TY - JOUR
T1 - Continuity of Genetic Risk for Aggressive Behavior Across the Life-Course
AU - the ACTION Consortium
AU - van der Laan, Camiel M.
AU - Morosoli-García, José J.
AU - van de Weijer, Steve G.A.
AU - Colodro-Conde, Lucía
AU - Ip, Hill F.
AU - van der Laan, Camiel M.
AU - Krapohl, Eva M.L.
AU - Brikell, Isabell
AU - Sánchez-Mora, Cristina
AU - Nolte, Ilja M.
AU - Pourcain, Beate St
AU - Bolhuis, Koen
AU - Palviainen, Teemu
AU - Zafarmand, Hadi
AU - Gordon, Scott
AU - Zayats, Tetyana
AU - Aliev, Fazil
AU - Jiang, Chang
AU - Wang, Carol A.
AU - Saunders, Gretchen
AU - Karhunen, Ville
AU - Hammerschlag, Anke R.
AU - Adkins, Daniel E.
AU - Border, Richard
AU - Peterson, Roseann E.
AU - Prinz, Joseph A.
AU - Thiering, Elisabeth
AU - Seppälä, Ilkka
AU - Vilor-Tejedor, Natàlia
AU - Ahluwalia, Tarunveer S.
AU - Day, Felix R.
AU - Allegrini, Andrea G.
AU - Rimfeld, Kaili
AU - Chen, Qi
AU - Lu, Yi
AU - Martin, Joanna
AU - Artigas, María Soler
AU - Rovira, Paula
AU - Bosch, Rosa
AU - Español, Gemma
AU - Quiroga, Josep Antoni Ramos
AU - Neumann, Alexander
AU - Ensink, Judith
AU - Grasby, Katrina
AU - Tong, Xiaoran
AU - Marrington, Shelby
AU - Middeldorp, Christel
AU - Snieder, Harold
AU - Hartman, Catharina A.
AU - Oldehinkel, Albertine J.
N1 - Funding Information:
CvdL was supported by the Amsterdam Law and Behavior Institute (A-LAB; Vrije Universtiteit, Amsterdam). SvdW was suppported by NWO-grant 451-16-014. Data collection was made possible by multiple grants from The Netherlands Organization for Scientific Research (NWO): 575-25-006, 480-04-004, 904-61-090, 904-61-193, 400-05-717, 311-60008, SPI 56-464-14192 and the Avera Institute for Human Genetics. We gratefully acknowledge grant NWO 480-15-001/674: Netherlands Twin Registry Repository: researching the interplay between genome and environment. MGN is supported by ZonMw grant: ‘Genetics as a research tool: a natural experiment to elucidate the causal effects of social mobility on health’ (pnr: 531003014) and ZonMw project: ‘Can sex- and gender-specific gene expression and epigenetics explain sex-differences in disease prevalence and etiology?’ (pnr: 849200011). Data collection in the Australian sample was made possible by multiple grants from NHMRC (APP1069141) and the John Templeton Foundation (Genetics and Human Agency Project). We also thank David Smyth and Scott Gordon for IT support and Richard Parker as project manager. The 16UP study was supported by the Young and Well Cooperative Research Centre, which was established and funded under the Australian Government’s Cooperative Research Centres Program. The Prospective Imaging Study of Aging: Genes, Brain and Behaviour (PISA) is funded by a National Health and Medical Research Council (NHMRC) Boosting Dementia Research Initiative—Team Grant (APP1095227). Genome-wide SNP genotyping data for PISA participants is sourced from several genetic epidemiology studies led by NGM (with colleagues and collaborators) at QIMR Berghofer and elsewhere over the past 40 years. Principal sources of funding for these early studies were from grants to NGM from Australian NHMRC and to Andrew Heath and Pam Madden (Washington University, St Louis) from NIH (mainly NIAAA and NIDA) and we gratefully acknowledge these contributions. JJM was supported by a QIMR Berghofer International PhD Scholarship. LC-C was supported by a QIMR Berghofer Research Fellowship. SEM and NGM were funded by NHMRC investigator grants (APP1172917 and APP1172990).
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/9
Y1 - 2021/9
N2 - We test whether genetic influences that explain individual differences in aggression in early life also explain individual differences across the life-course. In two cohorts from The Netherlands (N = 13,471) and Australia (N = 5628), polygenic scores (PGSs) were computed based on a genome-wide meta-analysis of childhood/adolescence aggression. In a novel analytic approach, we ran a mixed effects model for each age (Netherlands: 12–70 years, Australia: 16–73 years), with observations at the focus age weighted as 1, and decaying weights for ages further away. We call this approach a ‘rolling weights’ model. In The Netherlands, the estimated effect of the PGS was relatively similar from age 12 to age 41, and decreased from age 41–70. In Australia, there was a peak in the effect of the PGS around age 40 years. These results are a first indication from a molecular genetics perspective that genetic influences on aggressive behavior that are expressed in childhood continue to play a role later in life.
AB - We test whether genetic influences that explain individual differences in aggression in early life also explain individual differences across the life-course. In two cohorts from The Netherlands (N = 13,471) and Australia (N = 5628), polygenic scores (PGSs) were computed based on a genome-wide meta-analysis of childhood/adolescence aggression. In a novel analytic approach, we ran a mixed effects model for each age (Netherlands: 12–70 years, Australia: 16–73 years), with observations at the focus age weighted as 1, and decaying weights for ages further away. We call this approach a ‘rolling weights’ model. In The Netherlands, the estimated effect of the PGS was relatively similar from age 12 to age 41, and decreased from age 41–70. In Australia, there was a peak in the effect of the PGS around age 40 years. These results are a first indication from a molecular genetics perspective that genetic influences on aggressive behavior that are expressed in childhood continue to play a role later in life.
KW - Aggression
KW - Aggressive behavior
KW - Development
KW - Life-course
KW - Polygenic score
KW - Rolling weights
U2 - 10.1007/s10519-021-10076-6
DO - 10.1007/s10519-021-10076-6
M3 - Article
C2 - 34390460
AN - SCOPUS:85116861074
SN - 0001-8244
VL - 51
SP - 592
EP - 606
JO - Behavior Genetics
JF - Behavior Genetics
IS - 5
ER -