1
40
2
-
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.
Pages
36–42
Issue
6
Volume
3
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
Gender differences in neurotoxicity of the nigrostriatal dopaminergic system: implications for Parkinson's disease.
Publisher
An entity responsible for making the resource available
Journal of Gender-Specific Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
2000-09
Subject
The topic of the resource
Female; Male; Sex Factors; Postmenopause; Gender Specific Care; Toxins; Basal Ganglia – Pathology; Brain Stem – Pathology; Basal Ganglia – Physiopathology; Brain Stem – Physiopathology; Dopamine – Metabolism; Estrogens – Pharmacodynamics; Parkinson Disease – Metabolism; Parkinson Disease – Pathology; Parkinson Disease – Physiopathology
Creator
An entity primarily responsible for making the resource
Dluzen D E; McDermott J L
Description
An account of the resource
This article describes the progression of steps followed to demonstrate a gender difference associated with Parkinson's disease (PD) and to gain an understanding of the basis, mechanisms, and implications of this gender specificity. First, a review of the literature on PD shows a greater incidence in men. Next, data are presented from a series of laboratory studies in animal models of PD that suggest a basis for this gender difference: estrogen appears to act as a neuroprotectant of the striatal dopaminergic system. One mechanism for this effect may be that estrogen inhibits the uptake of neurotoxins capable of producing degeneration within dopaminergic neurons. Finally, some of the potential neurologic implications of manipulating estrogen in premenopausal and postmenopausal women are considered.
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).
2000
Basal Ganglia – Pathology
Basal Ganglia – Physiopathology
Brain Stem – Pathology
Brain Stem – Physiopathology
Dluzen D E
Dopamine – Metabolism
Estrogens – Pharmacodynamics
Female
Gender Specific Care
Journal of Gender-Specific Medicine
Male
McDermott J L
Parkinson Disease – Metabolism
Parkinson Disease – Pathology
Parkinson Disease – Physiopathology
Postmenopause
Sex Factors
Toxins
-
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