Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes
Abstract Twin studies indicate that 30–40% of the disease liability for depression can be attributed to genetic differences. Here, we assess the explanatory ability of polygenic scores (PGS) based on broad- (PGSBD) and clinical- (PGSMDD) depression summary statistics from the UK Biobank in an indepe...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2023-04-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-023-33645-7 |
| _version_ | 1827961254346489856 |
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| author | John E. McGeary Chelsie E. Benca-Bachman Victoria A. Risner Christopher G. Beevers Brandon E. Gibb Rohan H. C. Palmer |
| author_facet | John E. McGeary Chelsie E. Benca-Bachman Victoria A. Risner Christopher G. Beevers Brandon E. Gibb Rohan H. C. Palmer |
| author_sort | John E. McGeary |
| collection | DOAJ |
| description | Abstract Twin studies indicate that 30–40% of the disease liability for depression can be attributed to genetic differences. Here, we assess the explanatory ability of polygenic scores (PGS) based on broad- (PGSBD) and clinical- (PGSMDD) depression summary statistics from the UK Biobank in an independent sample of adults (N = 210; 100% European Ancestry) who were extensively phenotyped for depression and related neurocognitive traits (e.g., rumination, emotion regulation, anhedonia, and resting frontal alpha asymmetry). The UK Biobank-derived PGSBD had small associations with MDD, depression severity, anhedonia, cognitive reappraisal, brooding, and suicidal ideation but only the association with suicidal ideation remained statistically significant after correcting for multiple comparisons. Similarly small associations were observed for the PGSMDD but none remained significant after correcting for multiple comparisons. These findings provide important initial guidance about the expected effect sizes between current UKB PGSs for depression and depression-related neurocognitive phenotypes. |
| first_indexed | 2024-04-09T16:23:44Z |
| format | Article |
| id | doaj.art-3c55fb6b3382425a94faae7f17e1d0d3 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-04-09T16:23:44Z |
| publishDate | 2023-04-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-3c55fb6b3382425a94faae7f17e1d0d32023-04-23T11:17:58ZengNature PortfolioScientific Reports2045-23222023-04-011311810.1038/s41598-023-33645-7Associating broad and clinically defined polygenic scores for depression with depression-related phenotypesJohn E. McGeary0Chelsie E. Benca-Bachman1Victoria A. Risner2Christopher G. Beevers3Brandon E. Gibb4Rohan H. C. Palmer5Providence Veterans Affairs Medical CenterProvidence Veterans Affairs Medical CenterBehavioral Genetics of Addiction Laboratory, Department of Psychology, Emory UniversityDepartment of Psychology, University of Texas at AustinDepartment of Psychology State, University of New York at BinghamtonProvidence Veterans Affairs Medical CenterAbstract Twin studies indicate that 30–40% of the disease liability for depression can be attributed to genetic differences. Here, we assess the explanatory ability of polygenic scores (PGS) based on broad- (PGSBD) and clinical- (PGSMDD) depression summary statistics from the UK Biobank in an independent sample of adults (N = 210; 100% European Ancestry) who were extensively phenotyped for depression and related neurocognitive traits (e.g., rumination, emotion regulation, anhedonia, and resting frontal alpha asymmetry). The UK Biobank-derived PGSBD had small associations with MDD, depression severity, anhedonia, cognitive reappraisal, brooding, and suicidal ideation but only the association with suicidal ideation remained statistically significant after correcting for multiple comparisons. Similarly small associations were observed for the PGSMDD but none remained significant after correcting for multiple comparisons. These findings provide important initial guidance about the expected effect sizes between current UKB PGSs for depression and depression-related neurocognitive phenotypes.https://doi.org/10.1038/s41598-023-33645-7 |
| spellingShingle | John E. McGeary Chelsie E. Benca-Bachman Victoria A. Risner Christopher G. Beevers Brandon E. Gibb Rohan H. C. Palmer Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes Scientific Reports |
| title | Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes |
| title_full | Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes |
| title_fullStr | Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes |
| title_full_unstemmed | Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes |
| title_short | Associating broad and clinically defined polygenic scores for depression with depression-related phenotypes |
| title_sort | associating broad and clinically defined polygenic scores for depression with depression related phenotypes |
| url | https://doi.org/10.1038/s41598-023-33645-7 |
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