Signaling pathways mediating the neuroprotective effects of sex steroids and SERMs in Parkinson's disease.
Identifieur interne : 001130 ( Main/Exploration ); précédent : 001129; suivant : 001131Signaling pathways mediating the neuroprotective effects of sex steroids and SERMs in Parkinson's disease.
Auteurs : Mélanie Bourque [Canada] ; Dean E. Dluzen ; Thérèse Di PaoloSource :
- Frontiers in neuroendocrinology [ 1095-6808 ] ; 2012.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Estrogens (pharmacology), Gonadal Steroid Hormones (pharmacology), Humans, Models, Biological, Neuroprotective Agents (pharmacology), Parkinson Disease (genetics), Parkinson Disease (prevention & control), Parkinson Disease (psychology), Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (pathology), Receptors, Estrogen (genetics), Receptors, Estrogen (metabolism), Receptors, Estrogen (physiology), Selective Estrogen Receptor Modulators (pharmacology), Signal Transduction (drug effects), Signal Transduction (genetics), Signal Transduction (physiology).
- MESH :
- chemical , genetics : Receptors, Estrogen.
- chemical , metabolism : Receptors, Estrogen.
- chemical , pharmacology : Estrogens, Gonadal Steroid Hormones, Neuroprotective Agents, Selective Estrogen Receptor Modulators.
- chemical , physiology : Receptors, Estrogen.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemically induced : Parkinsonian Disorders.
- drug effects : Signal Transduction.
- genetics : Parkinson Disease, Signal Transduction.
- pathology : Parkinsonian Disorders.
- physiology : Signal Transduction.
- prevention & control : Parkinson Disease.
- psychology : Parkinson Disease.
- Animals, Humans, Models, Biological.
Abstract
Studies with the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease have shown the ability of 17β-estradiol to protect the nigrostriatal dopaminergic system. This paper reviews the signaling pathways mediating the neuroprotective effect of 17β-estradiol against MPTP-induced toxicity. The mechanisms of 17β-estradiol action implicate activation of signaling pathways such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. 17β-estradiol signaling is complex and integrates multiple interactions with signaling molecules that act to potentiate a protective effect. 17β-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 17β-estradiol. Compounds that stimulate GPER1 such as selective estrogen receptor modulators and phytoestrogens show neuroprotective activity and are alternatives to 17β-estradiol.
DOI: 10.1016/j.yfrne.2012.02.003
PubMed: 22387674
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Studies with the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease have shown the ability of 17β-estradiol to protect the nigrostriatal dopaminergic system. This paper reviews the signaling pathways mediating the neuroprotective effect of 17β-estradiol against MPTP-induced toxicity. The mechanisms of 17β-estradiol action implicate activation of signaling pathways such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. 17β-estradiol signaling is complex and integrates multiple interactions with signaling molecules that act to potentiate a protective effect. 17β-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 17β-estradiol. Compounds that stimulate GPER1 such as selective estrogen receptor modulators and phytoestrogens show neuroprotective activity and are alternatives to 17β-estradiol.</div>
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