microglia; Inflammation; Neuroprotection; AD; Barrier; CSF1R; Plaques
Creator
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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.
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<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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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
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URL Address
<a href="http://doi.org/10.3390/cells10040957" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/cells10040957</a>
Issue
4
Volume
10
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Update Year & Number
May 2021 List
NEOMED College
College of Pharmacy
NEOMED Department
Department of Pharmaceutical Sciences
NEOMED Postdoc Publications
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Title
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Microglial Function and Regulation during Development, Homeostasis and Alzheimer's Disease
Publisher
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Cells
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-04
Subject
The topic of the resource
inflammation; TREM2; neurodegenerative diseases; microglia; neuroinflammation; Alzheimer’s disease; s disease; Alzheimer’
Creator
An entity primarily responsible for making the resource
Casali BT; Reed-Geaghan EG
Description
An account of the resource
Microglia are the resident immune cells of the brain, deriving from yolk sac progenitors that populate the brain parenchyma during development. During development and homeostasis, microglia play critical roles in synaptogenesis and synaptic plasticity, in addition to their primary role as immune sentinels. In aging and neurodegenerative diseases generally, and Alzheimer's disease (AD) specifically, microglial function is altered in ways that significantly diverge from their homeostatic state, inducing a more detrimental inflammatory environment. In this review, we discuss the receptors, signaling, regulation and gene expression patterns of microglia that mediate their phenotype and function contributing to the inflammatory milieu of the AD brain, as well as strategies that target microglia to ameliorate the onset, progression and symptoms of AD.
Identifier
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<a href="http://doi.org/10.3390/cells10040957" target="_blank" rel="noreferrer noopener">10.3390/cells10040957</a>
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journalArticle
2021
Alzheimer’s disease
Alzheimer’
Casali BT
Cells
Department of Pharmaceutical Sciences
Inflammation
journalArticle
May 2021 List
Microglia
NEOMED College of Pharmacy
NEOMED College of Pharmacy Postdoc
NEOMED Postdoc Publications
Neurodegenerative Diseases
Neuroinflammation
Reed-Geaghan EG
s disease
TREM2
-
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
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.3390/cells10040957">http://doi.org/10.3390/cells10040957</a></td>
</tr></tbody></table>
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Pharmaceutical Sciences
Update Year & Number
Jan to Aug list 2021
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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Microglial Function and Regulation during Development, Homeostasis and Alzheimer's Disease
Creator
An entity primarily responsible for making the resource
Casali BT; Reed-Geaghan EG
Publisher
An entity responsible for making the resource available
Cells
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-04-20
Description
An account of the resource
Microglia are the resident immune cells of the brain, deriving from yolk sac progenitors that populate the brain parenchyma during development. During development and homeostasis, microglia play critical roles in synaptogenesis and synaptic plasticity, in addition to their primary role as immune sentinels. In aging and neurodegenerative diseases generally, and Alzheimer’s disease (AD) specifically, microglial function is altered in ways that significantly diverge from their homeostatic state, inducing a more detrimental inflammatory environment. In this review, we discuss the receptors, signaling, regulation and gene expression patterns of microglia that mediate their phenotype and function contributing to the inflammatory milieu of the AD brain, as well as strategies that target microglia to ameliorate the onset, progression and symptoms of AD.
Identifier
An unambiguous reference to the resource within a given context
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.3390/cells10040957">http://doi.org/10.3390/cells10040957</a></td>
</tr></tbody></table>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2021
Alzheimer disease
Inflammation
Microglia
neurodegenerative disease
Neuroinflammation
TREM2
-
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/10.1002/cne.24484" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cne.24484</a>
Pages
2921–2936
Issue
18
Volume
526
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 changes associated to Alzheimer's disease pathology in aged chimpanzees.
Publisher
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The Journal of comparative neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-12
Subject
The topic of the resource
Alzheimer's disease; amyloid beta protein; chimpanzee; microglia; neurofibrillary tangle; neuroinflammation; RRID: AB223647; RRID: AB2313890; RRID: AB2313952; RRID: AB2315150; RRID: AB839504
Creator
An entity primarily responsible for making the resource
Edler Melissa K; Sherwood Chet C; Meindl Richard S; Munger Emily L; Hopkins William D; Ely John J; Erwin Joseph M; Perl Daniel P; Mufson Elliott J; Hof Patrick R; Raghanti Mary Ann
Description
An account of the resource
In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Abeta) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees (n = 20, ages 37-62 years) with varying degrees of AD-like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Abeta42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Abeta42-positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes with Abeta deposition similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed.
Identifier
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<a href="http://doi.org/10.1002/cne.24484" target="_blank" rel="noreferrer noopener">10.1002/cne.24484</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).
2018
Alzheimer's disease
amyloid beta protein
Chimpanzee
Edler Melissa K
Ely John J
Erwin Joseph M
Hof Patrick R
Hopkins William D
Meindl Richard S
Microglia
Mufson Elliott J
Munger Emily L
Neurofibrillary tangle
Neuroinflammation
Perl Daniel P
Raghanti Mary Ann
RRID: AB223647
RRID: AB2313890
RRID: AB2313952
RRID: AB2315150
RRID: AB839504
Sherwood Chet C
The Journal of comparative neurology
-
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.nano.2019.102107" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nano.2019.102107</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
102107
Volume
23
ISSN
1549-9642
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.nano.2019.102107" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.nano.2019.102107</a>
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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
Nose-to-brain co-delivery of repurposed simvastatin and BDNF synergistically attenuates LPS-induced neuroinflammation
Publisher
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Nanomedicine: Nanotechnology, Biology, And Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10-23
Subject
The topic of the resource
Microglia; Nanoparticles; Drug repurposing; Polymersomes; Intranasal delivery
Creator
An entity primarily responsible for making the resource
Manickavasagam Dharani; Lin Li; Oyewumi Moses O
Description
An account of the resource
A therapeutic strategy that can combat the multifaceted nature of neuroinflammation pathology was investigated. Thus, we fabricated PEG-PdLLA polymersomes and evaluated the efficacy in co-delivery of simvastatin (Sim, as a repurposed anti-inflammatory agent) with brain derived neurotrophic factor (BDNF, as an exogeneous trophic factor supplementation). Using LPS model of neuroinflammation, intranasal administration of combination drug-loaded polymersomes (containing both Sim and BDNF; Sim-BDNF-Ps) markedly down-regulated brain levels of cytokines compared to free drug and single-drug-loaded polymersomes. Further, Sim-BDNF-Ps effectively replenished brain level of BDNF that was depleted following neuroinflammation, resulting in a 2-fold BDNF increase versus untreated LPS control group. We found out that the efficiency of the combination drug-loaded polymersomes to suppress microglia activation in brain regions followed the order: frontal cortex > striatum > hippocampus. Our findings indicated that Sim-BDNF-Ps could effectively inhibit microglial-mediated inflammation as well as potentially resolve the neurotoxic microenvironment that is often associated with neuroinflammation.
Identifier
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<a href="http://doi.org/10.1016/j.nano.2019.102107" target="_blank" rel="noreferrer noopener">10.1016/j.nano.2019.102107</a>
PMID: 31655202
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
And Medicine
Biology
Department of Pharmaceutical Sciences
Drug repurposing
Intranasal delivery
Journal Article
Lin Li
Manickavasagam Dharani
Microglia
Nanomedicine: Nanotechnology
Nanomedicine: Nanotechnology, Biology, And Medicine
Nanoparticles
NEOMED College of Pharmacy
NEOMED College of Pharmacy Student
NEOMED Student Publications
November 2019 Update
Oyewumi Moses O
polymersomes
-
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/10.1096/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
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fj.201900567RR" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fj.201900567RR</a>
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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
The file format, physical medium, or dimensions of the resource
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/10.4172/2155-9899.1000492" target="_blank" rel="noreferrer noopener">http://doi.org/10.4172/2155-9899.1000492</a>
Issue
2
Volume
8
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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Rebound from Inhibition: Self-Correction against Neurodegeneration?
Publisher
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Journal of clinical & cellular immunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-04
Subject
The topic of the resource
Astrocytes; Calcium buffering; Calcium channels; Microglia; Motor neuron degeneration; NG2 glia; Post-inhibitory rebound firing; Rhythmic neural networks
Creator
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Sivaramakrishnan Shobhana; Lynch William P
Description
An account of the resource
Neural networks play a critical role in establishing constraints on excitability in the central nervous system. Several recent studies have suggested that network dysfunction in the brain and spinal cord are compromised following insult by a neurodegenerative trigger and might precede eventual neuronal loss and neurological impairment. Early intervention of network excitability and plasticity might therefore be critical in resetting hyperexcitability and preventing later neuronal damage. Here, the behavior of neurons that generate burst firing upon recovery from inhibitory input or intrinsic membrane hyperpolarization (rebound neurons) is examined in the context of neural networks that underlie rhythmic activity observed in areas of the brain and spinal cord that are vulnerable to neurodegeneration. In a non-inflammatory rodent model of spongiform neurodegenerative disease triggered by retrovirus infection of glia, rebound neurons are particularly vulnerable to neurodegeneration, likely due to an inherently low calcium buffering capacity. The dysfunction of rebound neurons translates into a dysfunction of rhythmic neural circuits, compromising normal neurological function and leading to eventual morbidity. Understanding how virus infection of glia can mediate dysfunction of rebound neurons, induce hyperexcitability and loss of rhythmic function, pathologic features observed in neurodegenerative disorders ranging from epilepsy to motor neuron disease, might therefore suggest a common pathway for early therapeutic intervention.
Identifier
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<a href="http://doi.org/10.4172/2155-9899.1000492" target="_blank" rel="noreferrer noopener">10.4172/2155-9899.1000492</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).
2017
Astrocytes
Calcium buffering
Calcium Channels
Department of Integrative Medical Sciences
Journal of clinical & cellular immunology
Lynch William P
Microglia
Motor neuron degeneration
NEOMED College of Medicine
NG2 glia
Post-inhibitory rebound firing
Rhythmic neural networks
Sivaramakrishnan Shobhana