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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorHU, Li Wen-
dc.contributor.authorKAWAMOTO, Elisa Mitiko-
dc.contributor.authorBRIETZKE, Elisa-
dc.contributor.authorSCAVONE, Cristoforo-
dc.contributor.authorLAFER, Beny-
dc.date.accessioned2017-11-27T16:34:35Z-
dc.date.available2017-11-27T16:34:35Z-
dc.date.issued2011-
dc.identifier.citationPROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, v.35, n.1, p.11-17, 2011-
dc.identifier.issn0278-5846-
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/23425-
dc.description.abstractThe neurobiology of Bipolar Disorder (BD) is not completely understood, although abnormalities in neuroplasticity and control of apoptosis have been considered as central events in its pathophysiology. The molecules of the Wnt family comprise a class of proteins that control essential developmental processes such as embryonic patterning, cell growth, migration, and differentiation with their actions largely exerted by modulating gene transcription. The Wnt signaling pathway has interface with some mediators with a well documented action in neuroplasticity and regulation of cell surviving. In addition, mood stabilizers such as lithium and valproate may have their neuroprotective properties in part mediated by the Wnt pathway. This article is an overview of how the Wnt signaling cascade might be involved in the pathogenesis of BD and also in details of intracellular events related to this pathway. Further studies of Wnt signaling may lead to a better comprehension of the neuroprotective actions of mood stabilizers and contribute to improving the therapeutics of BD.-
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2008/06948-8, 2008/08191-1]-
dc.language.isoeng-
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD-
dc.relation.ispartofProgress in Neuro-Psychopharmacology & Biological Psychiatry-
dc.rightsrestrictedAccess-
dc.subjectBipolar disorder-
dc.subjectGSK3 beta-
dc.subjectInflammation-
dc.subjectNeuroplasticity-
dc.subjectWnt-
dc.subject.otherglycogen-synthase kinase-3-
dc.subject.othersubgenual prefrontal cortex-
dc.subject.othermajor depressive disorder-
dc.subject.otherneurotrophic factor-
dc.subject.otherlithium treatment-
dc.subject.otherbeta-catenin-
dc.subject.otheroxidative stress-
dc.subject.otherpsychiatric-disorders-
dc.subject.othertransduction pathways-
dc.subject.othereuthymic patients-
dc.titleThe role of Wnt signaling and its interaction with diverse mechanisms of cellular apoptosis in the pathophysiology of bipolar disorder-
dc.typearticle-
dc.rights.holderCopyright PERGAMON-ELSEVIER SCIENCE LTD-
dc.identifier.doi10.1016/j.pnpbp.2010.08.031-
dc.identifier.pmid20828594-
dc.subject.wosClinical Neurology-
dc.subject.wosNeurosciences-
dc.subject.wosPharmacology & Pharmacy-
dc.subject.wosPsychiatry-
dc.type.categoryreview-
dc.type.versionpublishedVersion-
hcfmusp.author.externalKAWAMOTO, Elisa Mitiko:Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, BR-01060970 Sao Paulo, Brazil-
hcfmusp.author.externalSCAVONE, Cristoforo:Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, BR-01060970 Sao Paulo, Brazil-
hcfmusp.description.beginpage11-
hcfmusp.description.endpage17-
hcfmusp.description.issue1-
hcfmusp.description.volume35-
hcfmusp.origemWOS-
hcfmusp.origem.id2-s2.0-78650958063-
hcfmusp.origem.idWOS:000287271400002-
hcfmusp.publisher.cityOXFORD-
hcfmusp.publisher.countryENGLAND-
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