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.
URL Address
<a href="http://doi.org/10.1016/j.yfrne.2012.02.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yfrne.2012.02.003</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
169-178
Issue
2
Volume
33
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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
Signaling pathways mediating the neuroprotective effects of sex steroids and SERMs in Parkinson's disease
Publisher
An entity responsible for making the resource available
Frontiers in Neuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-04
Subject
The topic of the resource
Signaling; Neuroprotection; MPTP; mice; Akt; 3; 2; 1-methyl-4-phenyl-1; 6-tetrahydropyridine; receptor; Neurosciences & Neurology; Endocrinology & Metabolism; nervous-system; plasma-membrane; estrogen-receptor-alpha; er-alpha; gender-differences; rat-brain; striatum; estrogen; ERK; estradiol; growth-factor-i; protein-coupled receptor-30; selective estrogen; SERMs; Substantia nigra
Creator
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Bourque M; Dluzen D E; Di Paolo T
Description
An account of the resource
Studies with the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease have shown the ability of 17 beta-estradiol to protect the nigrostriatal dopaminergic system. This paper reviews the signaling pathways mediating the neuroprotective effect of 17 beta-estradiol against MPTP-induced toxicity. The mechanisms of 17 beta-estradiol action implicate activation of signaling pathways such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. 17 beta-estradiol signaling is complex and integrates multiple interactions with signaling molecules that act to potentiate a protective effect. 17 beta-estradiol signaling is mediated via estrogen receptors, including GPER1, but others receptors, such as the IGF-1 receptor, are implicated in the neuroprotective effect. Glial and neuronal crosstalk is a critical factor in the maintenance of dopamine neuronal survival and in the neuroprotective action of 17 beta-estradiol. Compounds that stimulate GPER1 such as selective estrogen receptor modulators and phytoestrogens show neuroprotective activity and are alternatives to 17 beta-estradiol. (C) 2012 Published by Elsevier Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yfrne.2012.02.003" target="_blank" rel="noreferrer noopener">10.1016/j.yfrne.2012.02.003</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1-Methyl-4-phenyl-1
2
2012
3
6-tetrahydropyridine
Akt
Bourque M
Di Paolo T
Dluzen D E
Endocrinology & Metabolism
er-alpha
ERK
estradiol
estrogen
estrogen-receptor-alpha
Frontiers in Neuroendocrinology
gender-differences
growth-factor-i
Journal Article or Conference Abstract Publication
Mice
MPTP
nervous-system
Neuroprotection
Neurosciences & Neurology
plasma-membrane
protein-coupled receptor-30
rat-brain
Receptor
selective estrogen
SERMs
Signaling
striatum
SUBSTANTIA nigra
-
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/10.1111/j.1365-2826.2011.02193.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1365-2826.2011.02193.x</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
48-61
Issue
1
Volume
24
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<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
Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease
Publisher
An entity responsible for making the resource available
Journal of Neuroendocrinology
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
17 ss-oestradiol; Akt; beta messenger-rna; central-nervous-system; dopamine transporter; Endocrinology & Metabolism; er-alpha; GPER1; growth-factor receptor; GSK3 ss; induced dopamine depletion; ischemic brain-injury; monoamine transporter; MPTP; Neurosciences & Neurology; plasma-membrane; protein-coupled receptor; rat-brain; vesicular
Creator
An entity primarily responsible for making the resource
Al Sweidi S; Sanchez M G; Bourque M; Morissette M; Dluzen D; Di Paolo T
Description
An account of the resource
Parkinsons disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17 beta-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)a and beta distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57Bl/6 male mice. Intact ERKO beta mice had lower levels of striatal DAT and VMAT2, whereas ERKOa mice were the most sensitive to MPTP toxicity compared to WT and ERKO beta mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17 beta-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17 beta-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17 beta-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/beta III-tubulin, pGSK3 (Ser 9)/beta III-tubulin and Akt/beta III-tubulin. Hence, ERa, ER beta and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1365-2826.2011.02193.x" target="_blank" rel="noreferrer noopener">10.1111/j.1365-2826.2011.02193.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
17 ss-oestradiol
2012
Akt
Al Sweidi S
beta messenger-rna
Bourque M
central-nervous-system
Di Paolo T
Dluzen D
Dopamine transporter
Endocrinology & Metabolism
er-alpha
GPER1
growth-factor receptor
GSK3 ss
induced dopamine depletion
ischemic brain-injury
Journal Article or Conference Abstract Publication
Journal of neuroendocrinology
monoamine transporter
Morissette M
MPTP
Neurosciences & Neurology
plasma-membrane
protein-coupled receptor
rat-brain
Sanchez M G
vesicular