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dc.contributor.authorRamsay, Hughen
dc.contributor.authorSurcel, Heljä-Marjaen
dc.contributor.authorBjörnholm, Lassien
dc.contributor.authorKerkelä, Marttaen
dc.contributor.authorKhandaker, Golamen
dc.contributor.authorVeijola, Juhaen
dc.date.accessioned2020-09-24T23:30:50Z
dc.date.available2020-09-24T23:30:50Z
dc.date.issued2020-11-17en
dc.identifier.issn1787-9965
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/310709
dc.description.abstractPrenatal infection is associated with brain structural and functional abnormalities, and may increase risk for psychosis through a direct effect on neurodevelopment. Various infections may exert their effect through a pro-inflammatory immune response but studies of prenatal maternal inflammatory markers and offspring neurodevelopment are scarce. Using the longitudinal Northern Finland Birth Cohort 1986 study, we examined the associations of maternal prenatal C-reactive protein (CRP) levels with psychosis risk factors in adolescent offspring. CRP was measured in maternal sera collected in pregnancy. In offspring, school performance was measured at age 7 years, while school performance, psychotic experiences and cannabis use were measured at age 16 years. We tested associations of CRP with offspring measures using regression analysis controlling for offspring sex, maternal education level, and prenatal maternal body mass index, smoking and alcohol use in pregnancy, place of birth, maternal psychiatric admission, paternal psychiatric admission, mothers age at birth and gestational week of CRP sample. We also tested if adolescent cannabis use mediated the associations between maternal CRP and offspring outcomes. Controlling for covariates, maternal CRP was associated with academic performance at age 16 years (beta=0.062, 95% CI=0.036-0.088), but not with possible psychotic experiences at 16 years (odds ratio=1.09, 95% CI=0.96-1.24). Maternal CRP was also associated with adolescent cannabis use (odds ratio=1.24, 95% CI=1.07-1.43). These findings suggest that prenatal inflammation may influence later mental illness risk by affecting neurodevelopment, and also indirectly by increasing risk of exposure to cannabis.
dc.format.mediumPrint-Electronicen
dc.languageengen
dc.publisherOxford University Press
dc.rightsAll rights reserved
dc.rights.uri
dc.titleAssociations Between Maternal Prenatal C-Reactive Protein and Risk Factors for Psychosis in Adolescent Offspring: Findings From the Northern Finland Birth Cohort 1986.en
dc.typeArticle
prism.publicationDate2020en
prism.publicationNameSchizophrenia bulletinen
dc.identifier.doi10.17863/CAM.57799
dcterms.dateAccepted2020-09-22en
rioxxterms.versionofrecord10.1093/schbul/sbaa152en
rioxxterms.versionAM
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2020-11-17en
dc.contributor.orcidKhandaker, Golam [0000-0002-4935-9220]
dc.identifier.eissn1745-1701
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idWellcome Trust (201486/Z/16/Z)
pubs.funder-project-idMRC (MC_PC_17213)
pubs.funder-project-idMedical Research Council (MR/S037675/1)
cam.orpheus.successMon Nov 23 07:31:32 GMT 2020 - Embargo updated*
cam.orpheus.counter11*
rioxxterms.freetoread.startdate2021-11-17


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