1
40
2
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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
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
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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>
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/10.3233/JAD-160658" target="_blank" rel="noreferrer noopener">http://doi.org/10.3233/JAD-160658</a>
Pages
1605–1619
Issue
4
Volume
55
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
Early Evidence of Low Bone Density and Decreased Serotonergic Synthesis in the Dorsal Raphe of a Tauopathy Model of Alzheimer's Disease.
Publisher
An entity responsible for making the resource available
Journal of Alzheimer's disease : JAD
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
Female; Male; Animals; Mice; *Alzheimer's disease; Body Weight; Body Composition; Age Factors; Body Weight/genetics; Phosphorylation; Bone Density/*physiology; *Alzheimer Disease/complications/genetics/pathology; *bone density; *microtubule-associated protein; *serotonin; *tau proteins; *tauopathies; Body Composition/genetics; Bone Diseases/*etiology; Dorsal Raphe Nucleus/*pathology; Neurons/metabolism/pathology; Serotonin/*metabolism; tau Proteins/*genetics/metabolism; Tauopathies/complications/genetics; Tryptophan Hydroxylase/metabolism; Biological; Models; Inbred C57BL; Animal; Disease Models; Transgenic; Nerve Tissue Proteins; Neurodegenerative Diseases; Animal Studies; Alzheimer's Disease; Bone Density – Physiology; Nerve Tissue Proteins – Metabolism; Neurodegenerative Diseases – Complications; Alzheimer's Disease – Complications; Alzheimer's Disease – Pathology; Bone Diseases – Etiology; Brain Stem – Pathology; Neurons – Metabolism; Neurons – Pathology; Oxidoreductases – Metabolism; Serotonin – Metabolism
Creator
An entity primarily responsible for making the resource
Dengler-Crish Christine M; Smith Matthew A; Wilson Gina N
Description
An account of the resource
Reduced bone mineral density (BMD) and its clinical sequelae, osteoporosis, occur at a much greater rate in patients with Alzheimer's disease (AD), often emerging early in the disease before significant cognitive decline is seen. Reduced BMD translates to increased bone fracture risk, decreased quality of life, and increased mortality for AD patients. However, the mechanism responsible for this observation is unclear. We hypothesize that bone loss is an additional component of an AD prodrome-changes that emerge prior to dementia and are mediated by dysfunction of the central serotonergic pathways. We characterized the skeletal phenotype of htau mice that express human forms of the microtubule-associated protein tau that become pathologically hyperphosphorylated in AD. Using radiographic densitometry, we measured BMD in female and male htau mice from 2-6 months of age-time-points prior to the presence of significant tauopathy in the hippocampal/entorhinal regions characteristic of this model. We found a significantly reduced BMD phenotype in htau mice that was most pronounced in males. Using western blotting and immunofluorescence, we showed overall reduced tryptophan hydroxylase (TPH) protein in htau brainstem and a 70% reduction in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3233/JAD-160658" target="_blank" rel="noreferrer noopener">10.3233/JAD-160658</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).
*Alzheimer Disease/complications/genetics/pathology
*Alzheimer's disease
*bone density
*microtubule-associated protein
*serotonin
*tau proteins
*tauopathies
2017
Age Factors
Alzheimer's disease
Alzheimer's Disease – Complications
Alzheimer's Disease – Pathology
Animal
Animal Studies
Animals
Biological
Body Composition
Body Composition/genetics
Body Weight
Body Weight/genetics
Bone Density – Physiology
Bone Density/*physiology
Bone Diseases – Etiology
Bone Diseases/*etiology
Brain Stem – Pathology
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Disease Models
Dorsal Raphe Nucleus/*pathology
Female
Inbred C57BL
Journal of Alzheimer's disease : JAD
Male
Mice
Models
NEOMED College of Pharmacy
Nerve Tissue Proteins
Nerve Tissue Proteins – Metabolism
Neurodegenerative Diseases
Neurodegenerative Diseases – Complications
Neurons – Metabolism
Neurons – Pathology
Neurons/metabolism/pathology
Oxidoreductases – Metabolism
Phosphorylation
Serotonin – Metabolism
Serotonin/*metabolism
Smith Matthew A
tau Proteins/*genetics/metabolism
Tauopathies/complications/genetics
Transgenic
Tryptophan Hydroxylase/metabolism
Wilson Gina N