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DC Field | Value | Language |
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dc.contributor.author | DeMichele-Sweet, MAA | - |
dc.contributor.author | Klei, L | - |
dc.contributor.author | Creese, B | - |
dc.contributor.author | Harwood, JC | - |
dc.contributor.author | Weamer, EA | - |
dc.contributor.author | McClain, L | - |
dc.contributor.author | Sims, R | - |
dc.contributor.author | Hernandez, I | - |
dc.contributor.author | Moreno-Grau, S | - |
dc.contributor.author | Tárraga, L | - |
dc.contributor.author | Boada, M | - |
dc.contributor.author | Alarcón-Martín, E | - |
dc.contributor.author | Valero, S | - |
dc.contributor.author | Liu, Y | - |
dc.contributor.author | Hooli, B | - |
dc.contributor.author | Aarsland, D | - |
dc.contributor.author | Selbaek, G | - |
dc.contributor.author | Bergh, S | - |
dc.contributor.author | Rongve, A | - |
dc.contributor.author | Saltvedt, I | - |
dc.contributor.author | Skjellegrind, HK | - |
dc.contributor.author | Engdahl, B | - |
dc.contributor.author | Stordal, E | - |
dc.contributor.author | Andreassen, OA | - |
dc.contributor.author | Djurovic, S | - |
dc.contributor.author | Athanasiu, L | - |
dc.contributor.author | Seripa, D | - |
dc.contributor.author | Borroni, B | - |
dc.contributor.author | Albani, D | - |
dc.contributor.author | Forloni, G | - |
dc.contributor.author | Mecocci, P | - |
dc.contributor.author | Serretti, A | - |
dc.contributor.author | De Ronchi, D | - |
dc.contributor.author | Politis, A | - |
dc.contributor.author | Williams, J | - |
dc.contributor.author | Mayeux, R | - |
dc.contributor.author | Foroud, T | - |
dc.contributor.author | Ruiz, A | - |
dc.contributor.author | Ballard, C | - |
dc.contributor.author | Holmans, P | - |
dc.contributor.author | Lopez, OL | - |
dc.contributor.author | Kamboh, MI | - |
dc.contributor.author | Devlin, B | - |
dc.contributor.author | Sweet, RA | - |
dc.contributor.other | NIA-LOAD Family Based Study Consortium, Alzheimer’s Disease Genetics Consortium (ADGC) | - |
dc.contributor.other | Alzheimer’s Disease Genetics Consortium (ADGC) | - |
dc.date.accessioned | 2023-11-19T15:45:08Z | - |
dc.date.available | 2023-11-19T15:45:08Z | - |
dc.date.issued | 2021-06-10 | - |
dc.identifier | ORCID iD: Mary Ann A. DeMichele-Sweet https://orcid.org/0000-0002-6582-7813 | - |
dc.identifier | ORCID iD: Byron Creese https://orcid.org/0000-0001-6490-6037 | - |
dc.identifier | ORCID iD: Rebecca Sims https://orcid.org/0000-0002-3885-1199 | - |
dc.identifier | ORCID iD: Mercè Boada https://orcid.org/0000-0003-2617-3009 | - |
dc.identifier | ORCID iD: Yushi Liu https://orcid.org/0000-0003-4185-4187 | - |
dc.identifier | ORCID iD: Basavaraj Hooli https://orcid.org/0000-0002-5461-1507 | - |
dc.identifier | ORCID iD: Geir Selbaek https://orcid.org/0000-0001-6511-8219 | - |
dc.identifier | ORCID iD: Sverre Bergh https://orcid.org/0000-0001-9593-2967 | - |
dc.identifier | ORCID iD: Arvid Rongve https://orcid.org/0000-0002-0476-4134 | - |
dc.identifier | ORCID iD: Ingvild Saltvedt https://orcid.org/0000-0002-7897-9808 | - |
dc.identifier | ORCID iD: Håvard K. Skjellegrind https://orcid.org/0000-0003-3067-0016 | - |
dc.identifier | ORCID iD: Bo Engdahl https://orcid.org/0000-0002-9166-5782 | - |
dc.identifier | ORCID iD: Eystein Stordal https://orcid.org/0000-0002-2443-7923 | - |
dc.identifier | ORCID iD: Ole A. Andreassen https://orcid.org/0000-0002-4461-3568 | - |
dc.identifier | ORCID iD: Srdjan Djurovic https://orcid.org/0000-0002-8140-8061 | - |
dc.identifier | ORCID iD: Lavinia Athanasiu https://orcid.org/0000-0002-3321-6997 | - |
dc.identifier | ORCID iD: Barbara Borroni https://orcid.org/0000-0001-9340-9814 | - |
dc.identifier | ORCID iD: Diego Albani https://orcid.org/0000-0002-7050-6723 | - |
dc.identifier | ORCID iD: Alessandro Serretti https://orcid.org/0000-0003-4363-3759 | - |
dc.identifier | ORCID iD: Antonis Politis https://orcid.org/0000-0003-0261-7517 | - |
dc.identifier | ORCID iD: Julie Williams https://orcid.org/0000-0002-4069-0259 | - |
dc.identifier | ORCID iD: Tatiana Foroud https://orcid.org/0000-0002-5549-2212 | - |
dc.identifier | ORCID iD: Agustin Ruiz https://orcid.org/0000-0003-2633-2495 | - |
dc.identifier | ORCID iD: Clive Ballard https://orcid.org/0000-0003-0022-5632 | - |
dc.identifier | ORCID iD: Peter Holmans https://orcid.org/0000-0003-0870-9412 | - |
dc.identifier | ORCID iD: Oscar L. Lopez https://orcid.org/0000-0002-8546-8256 | - |
dc.identifier | ORCID iD: Bernie Devlin https://orcid.org/0000-0003-2524-4290 | - |
dc.identifier | ORCID iD: Robert A. Sweet https://orcid.org/0000-0001-9154-9709 | - |
dc.identifier.citation | DeMichele-Sweet, M.A.A. et al. (2021) 'Genome-wide association identifies the first risk loci for psychosis in Alzheimer disease', Molecular Psychiatry, 26 (10), pp. 5797 - 5811. doi: 10.1038/s41380-021-01152-8. | en_US |
dc.identifier.issn | 1359-4184 | - |
dc.identifier.uri | https://bura.brunel.ac.uk/handle/2438/27671 | - |
dc.description | Authors in the NIA-LOAD Family Based Study Consortium are Tatiana Foroud, M. Ilyas Kamboh, Oscar L. Lopez, and Richard Mayeux. Authors in the Alzheimer’s Disease Genetics Consortium (ADGC) are Tatiana Foroud, Richard Mayeux, and Robert A. Sweet. A complete list of contributing individuals, consortia, and their grant support can be found in Supplementary Acknowledgements online at: https://www.nature.com/articles/s41380-021-01152-8#Sec13 . | en_US |
dc.description.abstract | Psychotic symptoms, defined as the occurrence of delusions or hallucinations, are frequent in Alzheimer disease (AD with psychosis, AD + P). AD + P affects ~50% of individuals with AD, identifies a subgroup with poor outcomes, and is associated with a greater degree of cognitive impairment and depressive symptoms, compared to subjects without psychosis (AD − P). Although the estimated heritability of AD + P is 61%, genetic sources of risk are unknown. We report a genome-wide meta-analysis of 12,317 AD subjects, 5445 AD + P. Results showed common genetic variation accounted for a significant portion of heritability. Two loci, one in ENPP6 (rs9994623, O.R. (95%CI) 1.16 (1.10, 1.22), p = 1.26 × 10−8) and one spanning the 3′-UTR of an alternatively spliced transcript of SUMF1 (rs201109606, O.R. 0.65 (0.56–0.76), p = 3.24 × 10−8), had genome-wide significant associations with AD + P. Gene-based analysis identified a significant association with APOE, due to the APOE risk haplotype ε4. AD + P demonstrated negative genetic correlations with cognitive and educational attainment and positive genetic correlation with depressive symptoms. We previously observed a negative genetic correlation with schizophrenia; instead, we now found a stronger negative correlation with the related phenotype of bipolar disorder. Analysis of polygenic risk scores supported this genetic correlation and documented a positive genetic correlation with risk variation for AD, beyond the effect of ε4. We also document a small set of SNPs likely to affect risk for AD + P and AD or schizophrenia. These findings provide the first unbiased identification of the association of psychosis in AD with common genetic variation and provide insights into its genetic architecture. | en_US |
dc.description.sponsorship | This study was supported by the following federal grants: AG027224 (RAS), MH116046 (RAS), MH057881 (BD), AG030653 (MIK), AG041718 (MIK), AG066468 (OLL). | en_US |
dc.format.extent | 5797 - 5811 | - |
dc.format.medium | Print-Electronic | - |
dc.language | English | - |
dc.language.iso | en_US | en_US |
dc.publisher | Springer Nature | en_US |
dc.rights | Copyright © The Author(s), under exclusive licence to Springer Nature Limited 2021. This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use (see: https://www.springernature.com/gp/open-research/policies/journal-policies), but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1038/s41380-021-01152-8. | - |
dc.rights.uri | https://www.springernature.com/gp/open-research/policies/journal-policies | - |
dc.subject | diseases | en_US |
dc.subject | psychiatric disorders | en_US |
dc.title | Genome-wide association identifies the first risk loci for psychosis in Alzheimer disease | en_US |
dc.type | Article | en_US |
dc.identifier.doi | https://doi.org/10.1038/s41380-021-01152-8 | - |
dc.relation.isPartOf | Molecular Psychiatry | - |
pubs.issue | 10 | - |
pubs.publication-status | Published | - |
pubs.volume | 26 | - |
dc.identifier.eissn | 1476-5578 | - |
dc.rights.holder | The Author(s) | - |
Appears in Collections: | Dept of Life Sciences Research Papers |
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FullText.pdf | Copyright © The Author(s), under exclusive licence to Springer Nature Limited 2021. This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use (see: https://www.springernature.com/gp/open-research/policies/journal-policies), but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1038/s41380-021-01152-8. | 1.07 MB | Adobe PDF | View/Open |
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