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FAS -670A>G genetic polymorphism Is associated with treatment resistant depression

2015-10-01Journal article Open access
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dc.contributor.authorSantos, Marlene
dc.contributor.authorCarvalho, Serafim
dc.contributor.authorLima, Luís
dc.contributor.authorMota-Pereira, Jorge
dc.contributor.authorPimentel, Paulo
dc.contributor.authorMaia, Dulce
dc.contributor.authorCorreia, Diana
dc.contributor.authorGomes, Sofia
dc.contributor.authorCruz, Agostinho
dc.contributor.authorMedeiros, Rui
dc.date.accessioned2021-11-22T12:21:12Z
dc.date.available2021-11-22T12:21:12Z
dc.date.issued2015-10-01
dc.description.abstractHippocampal neurogenesis has been suggested as a downstream event of antidepressants (AD) mechanism of action and might explain the lag time between AD administration and the therapeutic effect. Despite the widespread use of AD in the context of Major Depressive Disorder (MDD) there are no reliable biomarkers of treatment response phenotypes, and a significant proportion of patients display Treatment Resistant Depression (TRD). Fas/FasL system is one of the best-known death-receptor mediated cell signaling systems and is recognized to regulate cell proliferation and tumor cell growth. Recently this pathway has been described to be involved in neurogenesis and neuroplasticity. Since FAS -670A>G and FASL -844T>C functional polymorphisms never been evaluated in the context of depression and antidepressant therapy, we genotyped FAS -670A>G and FASL -844T>C in a subset of 80 MDD patients to evaluate their role in antidepressant treatment response phenotypes. We found that the presence of FAS -670G allele was associated with antidepressant bad prognosis (relapse or TRD: OR=6.200; 95% CI: [1.875–20.499]; p=0.001), and we observed that patients carrying this allele have a higher risk to develop TRD (OR=10.895; 95% CI: [1.362–87.135]; p=0.008). Moreover, multivariate analysis adjusted to potentials confounders showed that patients carrying G allele have higher risk of early relapse (HR=3.827; 95% CI: [1.072–13.659]; p=0.039). FAS mRNA levels were down-regulated among G carriers, whose genotypes were more common in TRD patients. No association was found between FASL-844T>C genetic polymorphism and any treatment phenotypes. Small sample size. Patients used antidepressants with different mechanisms of action. To the best of our knowledge this is the first study to evaluate the role of FAS functional polymorphism in the outcome of antidepressant therapy. This preliminary report associates FAS -670A>G genetic polymorphism with Treatment Resistant Depression and with time to relapse. The current results may possibly be given to the recent recognized role of Fas in neurogenesis and/or neuroplasticity.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationSantos, M., Carvalho, S., Lima, L., Mota-Pereira, J., Pimentel, P., Maia, D., Correia, D., Gomes, S., Cruz, A., & Medeiros, R. (2015). FAS -670A>G genetic polymorphism Is associated with Treatment Resistant Depression. Journal of Affective Disorders, 185, 164-169. https://doi.org/https://doi.org/10.1016/j.jad.2015.06.027pt_PT
dc.identifier.doi10.1016/j.jad.2015.06.027pt_PT
dc.identifier.issn0165-0327
dc.identifier.urihttp://hdl.handle.net/10400.22/18918
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0165032715003997?via%3Dihubpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectNeurogenesispt_PT
dc.subjectNeuroplasticitypt_PT
dc.subjectFASpt_PT
dc.subjectAntidepressantspt_PT
dc.subjectTreatment resistant depressionpt_PT
dc.subjectPolymorphismspt_PT
dc.titleFAS -670A>G genetic polymorphism Is associated with treatment resistant depressionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage169pt_PT
oaire.citation.startPage164pt_PT
oaire.citation.titleJournal of Affective Disorderspt_PT
oaire.citation.volume185pt_PT
person.familyNameSantos
person.familyNameOliveira Lima
person.familyNameCruz
person.givenNameMarlene
person.givenNameLuís Carlos
person.givenNameAgostinho
person.identifier1508370
person.identifier.ciencia-id8311-B967-31C4
person.identifier.ciencia-id9F16-0E29-D9FC
person.identifier.orcid0000-0001-5020-5942
person.identifier.orcid0000-0001-8152-9237
person.identifier.orcid0000-0002-1157-8196
person.identifier.scopus-author-id57110502000
person.identifier.scopus-author-id23501978900
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication8ce9ee39-a4c6-46ae-99e2-49397b550f1b
relation.isAuthorOfPublicationc6b00c1f-f4c9-4f4f-b291-17cf30b1e1f8
relation.isAuthorOfPublicationd7ec3c5d-b3e0-4e34-8e24-4d1588876120
relation.isAuthorOfPublication.latestForDiscoveryc6b00c1f-f4c9-4f4f-b291-17cf30b1e1f8

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