1
40
20
-
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/10.1002/ardp.201500293" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/ardp.201500293</a>
Pages
252–267
Issue
4
Volume
349
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
Synthesis and Biological Evaluation of Pentacycloundecylamines and Triquinylamines as Voltage-Gated Calcium Channel Blockers.
Publisher
An entity responsible for making the resource available
Archiv der Pharmazie
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-04
Subject
The topic of the resource
Alicyclic/chemical synthesis/*chemistry/pharmacology; Amines/chemical synthesis/*chemistry/pharmacology; Animals; Apoptosis/drug effects; Calcium Channel Blockers/chemical synthesis/*chemistry/pharmacology; Calcium Channels; Calcium/*metabolism; Cell Survival/drug effects; Hydrocarbons; Hydrogen Peroxide/pharmacology; L-Lactate Dehydrogenase/metabolism; L-type calcium channel (LTCC) blockers; L-Type/*metabolism; Multifunctional drugs; Neurodegeneration; PC12 Cells; Pentacycloundecylamine; Quinones/chemical synthesis/*chemistry/pharmacology; Rats; Structure-Activity Relationship; Triquinylamine
Creator
An entity primarily responsible for making the resource
Young Lois-May; Geldenhuys Werner J; Domingo Olwen C; Malan Sarel F; Van der Schyf Cornelis J
Description
An account of the resource
Preclinical studies for neurodegenerative diseases have shown a multi-targeted approach to be successful in the treatment of these complex disorders with several pathoetiological pathways. Polycyclic compounds, such as NGP1-01 (7a), have demonstrated the ability to target multiple mechanisms of the complex etiology and are referred to as multifunctional compounds. These compounds have served as scaffolds with the ability to attenuate Ca(2+) overload and excitotoxicity through several pathways. In this study, our focus was on mitigating Ca(2+) overload through the L-type calcium channels (LTCC). Here, we report the synthesis and biological evaluation of several novel polycyclic compounds. We determined the IC50 values for both the pentacycloundecylamines and the triquinylamines by means of a high-throughput fluorescence calcium flux assay utilizing Fura-2/AM. The potential of these compounds to offer protection against hydrogen peroxide-induced cell death was also evaluated. Overall,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/ardp.201500293" target="_blank" rel="noreferrer noopener">10.1002/ardp.201500293</a>
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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).
2016
Alicyclic/chemical synthesis/*chemistry/pharmacology
Amines/chemical synthesis/*chemistry/pharmacology
Animals
Apoptosis/drug effects
Archiv der Pharmazie
Calcium Channel Blockers/chemical synthesis/*chemistry/pharmacology
Calcium Channels
Calcium/*metabolism
Cell Survival/drug effects
Domingo Olwen C
Geldenhuys Werner J
Hydrocarbons
Hydrogen Peroxide/pharmacology
L-Lactate Dehydrogenase/metabolism
L-type calcium channel (LTCC) blockers
L-Type/*metabolism
Malan Sarel F
Multifunctional drugs
Neurodegeneration
PC12 Cells
Pentacycloundecylamine
Quinones/chemical synthesis/*chemistry/pharmacology
Rats
Structure-Activity Relationship
Triquinylamine
Van der Schyf Cornelis J
Young Lois-May
-
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/s12035-017-0707-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s12035-017-0707-z</a>
Pages
5167–5176
Issue
6
Volume
55
Dublin Core
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Title
A name given to the resource
Glycoprotein NMB: an Emerging Role in Neurodegenerative Disease.
Publisher
An entity responsible for making the resource available
Molecular neurobiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-06
Subject
The topic of the resource
Animals; GPNMB; Humans; Immune System/metabolism; Membrane Glycoproteins/chemistry/*metabolism; Nerve Degeneration/pathology; Neurodegeneration; Neurodegenerative Diseases/*metabolism/therapy; Neuroinflammation; Neuroprotection
Creator
An entity primarily responsible for making the resource
Budge Kevin M; Neal Matthew L; Richardson Jason R; Safadi Fayez F
Description
An account of the resource
Neurodegeneration is characterized by severe neuronal loss leading to the cognitive and physical impairments that define various neurodegenerative diseases. Neuroinflammation is one hallmark of neurodegenerative diseases and can ultimately contribute to disease progression. Increased inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) are associated with Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Unfortunately, current therapeutic options lack ability to stop or effectively slow progression of these diseases and are primarily aimed at alleviating symptoms. Thus, it is crucial to discover novel treatment candidates for neurodegenerative diseases. Glycoprotein nonmetastatic melanoma protein B (GPNMB) is a type-I transmembrane glycoprotein first identified in a melanoma cell line. GPNMB augments bone mineral deposition by stimulating osteoblast differentiation. Aside from its anabolic function in the bone, emerging evidence suggests that GPNMB has anti-inflammatory and reparative functions. GPNMB has also been demonstrated to be neuroprotective in an animal model of ALS, cerebral ischemia, and other disease models. Given these discoveries, GPNMB should be investigated as a potential therapeutic option for multiple neurodegenerative diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s12035-017-0707-z" target="_blank" rel="noreferrer noopener">10.1007/s12035-017-0707-z</a>
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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).
2018
Animals
Budge Kevin M
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
GPNMB
Humans
Immune System/metabolism
Membrane Glycoproteins/chemistry/*metabolism
Molecular neurobiology
Neal Matthew L
NEOMED College of Medicine
NEOMED College of Pharmacy
Nerve Degeneration/pathology
Neurodegeneration
Neurodegenerative Diseases/*metabolism/therapy
Neuroinflammation
Neuroprotection
Richardson Jason R
Safadi Fayez F
-
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/10.3389/fnins.2014.00290" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnins.2014.00290</a>
Pages
290–290
Volume
8
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
Anterograde transport blockade precedes deficits in retrograde transport in the visual projection of the DBA/2J mouse model of glaucoma.
Publisher
An entity responsible for making the resource available
Frontiers in neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-07
Subject
The topic of the resource
glaucoma; optic nerve; axonal transport; axonopathy; neurodegeneration; ocular; superior colliculi; vision disorders
Creator
An entity primarily responsible for making the resource
Dengler-Crish Christine M; Smith Matthew A; Inman Denise M; Wilson Gina N; Young Jesse W; Crish Samuel D
Description
An account of the resource
Axonal transport deficits have been reported as an early pathology in several neurodegenerative disorders, including glaucoma. However, the progression and mechanisms of these deficits are poorly understood. Previous work suggests that anterograde transport is affected earlier and to a larger degree than retrograde transport, yet this has never been examined directly in vivo. Using combined anterograde and retrograde tract tracing methods, we examined the time-course of anterograde and retrograde transport deficits in the retinofugal projection in pre-glaucomatous (3 month-old) and glaucomatous (9-13 month old) DBA/2J mice. DBA/2J-Gpnmb (+) mice were used as a control strain and were shown to have similar retinal ganglion cell densities as C57BL/6J control mice-a strain commonly investigated in the field of vision research. Using cholera toxin-B injections into the eye and FluoroGold injections into the superior colliculus (SC), we were able to measure anterograde and retrograde transport in the primary visual projection. In DBA/2J, anterograde transport from the retina to SC was decreased by 69% in the 9-10 month-old age group, while retrograde transport was only reduced by 23% from levels seen in pre-glaucomatous mice. Despite this minor reduction, retrograde transport remained largely intact in these glaucomatous age groups until 13-months of age. These findings indicate that axonal transport deficits occur in semi-functional axons that are still connected to their brain targets. Structural persistence as determined by presence of estrogen-related receptor beta label in the superficial SC was maintained beyond time-points where reductions in retrograde transport occurred, also supporting that transport deficits may be due to physiological or functional abnormalities as opposed to overt structural loss.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3389/fnins.2014.00290" target="_blank" rel="noreferrer noopener">10.3389/fnins.2014.00290</a>
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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).
2014
Axonal Transport
Axonopathy
Crish Samuel D
Dengler-Crish Christine M
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
Frontiers in neuroscience
Glaucoma
Inman Denise M
NEOMED College of Medicine
NEOMED College of Pharmacy
Neurodegeneration
ocular
optic nerve
Smith Matthew A
superior colliculi
vision disorders
Wilson Gina N
Young Jesse W
-
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/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</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
Neurotoxicity of pesticides
Publisher
An entity responsible for making the resource available
Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; Fungicide; Glyphosate; iPSC; Microelectrode array; Mitochondrial Complex I; Neurodegeneration; Neurotoxicity; Organochlorine; Organophosphate; Paraquat; Pesticide; Pyrethroid; Pyridaben; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
Department of Pharmaceutical Sciences
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
Fitsanakis Vanessa
Fungicide
Glyphosate
IPSC
June 2019 Update
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
NEOMED College of Pharmacy
Neurodegeneration
Neurotoxicity
Organochlorine
Organophosphate
Paraquat
Pesticide
Pyrethroid
Pyridaben
Richardson Jason R
Rotenone
Westerink Remco H S
Zebrafish
-
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/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00401-019-02033-9</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).
Pages
343-362
Issue
3
Volume
138
Search for Full-text
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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
Neurotoxicity of pesticides.
Publisher
An entity responsible for making the resource available
Acta Neuropathologica
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
activity; cell-culture; developmental; Dichlorodiphenyltrichloroethane; Dieldrin; Endosulfan; exposure; Fungicide; Glyphosate; glyphosate-based herbicide; induced oxidative stress; iPSC; Microelectrode array; Mitochondrial Complex I; mitochondrial complex-i; Neurodegeneration; neuronal network; Neurosciences & Neurology; Neurotoxicity; Neurotoxicity; nigrostriatal dopamine system; Organochlorine; Organophosphate; Paraquat; parkinsons-disease; Pathology; Pesticide; Pyrethroid; pyrethroid insecticides; Pyridaben; reproduces features; Rotenone; Zebrafish
Creator
An entity primarily responsible for making the resource
Richardson Jason R; Fitsanakis Vanessa; Westerink Remco H S; Kanthasamy Anumantha G
Description
An account of the resource
Pesticides are unique environmental contaminants that are specifically introduced into the environment to control pests, often by killing them. Although pesticide application serves many important purposes, including protection against crop loss and against vector-borne diseases, there are significant concerns over the potential toxic effects of pesticides to non-target organisms, including humans. In many cases, the molecular target of a pesticide is shared by non-target species, leading to the potential for untoward effects. Here, we review the history of pesticide usage and the neurotoxicity of selected classes of pesticides, including insecticides, herbicides, and fungicides, to humans and experimental animals. Specific emphasis is given to linkages between exposure to pesticides and risk of neurological disease and dysfunction in humans coupled with mechanistic findings in humans and animal models. Finally, we discuss emerging techniques and strategies to improve translation from animal models to humans. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00401-019-02033-9" target="_blank" rel="noreferrer noopener">10.1007/s00401-019-02033-9</a>
2019
Acta Neuropathologica
activity
cell-culture
Department of Pharmaceutical Sciences
Developmental
Dichlorodiphenyltrichloroethane
Dieldrin
Endosulfan
exposure
Fitsanakis Vanessa
Fungicide
Glyphosate
glyphosate-based herbicide
induced oxidative stress
IPSC
Kanthasamy Anumantha G
Microelectrode array
Mitochondrial Complex I
mitochondrial complex-i
NEOMED College of Pharmacy
Neurodegeneration
neuronal network
Neurosciences & Neurology
Neurotoxicity
nigrostriatal dopamine system
Organochlorine
Organophosphate
Paraquat
parkinsons-disease
Pathology
Pesticide
Pyrethroid
pyrethroid insecticides
Pyridaben
reproduces features
Richardson Jason R
Rotenone
September 2019 Update
Westerink Remco H S
Zebrafish
-
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/10.1002/stem.227" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/stem.227</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).
Pages
2846-2856
Issue
11
Volume
27
Search for Full-text
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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
Cross-Talk Between Stem Cells and the Dysfunctional Brain is Facilitated by Manipulating the Niche: Evidence from an Adhesion Molecule
Publisher
An entity responsible for making the resource available
Stem Cells
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-11
Subject
The topic of the resource
adhesion molecule; Aging; aging and age-related diseases; astrocytes; axonal regeneration; Biotechnology & Applied Microbiology; Cell Biology; central-nervous-system; chaperone effect; differentiation; dopamine; extracellular; functional recovery; Hematology; L1; matrix; migration; model; molecules; motor-neurons; mouse; MPTP; neural stem cells; neurodegeneration; neuroprotection; neurotrophic factors; niche; Oncology; oxidative stress; parkinsons-disease; parkinsons-disease; protect neurons; recognition; spinal-cord-injury; transplantation
Creator
An entity primarily responsible for making the resource
Ourednik V; Ourednik J; Xu Y F; Zhang Y; Lynch W P; Snyder E Y; Schachner M
Description
An account of the resource
In the injured brain, the behavior of neural stem/progenitor cells (NSCs) is regulated by multiple converging factors encountered in the niche, which is composed of several neural and non-neural cell types. Signals emanating from the host influence the migration, survival, distribution, and fate of transplanted NSCs, which in turn can create host microenvironments that favor a return to homeostasis. We tested the hypothesis that overexpression of key facilitatory molecules that de. ne the injury niche might enhance this bidirectional stem cell host interaction to therapeutic advantage. As proof of concept, we investigated whether conditioning the niche with the neural cell adhesion molecule L1 might enhance recovery in a prototypical neurodegenerative milieu-the MPTP-induced model of Parkinson's disease in aged mice-where cross-talk between NSCs and imperiled host dopaminergic neurons is known to be pivotal in rescuing the function and connectivity of the latter. In lesioned mice (and in unlesioned controls), we overexpressed L1 in the NSCs to be transplanted into the ventral mesencephalon. Several pairwise experimental combinations were tested based on variations of engrafting L1 overexpressing versus nonoverexpressing NSCs into wild-type (WT) versus L1-overexpressing transgenic mice (specifically L1 transcribed from the GFAP promoter and, hence, overexpressed in host astrocytes). Enrichment for L1-particularly when expressed simultaneously in both donor NSCs and host brain-led to rapid and extensive distribution of exogenous NSCs, which in turn rescued (with an efficacy greater than in nonengineered controls) dysfunctional host dopaminergic nigral neurons, even when grafting was delayed by a month. L1 overexpression by NSCs also enhanced their own differentiation into tyrosine hydroxylase-expressing neurons in both WT and transgenic hosts. Graft-host interactions were thus favored by progressively increasing levels of L1. More broadly, this study supports the view that manipulating components of the niche (such as an adhesion molecule) that facilitate cross-talk between stem cells and the dysfunctional brain may offer new strategies for more efficacious neurotransplantation, particularly when treatment is delayed as in chronic lesions or advanced stages of a neurodegenerative disease. STEM CELLS 2009; 27: 2846-2856
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/stem.227" target="_blank" rel="noreferrer noopener">10.1002/stem.227</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2009
adhesion molecule
Aging
aging and age-related diseases
Astrocytes
axonal regeneration
Biotechnology & Applied Microbiology
Cell Biology
central-nervous-system
chaperone effect
differentiation
Dopamine
extracellular
functional recovery
Hematology
Journal Article
L1
Lynch W P
matrix
migration
model
molecules
motor-neurons
mouse
MPTP
Neural stem cells
Neurodegeneration
Neuroprotection
neurotrophic factors
niche
oncology
Ourednik J
Ourednik V
Oxidative Stress
parkinsons-disease
protect neurons
recognition
Schachner M
Snyder E Y
spinal-cord-injury
stem cells
Transplantation
Xu Y F
Zhang Y
-
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/10.1006/viro.1998.9240" target="_blank" rel="noreferrer noopener">http://doi.org/10.1006/viro.1998.9240</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).
Pages
127-136
Issue
2
Volume
247
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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
Dissecting the determinants of neuropathogenesis of the murine oncornaviruses
Publisher
An entity responsible for making the resource available
Virology
Date
A point or period of time associated with an event in the lifecycle of the resource
1998
1998-08
Subject
The topic of the resource
c rna virus; central-nervous-system; endothelial-cell tropism; induced spongiform; infection; leukemia-virus; motor neuron disease; neurodegeneration; neurological disease; neurotropic retrovirus; temperature-sensitive mutant; Virology; wild mouse retrovirus
Creator
An entity primarily responsible for making the resource
Portis J L; Lynch W P
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1006/viro.1998.9240" target="_blank" rel="noreferrer noopener">10.1006/viro.1998.9240</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
1998
c rna virus
central-nervous-system
endothelial-cell tropism
induced spongiform
Infection
Journal Article
leukemia-virus
Lynch W P
motor neuron disease
Neurodegeneration
neurological disease
neurotropic retrovirus
Portis J L
temperature-sensitive mutant
Virology
wild mouse retrovirus
-
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/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-015-0399-0</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).
Pages
13-13
Volume
12
Search for Full-text
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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 pro-inflammatory cytokine elevations in the DBA/2J mouse model of 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
2015
2015-09
Subject
The topic of the resource
Aging; axonal-transport; axoplasmic-transport; Cytokines; fibroblast-growth-factor; gene-expression; glaucoma; Immunology; inflammation; Intraocular pressure; Intraocular pressure; necrosis-factor-alpha; neurodegeneration; Neurosciences & Neurology; ocular hypertension; optic-nerve head; retinal ganglion-cells; tnf-alpha
Creator
An entity primarily responsible for making the resource
Wilson G N; Inman D M; Denger-Crish C M; Smith M A; Crish S D
Description
An account of the resource
Background: Neuroinflammation-astrogliosis, microglial activation, and changes in cytokine signaling-is a prominent feature of neurodegenerative disorders. Glaucoma is a group of chronic neurodegenerative conditions that make up the leading cause of irreversible blindness worldwide. Neuroinflammation has been postulated to play a significant role in the pathogenesis and progression of glaucomatous neurodegeneration. Though much is known regarding inflammation in the eye in glaucoma, little is known about cytokine activity outside of the retina where pathologies develop early. Methods: We traced the primary visual projection from the eye to the superior colliculus (SC) in DBA/2J and DBA/2J. Gpnmb(+) (control) mice using the anterograde tracer cholera toxin-B (CTB) to assay axonal transport deficits. Forty-eight hours later, visual structures were microdissected from fresh tissue based on transport outcome. Using magnetic bead multiplexing assays, we measured levels of 20 cytokines in the retina, proximal and distal optic nerves, CTB-positive and negative SC subdivisions, cerebellum, and serum at different ages representing different stages of pathology. Results: Pro-and anti-inflammatory cytokine levels in mice often changed in the same direction based on strain, age, and tissue. Significant elevations in retinal pro-inflammatory cytokines were observed in young DBA/2J mice compared to controls, followed by an age-dependent decrease in the DBA/2J mice. Proximal optic nerve of young DBA/2J mice showed a 50 % or greater decrease in levels of certain cytokines compared to older DBA/2J cohorts and controls, while both proximal and distal optic nerve of DBA/2Js showed elevations in IL-1 beta at all ages compared to controls. Pro-inflammatory cytokine IL-6 levels varied in accordance with transport outcome in the SC: IL-6 was elevated 44-80 % in glaucomatous DBA/2J collicular regions deficient in anterograde transport from retinal ganglion cells (RGCs) compared to areas with intact transport. Conclusion: Dysregulation of cytokine signaling in the RGC projection of DBA/2J mice was evident early in distal retinal targets, well before intraocular pressure elevation or axonal degeneration begins.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">10.1186/s12974-015-0399-0</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2015
Aging
axonal-transport
axoplasmic-transport
Crish S D
Cytokines
Denger-Crish C M
Department of Pharmaceutical Sciences
fibroblast-growth-factor
gene-expression
Glaucoma
Immunology
Inflammation
Inman D M
Intraocular Pressure
Journal Article
Journal of neuroinflammation
necrosis-factor-alpha
NEOMED College of Pharmacy
Neurodegeneration
Neurosciences & Neurology
Ocular Hypertension
optic-nerve head
retinal ganglion-cells
Smith M A
TNF-alpha
Wilson G N
-
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/10.1016/j.nbd.2013.07.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2013.07.001</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).
Pages
26-37
Volume
59
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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
Proximal inhibition of p38 MAPK stress signaling prevents distal axonopathy
Publisher
An entity responsible for making the resource available
Neurobiology of Disease
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-11
Subject
The topic of the resource
Glaucoma; Neurodegeneration; Neurosciences & Neurology; death; amyotrophic-lateral-sclerosis; mouse model; ocular hypertension; activated protein-kinase; up-regulation; alzheimers-disease brain; Axonopathy; experimental glaucoma; ganglion-cell neurons; Heat shock protein; p38 MAPK; rat retina; Retinal ganglion cell
Creator
An entity primarily responsible for making the resource
Dapper J D; Crish S D; Pang I H; Calkins D J
Description
An account of the resource
The p38 mitogen-activated protein kinase (MAPK) isoforms are phosphorylated by a variety of stress stimuli in neurodegenerative disease and act as upstream activators of myriad pathogenic processes. Thus, p38 MAPK inhibitors are of growing interest as possible therapeutic interventions. Axonal dysfunction is an early component of most neurodegenerative disorders, including the most prevalent optic neuropathy, glaucoma. Sensitivity to intraocular pressure at an early stage disrupts anterograde transport along retinal ganglion cell (RGC) axons to projection targets in the brain with subsequent degeneration of the axons themselves; RGC body loss is much later. Here we show that elevated ocular pressure in rats increases p38 MAPK activation in retina, especially in RGC bodies. Topical eye-drop application of a potent and selective inhibitor of the p38 MAPK catalytic domain (Ro3206145) prevented both the degradation of anterograde transport to the brain and degeneration of axons in the optic nerve. Ro3206145 reduced in the retina phosphorylation of tau and heat-shock protein 27, both down-stream targets of p38 IVIAPK activation implicated in glaucoma, as well as expression of two inflammatory responses. We also observed increased p38 MAPK activation in mouse models. Thus, inhibition of p38 MAPK signaling in the retina may represent a therapeutic target for preventing early pathogenesis in optic neuropathies. (C) 2013 Elsevier Inc. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.nbd.2013.07.001" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2013.07.001</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
activated protein-kinase
alzheimers-disease brain
amyotrophic-lateral-sclerosis
Axonopathy
Calkins D J
Crish S D
Dapper J D
Death
Department of Pharmaceutical Sciences
experimental glaucoma
ganglion-cell neurons
Glaucoma
Heat shock protein
Journal Article or Conference Abstract Publication
Mouse model
NEOMED College of Pharmacy
Neurobiology of disease
Neurodegeneration
Neurosciences & Neurology
Ocular Hypertension
p38 MAPK
Pang I H
rat retina
Retinal ganglion cell
Up-Regulation
-
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/10.1021/ml200196p" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/ml200196p</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).
Pages
39-42
Issue
1
Volume
3
Search for Full-text
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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
Molecular Insights Into Human Monoamine Oxidase B Inhibition By The Glitazone Antidiabetes Drugs
Publisher
An entity responsible for making the resource available
Acs Medicinal Chemistry Letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
Antidiabetes drug; Chemistry; drug design; gamma agonist pioglitazone; high-level expression; lsd1; monoamine oxidase; mouse model; neurodegeneration; neuroprotection; parkinsons-disease; parkinsons-disease; Pharmacology & Pharmacy; pichia-pastoris; pioglitazone; rosiglitazone
Creator
An entity primarily responsible for making the resource
Binda C; Aldeco M; Geldenhuys W J; Tortorici M; Mattevi A; Edmondson D E
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/ml200196p" target="_blank" rel="noreferrer noopener">10.1021/ml200196p</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Acs Medicinal Chemistry Letters
Aldeco M
Antidiabetes drug
Binda C
Chemistry
Drug Design
Edmondson D E
gamma agonist pioglitazone
Geldenhuys W J
high-level expression
lsd1
Mattevi A
monoamine oxidase
Mouse model
Neurodegeneration
Neuroprotection
parkinsons-disease
Pharmacology & Pharmacy
pichia-pastoris
pioglitazone
Rosiglitazone
Tortorici M
-
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/s10534-014-9790-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10534-014-9790-z</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).
Pages
1291-1301
Issue
6
Volume
27
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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
Abnormal Metal Levels In The Primary Visual Pathway Of The Dba/2j Mouse Model Of Glaucoma
Publisher
An entity responsible for making the resource available
Biometals
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-12
Subject
The topic of the resource
alzheimers-disease; amyloid-beta; aqueous-humor; Biochemistry & Molecular Biology; ganglion-cell degeneration; gene-expression; Glaucoma; ICP-MS; iron; microarray analysis; neurodegeneration; neurodegeneration; Retina; Retina; Superior colliculus; synapse
Creator
An entity primarily responsible for making the resource
DeToma A S; Dengler-Crish C M; Deb A; Braymer J J; Penner-Hahn J E; Van der Schyf C J; Lim M H; Crish S D
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s10534-014-9790-z" target="_blank" rel="noreferrer noopener">10.1007/s10534-014-9790-z</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2014
alzheimers-disease
amyloid-beta
aqueous-humor
Biochemistry & Molecular Biology
Biometals
Braymer J J
Crish S D
Deb A
Dengler-Crish C M
Department of Pharmaceutical Sciences
DeToma A S
ganglion-cell degeneration
gene-expression
Glaucoma
ICP-MS
iron
Lim M H
Microarray Analysis
NEOMED College of Pharmacy
Neurodegeneration
Penner-Hahn J E
retina
superior colliculus
synapse
Van der Schyf C J
-
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
n/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).
Pages
205-220
Volume
1025
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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
Developmental And Genetic Influences Upon Gender Differences In Methamphetamine-induced Nigrostriatal Dopaminergic Neurotoxicity
Publisher
An entity responsible for making the resource available
Current Status of Drug Dependence / Abuse Studies: Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
2004
Subject
The topic of the resource
bdnf mutant mice; brain; brain-derived neurotrophic factor (BDNF); differentiation; dopamine; estrogen; female mice; gonadal-hormones; messenger-rna; mptp-induced neurotoxicity; neurodegeneration; neuroprotection; neurotrophic factor; parkinsons-disease; sexual; sexual differences; testosterone; ventral mesencephalon
Creator
An entity primarily responsible for making the resource
Dluzen D E; McDermott J L
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Book Chapter
2004
bdnf mutant mice
Brain
brain-derived neurotrophic factor (BDNF)
Current Status of Drug Dependence / Abuse Studies: Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity
differentiation
Dluzen D E
Dopamine
estrogen
female mice
gonadal-hormones
McDermott J L
messenger-rna
mptp-induced neurotoxicity
Neurodegeneration
Neuroprotection
neurotrophic factor
parkinsons-disease
sexual
sexual differences
Testosterone
ventral mesencephalon
-
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
n/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).
Pages
282-294
Volume
1074
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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
Estrogen, Testosterone, And Methamphetamine Toxicity
Publisher
An entity responsible for making the resource available
Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity: Cocaine, Ghb, and Substituted Amphetamines
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
2006
Subject
The topic of the resource
17-beta-estradiol; c57/b1 mice; differences; female; gonadal steroids; inhibition; mptp-induced neurotoxicity; neurodegeneration; neuroprotection; neurotoxicity; nigrostriatal; nigrostriatal dopaminergic system; parkinsons-disease; sex; sexual differences; striatum; tamoxifen
Creator
An entity primarily responsible for making the resource
Dluzen D E; McDermott J L
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Book Chapter
17-beta-estradiol
2006
c57/b1 mice
Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity: Cocaine, Ghb, and Substituted Amphetamines
differences
Dluzen D E
Female
gonadal steroids
inhibition
McDermott J L
mptp-induced neurotoxicity
Neurodegeneration
Neuroprotection
Neurotoxicity
nigrostriatal
nigrostriatal dopaminergic system
parkinsons-disease
sex
sexual differences
striatum
Tamoxifen
-
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/s11064-007-9313-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11064-007-9313-1</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).
Pages
1686-1693
Issue
10
Volume
32
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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
Voltage-gated Calcium Channels Provide An Alternate Route For Iron Uptake In Neuronal Cell Cultures
Publisher
An entity responsible for making the resource available
Neurochemical Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-10
Subject
The topic of the resource
alzheimer-disease; alzheimers-disease; Biochemistry & Molecular Biology; fpl-64176; iron-overload toxicity; metabolism; mouse-brain; nerve growth-factor; neuroblastoma-cells; neurodegeneration; Neurosciences & Neurology; nimodipine; parkinsons-disease; parkinsons-disease; redox-active iron; substantia nigra; transferrin receptor; voltage-gated calcium channels
Creator
An entity primarily responsible for making the resource
Gaasch J A; Geldenhuys W J; Lockman P R; Allen D D; Van der Schyf C J
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11064-007-9313-1" target="_blank" rel="noreferrer noopener">10.1007/s11064-007-9313-1</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2007
Allen D D
alzheimer-disease
alzheimers-disease
Biochemistry & Molecular Biology
fpl-64176
Gaasch J A
Geldenhuys W J
iron-overload toxicity
Lockman P R
Metabolism
mouse-brain
nerve growth-factor
neuroblastoma-cells
Neurochemical Research
Neurodegeneration
Neurosciences & Neurology
nimodipine
parkinsons-disease
redox-active iron
SUBSTANTIA nigra
transferrin receptor
Van der Schyf C J
voltage-gated calcium channels
-
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/s11064-007-9290-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11064-007-9290-4</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).
Pages
1196-1208
Issue
7
Volume
32
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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
Brain Iron Toxicity: Differential Responses Of Astrocytes, Neurons, And Endothelial Cells
Publisher
An entity responsible for making the resource available
Neurochemical Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-07
Subject
The topic of the resource
astrocyte; Biochemistry & Molecular Biology; brain iron toxicity; central-nervous-system; cerebrospinal-fluid; endothelial cell; experimental intracerebral hemorrhage; low-molecular-weight; multifunctional neuroprotective drugs; neurodegeneration; neuron; Neurosciences & Neurology; oxidative stress; parkinsons-disease; protein messenger-rna; receptor-mediated transcytosis; toxic mechanisms; transferrin receptor
Creator
An entity primarily responsible for making the resource
Gaasch J A; Lockman P R; Geldenhuys W J; Allen D D; Van der Schyf C J
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11064-007-9290-4" target="_blank" rel="noreferrer noopener">10.1007/s11064-007-9290-4</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2007
Allen D D
Astrocyte
Biochemistry & Molecular Biology
brain iron toxicity
central-nervous-system
cerebrospinal-fluid
endothelial cell
experimental intracerebral hemorrhage
Gaasch J A
Geldenhuys W J
Lockman P R
low-molecular-weight
multifunctional neuroprotective drugs
Neurochemical Research
Neurodegeneration
Neuron
Neurosciences & Neurology
Oxidative Stress
parkinsons-disease
protein messenger-rna
receptor-mediated transcytosis
toxic mechanisms
transferrin receptor
Van der Schyf C J
-
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/10.1021/ml200196p" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/ml200196p</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).
Pages
39-42
Issue
1
Volume
3
Search for Full-text
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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
Molecular Insights Into Human Monoamine Oxidase B Inhibition By The Glitazone Antidiabetes Drugs
Publisher
An entity responsible for making the resource available
Acs Medicinal Chemistry Letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
Antidiabetes drug; Chemistry; drug design; gamma agonist pioglitazone; high-level expression; lsd1; monoamine oxidase; mouse model; neurodegeneration; neuroprotection; parkinsons-disease; parkinsons-disease; Pharmacology & Pharmacy; pichia-pastoris; pioglitazone; rosiglitazone
Creator
An entity primarily responsible for making the resource
Binda C; Aldeco M; Geldenhuys W J; Tortorici M; Mattevi A; Edmondson D E
Description
An account of the resource
The widely employed antidiabetic drug pioglitazone (Actos) is shown to be a specific and reversible inhibitor of human monoamine oxidase B (MAO B). The crystal structure of the enzyme-inhibitor complex shows that the R-enantiomer is bound with the thiazolidinedione ring near the flavin. The molecule occupies both substrate and entrance cavities of the active site, establishing noncovalent interactions with the surrounding amino acids. These binding properties differentiate pioglitazone from the clinically used MAO inhibitors, which act through covalent inhibition mechanisms and do not exhibit a high degree of MAO A versus B selectivity. Rosiglitazone (Avandia) and troglitazone, other members of the glitazone class, are less selective in that they are weaker inhibitors of both MAO A and MAO B. These results suggest that pioglitazone may have utility as a "repurposed" neuroprotectant drug in retarding the progression of disease in Parkinson's patients. They also provide new insights for the development of reversible isoenzyme-specific MAO inhibitors.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/ml200196p" target="_blank" rel="noreferrer noopener">10.1021/ml200196p</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Acs Medicinal Chemistry Letters
Aldeco M
Antidiabetes drug
Binda C
Chemistry
Drug Design
Edmondson D E
gamma agonist pioglitazone
Geldenhuys W J
high-level expression
Journal Article or Conference Abstract Publication
lsd1
Mattevi A
monoamine oxidase
Mouse model
Neurodegeneration
Neuroprotection
parkinsons-disease
Pharmacology & Pharmacy
pichia-pastoris
pioglitazone
Rosiglitazone
Tortorici M
-
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/10.1016/j.ejmg.2015.05.009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ejmg.2015.05.009</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).
Pages
381-386
Issue
8
Volume
58
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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
Exome Sequencing Reveals A Novel Wdr45 Frameshift Mutation And Inherited Polr3a Heterozygous Variants In A Female With A Complex Phenotype And Mixed Brain Mri Findings
Publisher
An entity responsible for making the resource available
European Journal of Medical Genetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-08
Subject
The topic of the resource
4H syndrome; accumulation; atp13a2 mutations; clinical spectrum; Demyelinating disease; diabetes-mellitus; gene; Genetics & Heredity; hallervorden-spatz-syndrome; hypogonadism; iron; Leukodystrophy; Leukodystrophy; NBIA; neurodegeneration; POLR3A; spastic paraplegia spg35; WDR45; Whole exome sequencing
Creator
An entity primarily responsible for making the resource
Khalifa M; Naffaa L
Description
An account of the resource
WDR45 and POLR3A are newly recognized genes; each is associated with a distinct neurodegenerative disease. WDR45 is an X-linked gene associated with a dominant form of Neurodegeneration with Brain Iron Accumulation (NBIA), manifested by progressive disabilities, dystonia, cognitive decline, spastic paraplegia, neuropsychiatric abnormalities and iron deposition in the basal ganglia on brain imaging. POLR3A, on the other hand, is an autosomal gene, and its mutations cause a recessive form of a hypomyelination with leukodystrophy disease, also known as 4H syndrome, characterized by congenital Hypomyelination with thinning of the corpus callosum, Hypodontia and Hypogonadotropic Hypogonadism. We report on a female child with severe intellectual disability, aphasia, short stature, ataxia, failure to thrive and structural brain abnormalities. Brain MRI obtained in late infancy showed hypomyelination involving the central periventricular white matter and thinning of the corpus callosum with no evidence of iron accumulation. Brain MRI obtained in childhood showed stable hypomyelination, with progressive iron accumulation in the basal ganglia, in particular in the globus pallidus and substantia nigra. Whole Exome Sequencing (WES) identified a novel WDR45 frameshift deleterious mutation in Exon 9 (c.587-588del) and also revealed three POLR3A missense heterozygous variants. The first is a maternally inherited novel missense variant in exon 4 (c.346A > G). Exon 13 carried two heterozygous missense variants, a maternally inherited variant (c.1724A > T) and a paternally inherited variant (1745G > A). These variants are considered likely damaging. The patient's complex clinical phenotype and mixed brain MRI findings might be attributed to the confounding effects of the expression of these two mutant genes. (C) 2015 Elsevier Masson SAS. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ejmg.2015.05.009" target="_blank" rel="noreferrer noopener">10.1016/j.ejmg.2015.05.009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2015
4H syndrome
accumulation
atp13a2 mutations
clinical spectrum
Demyelinating disease
diabetes-mellitus
European journal of medical genetics
gene
Genetics & Heredity
hallervorden-spatz-syndrome
hypogonadism
iron
Journal Article or Conference Abstract Publication
Khalifa M
Leukodystrophy
Naffaa L
NBIA
Neurodegeneration
POLR3A
spastic paraplegia spg35
WDR45
Whole Exome Sequencing
-
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/10.1016/j.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2012.10.029</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).
Pages
133-139
Volume
1489
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Dublin Core
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Title
A name given to the resource
Ngp1-01, A Multi-targeted Polycyclic Cage Amine, Attenuates Brain Endothelial Cell Death In Iron Overload Conditions
Publisher
An entity responsible for making the resource available
Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-12
Subject
The topic of the resource
activator; barrier; calcium channels; channels provide; intracerebral hemorrhage; Iron-overload; neurodegeneration; neurodegenerative disorders; neuroprotection; Neurosciences & Neurology; Nimodipine; parkinsons-disease; permeability; rat-brain; toxicity; transport; Vascular endothelial cells; Voltage-gated calcium channel
Creator
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Lockman J A; Geldenhuys W J; Jones-Higgins M R; Patrick J D; Allen D D; Van der Schyf C J
Description
An account of the resource
Development and progression of neurodegenerative disorders have, amongst other potential causes, been attributed to a disruption of iron regulatory mechanisms and iron accumulation. Excess extracellular iron may enter cells via nontraditional routes such as voltage-gated calcium channels and N-methyl-D-aspartate (NMDA) receptors leading to intracellular oxidative damage and ultimately mitochondrial failure. Nimodipine, an L-type calcium channel blocker has been shown to reduce iron-induced toxicity in neuronal and brain endothelial cells. Our current study investigates NGP1-01, a multimodal drug acting as an antagonist at both the NMDA receptor and the L-type calcium channel. Our previous studies support NGP1-01. as a promising neuroprotective agent in diseases involving calcium-related excitotoxicity. We demonstrate here that NGP1-01 (1 and 10 mu M) pretreatment abrogates the effects of iron overload in brain endothelial cells protecting cellular viability. Both concentrations of NGP1-01 were found to attenuate iron-induced reduction in cellular viability to a similar extent, and were statistically significant. To further verify the mechanism, the L-type calcium channel agonist FPL 64176 was administered to promote iron uptake. Addition of NGP1-01 dose-dependently reduced FPL 64176 stimulated uptake of iron. These data support further evaluation of NGP1-01 as a neuroprotective agent, not only in diseases associated with excitotoxicity, but also in those of iron overload. (C) 2012 Elsevier B.V. All rights reserved.
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<a href="http://doi.org/10.1016/j.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2012.10.029</a>
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Journal Article or Conference Abstract Publication
2012
activator
Allen D D
barrier
Brain research
Calcium Channels
channels provide
Geldenhuys W J
intracerebral hemorrhage
Iron-overload
Jones-Higgins M R
Journal Article or Conference Abstract Publication
Lockman J A
Neurodegeneration
neurodegenerative disorders
Neuroprotection
Neurosciences & Neurology
nimodipine
parkinsons-disease
Patrick J D
Permeability
rat-brain
toxicity
transport
Van der Schyf C J
Vascular endothelial cells
Voltage-gated calcium channel
-
Text
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<a href="http://doi.org/10.1080/15548627.2020.1797280" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/15548627.2020.1797280</a>
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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).
Pages
1-382
ISSN
1554-8635 1554-8627
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Update Year & Number
March 2021 List
NEOMED College
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Department of Anatomy & Neurobiology
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Title
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).
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Autophagy
Date
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2021
2021-02-08
Subject
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Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuole
Description
An account of the resource
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
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<a href="http://doi.org/10.1080/15548627.2020.1797280" target="_blank" rel="noreferrer noopener">10.1080/15548627.2020.1797280</a>
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journalArticle
2021
autophagosome
Autophagy
Cancer
Department of Anatomy & Neurobiology
Flux
journalArticle
LC3
lysosome
macroautophagy
March 2021 List
NEOMED College of Medicine
Neurodegeneration
phagophore
Stress
vacuole
-
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/10.1080/15548627.2020.1797280">http://doi.org/10.1080/15548627.2020.1797280</a></td>
</tr></tbody></table>
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Anatomy & Neurobiology
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
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).
Creator
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Multiple
Publisher
An entity responsible for making the resource available
Autophagy
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
Description
An account of the resource
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
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/10.1080/15548627.2020.1797280">http://doi.org/10.1080/15548627.2020.1797280</a></td>
</tr></tbody></table>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2021
autophagosome
Cancer
Flux
LC3
lysosome
macroautophagy
Neurodegeneration
phagophore
Stress
vacuole