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dc.contributor.authorKusters, Cynthia D.J.
dc.contributor.authorPaul, Kimberly C.
dc.contributor.authorFolle, Aline Duarte
dc.contributor.authorKeener, Adrienne M.
dc.contributor.authorBronstein, Jeff M.
dc.contributor.authorDobricic, Valerija
dc.contributor.authorTysnes, Ole-Bjørn
dc.contributor.authorBertram, Lars
dc.contributor.authorAlves, Guido Werner
dc.contributor.authorSinsheimer, Janet S.
dc.contributor.authorLill, Christina M.
dc.contributor.authorMaple-Grødem, Jodi
dc.contributor.authorRitz, Beate R.
dc.date.accessioned2021-05-07T10:47:58Z
dc.date.available2021-05-07T10:47:58Z
dc.date.created2020-12-21T12:59:47Z
dc.date.issued2020
dc.PublishedNeurology: Genetics. 2020, 6 (5), .
dc.identifier.issn2376-7839
dc.identifier.urihttps://hdl.handle.net/11250/2754133
dc.description.abstractObjective We examine the hypothesized overlap of genetic architecture for Alzheimer disease (AD), schizophrenia (SZ), and Parkinson disease (PD) through the use of polygenic risk scores (PRSs) with the occurrence of hallucinations in PD. Methods We used 2 population-based studies (ParkWest, Norway, and Parkinson's Environment and Gene, USA) providing us with 399 patients with PD with European ancestry and a PD diagnosis after age 55 years to assess the associations between 4 PRSs and hallucinations after 5 years of mean disease duration. Based on the existing genome-wide association study of other large consortia, 4 PRSs were created: one each using AD, SZ, and PD cohorts and another PRS for height, which served as a negative control. Results A higher prevalence of hallucinations was observed with each SD increase of the AD-PRS (odds ratio [OR]: 1.37, 95% confidence interval [CI]: 1.03–1.83). This effect was mainly driven by APOE (OR: 1.92, 95% CI: 1.14–3.22). In addition, a suggestive decrease and increase, respectively, in hallucination prevalence were observed with the SZ-PRS and the PD-PRS (OR: 0.77, 95% CI: 0.59–1.01; and OR: 1.29, 95% CI: 0.95–1.76, respectively). No association was observed with the height PRS. Conclusions These results suggest that mechanisms for hallucinations in PD may in part be driven by the same genetic architecture that leads to cognitive decline in AD, especially by APOE.en_US
dc.language.isoengen_US
dc.publisherWolters Kluwer Healthen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleGenetic risk scores and hallucinations in patients with Parkinson diseaseen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2020 The Author(s).en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.1212/NXG.0000000000000492
dc.identifier.cristin1862368
dc.source.journalNeurology: Geneticsen_US
dc.source.406
dc.source.145
dc.identifier.citationNeurology: Genetics. 2020, 6 (5)en_US
dc.source.volume6en_US
dc.source.issue5en_US


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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