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Bdnf-NRF2 crosstalk in depression disorder

dc.contributor.authorSantos, Marlene
dc.contributor.authorCaldevilla, Renato
dc.contributor.authorMorais, Stephanie
dc.contributor.authorCarvalho, Serafim
dc.contributor.authorMedeiros, Rui
dc.contributor.authorBarroso, Maria Fátima
dc.date.accessioned2024-10-15T14:52:47Z
dc.date.available2024-10-15T14:52:47Z
dc.date.issued2024-10
dc.description.abstractThe World Health Organization estimates that major depressive disorder (MDD) affects over 264 million individuals globally, posing a significant public health challenge. Treatment-resistant depression (TRD) represents a severe form of MDD with poor treatment outcomes. Genetic variations are known to impact MDD treatment responses, yet genome-wide association studies have struggled to identify consistent marker alleles. Previous research has linked the Brain Derived Neurotrophic Factor (BDNF) genetic polymorphism with TRD. BDNF is essential for neuronal survival and neuroplasticity, processes influenced by antidepressant treatment, and regulated by transcription factors like Nuclear factor erythroid 2-related factor 2 (NRF2). NRF2 regulates antioxidant and anti-inflammatory responses and plays a crucial role in depression pathogenesis. NRF2 knockout mice exhibit reduced BDNF levels and depression-like behaviors, indicating that NRF2activation enhances BDNF expression and antidepressant efficacy. The BDNF rs6265 (Val66Met) polymorphism is associated with variations in antidepressant response rates. Research suggests that the interaction between BDNF and NRF2 pathways could enhance antidepressant effectiveness. NRF2 activation, such as through the compound sulforaphane, has demonstrated rapid antidepressant effects by increasing BDNF expression. Lower levels of NRF2 and BDNF are observed in stress-induced depression models, and ketamine treatment influences NRF2-related genes. Simultaneously, there is a growing need for efficient genotyping methods, and genosensors offer a promising solution. This presentation will address the interplay between BDNF and NRF2 in depression, explore its relationship in antidepressant response, and present a putative genosensor for BDNF rs6265 (Val66Met) polymorphism identification, improving antidepressant treatment outcome.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationSantos, M., Caldevilla, R., Morais, S. L., Carvalho, S., Medeiros, R., & Barroso, M. F. (2024). Bdnf-NRF2 crosstalk in depression disorder. 8th BenBedPhar Scientific Meeting; COST Action CA20121, 31.pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.22/26251
dc.language.isoengpt_PT
dc.publisherNOVA Medical School; NOVA University of Lisbonpt_PT
dc.relationThis work received financial support from FCT/MCTES (UIDP/50006/2020 DOI 10.54499/UIDP/50006/2020) through national funds and the Ibero-American Program on Science and Technology CYTED (GENOPSYSEN, P222RT011).pt_PT
dc.subjectBdnf-NRF2pt_PT
dc.subjectMajor Depressive Disorderpt_PT
dc.titleBdnf-NRF2 crosstalk in depression disorderpt_PT
dc.typeconference object
dspace.entity.typePublication
oaire.citation.conferencePlaceLisboapt_PT
oaire.citation.startPage31pt_PT
oaire.citation.title8th BenBedPhar Scientific Meeting; COST Action CA20121pt_PT
person.familyNameSantos
person.familyNameManuel de Caldevilla Carvalho
person.givenNameMarlene
person.givenNameRenato
person.identifier1508370
person.identifier2868531
person.identifier.ciencia-id8311-B967-31C4
person.identifier.ciencia-id4817-5B7F-4D35
person.identifier.orcid0000-0001-5020-5942
person.identifier.orcid0009-0009-5272-4178
person.identifier.scopus-author-id57110502000
rcaap.rightsopenAccesspt_PT
rcaap.typeconferenceObjectpt_PT
relation.isAuthorOfPublication8ce9ee39-a4c6-46ae-99e2-49397b550f1b
relation.isAuthorOfPublicationfa11c04f-84f8-4db3-8a2d-8e9fe13fe991
relation.isAuthorOfPublication.latestForDiscoveryfa11c04f-84f8-4db3-8a2d-8e9fe13fe991

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