Najada Stringa1, Yuri Milaneschi2, Natasja M van Schoor3, Bianca Suanet4, Sven van der Lee5, Henne Holstege5, Marcel J T Reinders6, Aartjan T F Beekman2, Martijn Huisman7. 1. Amsterdam UMC- Vrije Universiteit Amsterdam, Department of Epidemiology and Biostatistics, Amsterdam Public Health Research Institute, (NS, NMS, MH) Amsterdam, the Netherlands. Electronic address: n.stringa@amsterdamumc.nl. 2. Amsterdam UMC- Vrije Universiteit Amsterdam, Department of Psychiatry, Amsterdam Public Health Research Institute, (YM, ATFB) Amsterdam, the Netherlands; GGZ in Geest, (YM, ATFB) Amsterdam, the Netherlands. 3. Amsterdam UMC- Vrije Universiteit Amsterdam, Department of Epidemiology and Biostatistics, Amsterdam Public Health Research Institute, (NS, NMS, MH) Amsterdam, the Netherlands. 4. Department of Sociology, Vrije Universiteit, (BS, MH) Amsterdam, the Netherlands. 5. Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, (SVNL, HH) Amsterdam, the Netherlands; Department of Clinical Genetics, VU University Medical Centre, (SVDL, HH) Amsterdam, the Netherlands. 6. Pattern Recognition and Bioinformatics, Delft University of Technology, (MJTR) Delft, the Netherlands. 7. Amsterdam UMC- Vrije Universiteit Amsterdam, Department of Epidemiology and Biostatistics, Amsterdam Public Health Research Institute, (NS, NMS, MH) Amsterdam, the Netherlands; Department of Sociology, Vrije Universiteit, (BS, MH) Amsterdam, the Netherlands.
Abstract
OBJECTIVES: The objectives of this study were to investigate the effect of genetic and social factors on depressive symptoms and depression over time and to test whether social factors moderate the relationship between depressive symptoms and its underlying genetics in later life. METHODS: The study included 2,279 participants with a mean follow-up of 15 years from the Longitudinal Aging Study Amsterdam with genotyping data. The personal genetic loading for depression was estimated for each participant by calculating a polygenic risk scores (PRS-D), based on 23,032 single nucleotide polymorphisms associated with major depression in a large genome-wide association study. Partner status, network size, received and given emotional support were assessed via questionnaires and depressive symptoms were assessed using the CES-D Scale. A CES-D Scale of 16 and higher was considered as clinically relevant depression. RESULTS: Higher PRS-D was associated with more depressive symptoms whereas having a partner and having a larger network size were independently associated with less depressive symptoms. After extra adjustment for education, cognitive function and functional limitations, giving more emotional support was also associated with less depressive symptoms. No evidence for gene-environment interaction between PRS-D and social factors was found. Similar results were found for clinically relevant depression. CONCLUSION: Genetic and social factors are independently associated with depressive symptoms over time in older adults. Strategies that boost social functioning should be encouraged in the general population of older adults regardless of the genetic liability for depression.
OBJECTIVES: The objectives of this study were to investigate the effect of genetic and social factors on depressive symptoms and depression over time and to test whether social factors moderate the relationship between depressive symptoms and its underlying genetics in later life. METHODS: The study included 2,279 participants with a mean follow-up of 15 years from the Longitudinal Aging Study Amsterdam with genotyping data. The personal genetic loading for depression was estimated for each participant by calculating a polygenic risk scores (PRS-D), based on 23,032 single nucleotide polymorphisms associated with major depression in a large genome-wide association study. Partner status, network size, received and given emotional support were assessed via questionnaires and depressive symptoms were assessed using the CES-D Scale. A CES-D Scale of 16 and higher was considered as clinically relevant depression. RESULTS: Higher PRS-D was associated with more depressive symptoms whereas having a partner and having a larger network size were independently associated with less depressive symptoms. After extra adjustment for education, cognitive function and functional limitations, giving more emotional support was also associated with less depressive symptoms. No evidence for gene-environment interaction between PRS-D and social factors was found. Similar results were found for clinically relevant depression. CONCLUSION: Genetic and social factors are independently associated with depressive symptoms over time in older adults. Strategies that boost social functioning should be encouraged in the general population of older adults regardless of the genetic liability for depression.
Authors: Lianne M Reus; Iris E Jansen; Merel O Mol; Fred van Ruissen; Jeroen van Rooij; Natasja M van Schoor; Niccolò Tesi; Marcel J T Reinders; Martijn A Huisman; Henne Holstege; Pieter Jelle Visser; Sterre C M de Boer; Marc Hulsman; Shahzad Ahmad; Najaf Amin; Andre G Uitterlinden; Arfan Ikram; Cornelia M van Duijn; Harro Seelaar; Inez H G B Ramakers; Frans R J Verhey; Aad van der Lugt; Jurgen A H R Claassen; Geert Jan Biessels; Peter Paul De Deyn; Philip Scheltens; Wiesje M van der Flier; John C van Swieten; Yolande A L Pijnenburg; Sven J van der Lee Journal: Transl Psychiatry Date: 2021-09-02 Impact factor: 6.222