1
40
3
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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
A name given to the resource
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
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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/s12011-019-01964-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s12011-019-01964-4</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).
ISSN
1559-0720
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/10.1007/s12011-019-01964-4" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s12011-019-01964-4</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
Fluoride-Free Diet Stimulates Pineal Growth in Aged Male Rats
Publisher
An entity responsible for making the resource available
Biological Trace Element Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-11-12
Subject
The topic of the resource
Aging; Calcification; Melatonin; Drinking water; Fluoridation; Fluoride; Neurodegenerative disease; Pineal gland; Pinealocytes
Creator
An entity primarily responsible for making the resource
Mrvelj Aaron; Womble Mark D
Description
An account of the resource
The pineal gland is a naturally calcifying endocrine organ which secretes the sleep-promoting hormone melatonin. Age-related changes of the pineal have been observed, including decreased pinealocyte numbers, increased calcification, and a reduction in melatonin production. Since fluoride is attracted to calcium within the pineal gland, this study sought to examine the effects of a fluoride-free diet on the morphology of the pineal gland of aged male rats (26 months old). All animals had previously been raised on standard fluoridated food and drinking water. These control animals were compared to other animals that were placed on a fluoride-free diet ("fluoride flush") for 4 or 8 weeks. At 4 weeks, pineal glands from fluoride-free animals showed a 96% increase in supporting cell numbers and at 8 weeks a 73% increase in the number of pinealocytes compared to control animals. In contrast, the number of pinealocytes and supporting cells in animals given an initial 4-week fluoride flush followed by a return to fluoridated drinking water (1.2 ppm NaF) for 4 weeks were not different from control animals. Our findings therefore demonstrate that a fluoride-free diet encouraged pinealocyte proliferation and pineal gland growth in aged animals and fluoride treatment inhibited gland growth. These findings suggest that dietary fluoride may be detrimental to the pineal gland.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s12011-019-01964-4" target="_blank" rel="noreferrer noopener">10.1007/s12011-019-01964-4</a>
PMID: 31713773
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
Aging
Biological Trace Element Research
Calcification
Department of Anatomy & Neurobiology
drinking water
Fluoridation
Fluoride
Journal Article
Melatonin
Mrvelj Aaron
NEOMED College of Medicine
neurodegenerative disease
November 2019 Update
Pineal gland
Pinealocytes
Womble Mark D
-
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/10.1074/jbc.RA119.007743" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.RA119.007743</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).
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
Defining α-synuclein species responsible for Parkinson disease phenotypes in mice
Publisher
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The Journal of Biological Chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Subject
The topic of the resource
alpha-synuclein (a-synuclein); amyloid; cytotoxicity; fibril; Lewy Body; motor behavior defect; neurodegenerative disease; oligomer; Parkinson disease; protein aggregation
Creator
An entity primarily responsible for making the resource
Froula Jessica M; Castellana-Cruz Marta; Anabtawi Nadia M; Camino José D; Chen Serene W; Thrasher Drake R; Freire Jennifer; Yazdi Allen A; Fleming Sheila; Dobson Christopher M; Kumita Janet R; Cremades Nunilo; Volpicelli-Daley Laura A
Description
An account of the resource
Parkinson disease (PD) is a neurodegenerative disorder characterized by fibrillar neuronal inclusions composed of aggregated α-synuclein. These inclusions are associated with behavioral and pathological PD phenotypes. One strategy for therapeutic interventions is to prevent the formation of these inclusions in order to halt disease progression. α-Synuclein exists in multiple structural forms, including disordered, non-amyloid oligomers, ordered amyloid oligomers, and fibrils. It is critical to understand which conformers contribute to specific PD phenotypes. Here, we utilized a mouse model to explore the pathological effects of stable amyloid β-sheet oligomers compared with those of fibrillar α-synuclein. We biophysically characterized these species with transmission EM, atomic-force microscopy, CD spectroscopy, FTIR spectroscopy, analytical ultracentrifugation, and thioflavin T assays. We then injected these different α-synuclein forms into the mouse striatum to determine their ability to induce PD-related phenotypes. We found that β-sheet oligomers produce a small but significant loss of dopamine neurons in the substantia nigra pars compacta (SNc). Injection of small β-sheet fibril fragments, however, produced the most robust phenotypes, including reduction of striatal dopamine terminals, SNc loss of dopamine neurons, and motor behavior defects. We conclude that although the β-sheet oligomers cause some toxicity, the potent effects of the short fibrillar fragments can be attributed to their ability to recruit monomeric α-synuclein and spread in vivo and hence contribute to the development of PD-like phenotypes. These results suggest that strategies to reduce the formation and propagation of β-sheet fibrillar species could be an important route for therapeutic intervention in PD and related disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.RA119.007743" target="_blank" rel="noreferrer noopener">10.1074/jbc.RA119.007743</a>
2019
alpha-synuclein (a-synuclein)
amyloid
Anabtawi Nadia M
Camino José D
Castellana-Cruz Marta
Chen Serene W
Cremades Nunilo
cytotoxicity
Department of Pharmaceutical Sciences
Dobson Christopher M
fibril
Fleming Sheila
Freire Jennifer
Froula Jessica M
June 2019 Update
Kumita Janet R
Lewy Body
motor behavior defect
NEOMED College of Pharmacy
neurodegenerative disease
oligomer
Parkinson Disease
Protein Aggregation
The Journal of biological chemistry
Thrasher Drake R
Volpicelli-Daley Laura A
Yazdi Allen A