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Text
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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
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Title
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Early Evidence of Low Bone Density and Decreased Serotonergic Synthesis in the Dorsal Raphe of a Tauopathy Model of Alzheimer's Disease.
Publisher
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Journal of Alzheimer's disease : JAD
Date
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2017
1905-07
Subject
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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
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Dengler-Crish Christine M; Smith Matthew A; Wilson Gina N
Description
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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
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<a href="http://doi.org/10.3233/JAD-160658" target="_blank" rel="noreferrer noopener">10.3233/JAD-160658</a>
Rights
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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).
*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