Neuroprotective actions of sex steroids in Parkinson's disease.
Identifieur interne : 000E22 ( PubMed/Checkpoint ); précédent : 000E21; suivant : 000E23Neuroprotective actions of sex steroids in Parkinson's disease.
Auteurs : Mélanie Bourque [Canada] ; Dean E. Dluzen ; Thérèse Di PaoloSource :
- Frontiers in neuroendocrinology [ 1095-6808 ] ; 2009.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animals, Disease Models, Animal, Dopamine (metabolism), Dopamine Agents (toxicity), Estrogens (metabolism), Estrogens (therapeutic use), Humans, Methamphetamine (toxicity), Mitogen-Activated Protein Kinases (metabolism), Neural Pathways (physiology), Neuroprotective Agents (metabolism), Neuroprotective Agents (therapeutic use), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Phosphatidylinositol 3-Kinases (metabolism), Progesterone (metabolism), Receptors, Estrogen (metabolism), Sex Characteristics, Signal Transduction (physiology), Steroids (metabolism), Steroids (therapeutic use).
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemical , metabolism : Dopamine, Estrogens, Mitogen-Activated Protein Kinases, Neuroprotective Agents, Phosphatidylinositol 3-Kinases, Progesterone, Receptors, Estrogen, Steroids.
- chemical , therapeutic use : Estrogens, Neuroprotective Agents, Steroids.
- chemical , toxicity : Dopamine Agents, Methamphetamine.
- drug therapy : Parkinson Disease.
- physiology : Neural Pathways, Signal Transduction.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Humans, Sex Characteristics.
Abstract
The sex difference in Parkinson's disease, with a higher susceptibility in men, suggests a modulatory effect of sex steroids in the brain. Numerous studies highlight that sex steroids have neuroprotective properties against various brain injuries. This paper reviews the protective effects of sex hormones, particularly estradiol, progesterone and androgens, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease as compared to methamphetamine toxicity. The molecular mechanisms underlying beneficial actions of sex steroids on the brain have been investigated showing steroid, dose, timing and duration specificities and presently focus is on the dopamine signaling pathways, the next frontier. Both genomic and non-genomic actions of estrogen converge to promote survival factors and show sex differences. Neuroprotection by estrogen involves activation of signaling molecules such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. Interaction with growth factors, such as insulin-like growth factor 1, also contributes to protective actions of estrogen.
DOI: 10.1016/j.yfrne.2009.04.014
PubMed: 19410597
Affiliations:
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Numerous studies highlight that sex steroids have neuroprotective properties against various brain injuries. This paper reviews the protective effects of sex hormones, particularly estradiol, progesterone and androgens, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease as compared to methamphetamine toxicity. The molecular mechanisms underlying beneficial actions of sex steroids on the brain have been investigated showing steroid, dose, timing and duration specificities and presently focus is on the dopamine signaling pathways, the next frontier. Both genomic and non-genomic actions of estrogen converge to promote survival factors and show sex differences. Neuroprotection by estrogen involves activation of signaling molecules such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. Interaction with growth factors, such as insulin-like growth factor 1, also contributes to protective actions of estrogen.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19410597</PMID><DateCreated><Year>2009</Year><Month>06</Month><Day>23</Day></DateCreated><DateCompleted><Year>2009</Year><Month>08</Month><Day>17</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-6808</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>2</Issue><PubDate><Year>2009</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Frontiers in neuroendocrinology</Title><ISOAbbreviation>Front Neuroendocrinol</ISOAbbreviation></Journal><ArticleTitle>Neuroprotective actions of sex steroids in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>142-57</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.yfrne.2009.04.014</ELocationID><Abstract><AbstractText>The sex difference in Parkinson's disease, with a higher susceptibility in men, suggests a modulatory effect of sex steroids in the brain. Numerous studies highlight that sex steroids have neuroprotective properties against various brain injuries. This paper reviews the protective effects of sex hormones, particularly estradiol, progesterone and androgens, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease as compared to methamphetamine toxicity. The molecular mechanisms underlying beneficial actions of sex steroids on the brain have been investigated showing steroid, dose, timing and duration specificities and presently focus is on the dopamine signaling pathways, the next frontier. Both genomic and non-genomic actions of estrogen converge to promote survival factors and show sex differences. Neuroprotection by estrogen involves activation of signaling molecules such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. 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DateType="Electronic"><Year>2009</Year><Month>05</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Front Neuroendocrinol</MedlineTA><NlmUniqueID>7513292</NlmUniqueID><ISSNLinking>0091-3022</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004967">Estrogens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011960">Receptors, Estrogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013256">Steroids</NameOfSubstance></Chemical><Chemical><RegistryNumber>44RAL3456C</RegistryNumber><NameOfSubstance 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effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="N">Dopamine Agents</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004967" MajorTopicYN="Y">Estrogens</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008694" 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UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>199</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>02</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>04</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>04</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>5</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>5</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>8</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19410597</ArticleId><ArticleId IdType="pii">S0091-3022(09)00023-5</ArticleId><ArticleId IdType="doi">10.1016/j.yfrne.2009.04.014</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><name sortKey="Dluzen, Dean E" sort="Dluzen, Dean E" uniqKey="Dluzen D" first="Dean E" last="Dluzen">Dean E. Dluzen</name></noCountry><country name="Canada"><noRegion><name sortKey="Bourque, Melanie" sort="Bourque, Melanie" uniqKey="Bourque M" first="Mélanie" last="Bourque">Mélanie Bourque</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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