1
40
3
-
Text
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URL Address
<a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1346-7</a>
Pages
313–313
Issue
1
Volume
15
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
Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-11
Subject
The topic of the resource
AMP-activated protein kinase; AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Pathology; Diet; Disease Models; Eye Proteins/genetics; Female; G-Protein-Coupled – Metabolism; G-Protein-Coupled/*metabolism; Glaucoma; Glaucoma – Complications; Glaucoma – Pathology; Glaucoma/*complications/pathology; Impact of Events Scale; Inbred DBA; Inflammation – Etiology; Inflammation – Prevention and Control; Inflammation hydroxycarboxylic acid receptor; Inflammation/*etiology/*prevention & control; Ketogenic diet; Ketogenic/methods; Male; Membrane Glycoproteins; Membrane Glycoproteins/genetics; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia/drug effects/pathology; Models; Mutation; Mutation/genetics; Neuroprotection/drug effects/*physiology; NLR Family; Optic Nerve – Pathology; Optic Nerve/pathology; Phosphotransferases – Metabolism; Proteins; Pyrin Domain-Containing 3 Protein/genetics/metabolism; Receptors; Retina – Drug Effects; Retina – Pathology; Retinal Ganglion Cells/drug effects/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Harun-Or-Rashid Mohammad; Inman Denise M
Description
An account of the resource
BACKGROUND: Glaucoma is a chronic degenerative disease for which inflammation is considered to play a pivotal role in the pathogenesis and progression. In this study, we examined the impact of a ketogenic diet on the inflammation evident in glaucoma as a follow-up to a recent set of experiments in which we determined that a ketogenic diet protected retinal ganglion cell structure and function. METHODS: Both sexes of DBA/2J (D2) mice were placed on a ketogenic diet (keto) or standard rodent chow (untreated) for 8 weeks beginning at 9 months of age. DBA/2J-Gpnmb(+) (D2G) mice were also used as a non-pathological genetic control for the D2 mice. Retina and optic nerve (ON) tissues were micro-dissected and used for the analysis of microglia activation, expression of pro- and anti-inflammatory molecules, and lactate- or ketone-mediated anti-inflammatory signaling. Data were analyzed by immunohistochemistry, quantitative RT-PCR, ELISA, western blot, and capillary tube-based electrophoresis techniques. RESULTS: Microglia activation was observed in D2 retina and ON as documented by intense microglial-specific Iba1 immunolabeling of rounded-up and enlarged microglia. Ketogenic diet treatment reduced Iba1 expression and the activated microglial phenotype. We detected low energy-induced AMP-activated protein kinase (AMPK) phosphorylation in D2 retina and ON that triggered NF-kappaB p65 signaling through its nuclear translocation. NF-kappaB induced pro-inflammatory TNF-alpha,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1346-7</a>
Rights
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).
2018
AMP-activated protein kinase
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cells – Drug Effects
Cells – Pathology
Department of Pharmaceutical Sciences
Diet
Disease Models
Eye Proteins/genetics
Female
G-Protein-Coupled – Metabolism
G-Protein-Coupled/*metabolism
Glaucoma
Glaucoma – Complications
Glaucoma – Pathology
Glaucoma/*complications/pathology
Harun-Or-Rashid Mohammad
Impact of Events Scale
Inbred DBA
Inflammation – Etiology
Inflammation – Prevention and Control
Inflammation hydroxycarboxylic acid receptor
Inflammation/*etiology/*prevention & control
Inman Denise M
Journal of neuroinflammation
Ketogenic diet
Ketogenic/methods
Male
Membrane Glycoproteins
Membrane Glycoproteins/genetics
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia/drug effects/pathology
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Neuroprotection/drug effects/*physiology
NLR Family
Optic Nerve – Pathology
Optic Nerve/pathology
Phosphotransferases – Metabolism
Proteins
Pyrin Domain-Containing 3 Protein/genetics/metabolism
Receptors
Retina – Drug Effects
Retina – Pathology
Retinal Ganglion Cells/drug effects/*pathology
Transgenic
-
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/10.1186/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
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
Genetically enhancing the expression of chemokine domain of CX3CL1 fails to prevent tau pathology in mouse models of tauopathy.
Publisher
An entity responsible for making the resource available
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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1310-6" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1310-6</a>
Rights
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).
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/s40572-017-0143-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s40572-017-0143-2</a>
Pages
192–199
Issue
2
Volume
4
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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Mechanisms of Gene-Environment Interactions in Parkinson's Disease.
Publisher
An entity responsible for making the resource available
Current environmental health reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-06
Subject
The topic of the resource
*Alpha-synuclein; *ATP13A2; *Gene-Environment Interaction; *Genetic Predisposition to Disease; *Manganese; *Paraquat; *Parkinson Disease; *Parkinson's disease; *Rotenone; Environmental Exposure/*adverse effects; Herbicides/adverse effects; Humans; Insecticides/adverse effects; Mutation/genetics; Paraquat/adverse effects; Risk Factors; Rotenone/adverse effects
Creator
An entity primarily responsible for making the resource
Fleming Sheila M
Description
An account of the resource
PURPOSE OF REVIEW: The purpose of the study was to discuss the main mechanisms associated with environmental and genetic factors that contribute to the development of Parkinson's disease (PD). RECENT FINDINGS: Novel genetic contributors to PD are being identified at a rapid pace in addition to novel environmental factors. The discovery of mutations in alpha-synuclein and leucine-rich repeat kinase 2 causing inherited forms of PD along with epidemiological, in vitro, and in vivo studies identifying herbicides, pesticides, and metals as risk factors have dramatically improved our understanding of mechanisms involved in the development of PD. However, at the same time, these discoveries have also added layers of complexity to the disease. Within the last several years, the genetics associated with PD has dominated the field in many ways; however, the majority of PD cases are likely due to different combinations of environmental exposures and genetic susceptibility. The most common toxicants used to model PD including rotenone, paraquat, and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s40572-017-0143-2" target="_blank" rel="noreferrer noopener">10.1007/s40572-017-0143-2</a>
Rights
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).
*Alpha-synuclein
*ATP13A2
*Gene-Environment Interaction
*Genetic Predisposition to Disease
*Manganese
*Paraquat
*Parkinson Disease
*Parkinson's disease
*Rotenone
2017
Current environmental health reports
Department of Pharmaceutical Sciences
Environmental Exposure/*adverse effects
Fleming Sheila M
Herbicides/adverse effects
Humans
Insecticides/adverse effects
Mutation/genetics
NEOMED College of Pharmacy
Paraquat/adverse effects
Risk Factors
Rotenone/adverse effects