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GWAS Study

Identification of common genetic risk variants for autism spectrum disorder.

Grove J, Ripke S, Als TD et al.

30804558 PubMed ID
GWAS Study Type
190848 Participants
433 Views
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

GJ
Grove J
RS
Ripke S
AT
Als TD
MM
Mattheisen M
WR
Walters RK
WH
Won H
PJ
Pallesen J
AE
Agerbo E
AO
Andreassen OA
AR
Anney R
AS
Awashti S
BR
Belliveau R
BF
Bettella F
BJ
Buxbaum JD
BJ
Bybjerg-Grauholm J
BM
Bækvad-Hansen M
CF
Cerrato F
CK
Chambert K
CJ
Christensen JH
CC
Churchhouse C
DK
Dellenvall K
DD
Demontis D
DR
De Rubeis S
DB
Devlin B
DS
Djurovic S
DA
Dumont AL
GJ
Goldstein JI
HC
Hansen CS
HM
Hauberg ME
HM
Hollegaard MV
HS
Hope S
HD
Howrigan DP
HH
Huang H
HC
Hultman CM
KL
Klei L
MJ
Maller J
MJ
Martin J
MA
Martin AR
MJ
Moran JL
NM
Nyegaard M
NT
Nærland T
PD
Palmer DS
PA
Palotie A
PC
Pedersen CB
PM
Pedersen MG
DT
dPoterba T
PJ
Poulsen JB
PB
Pourcain BS
QP
Qvist P
RK
Rehnström K
RA
Reichenberg A
RJ
Reichert J
RE
Robinson EB
RK
Roeder K
RP
Roussos P
SE
Saemundsen E
SS
Sandin S
SF
Satterstrom FK
DS
Davey Smith G
SH
Stefansson H
SS
Steinberg S
SC
Stevens CR
SP
Sullivan PF
TP
Turley P
WG
Walters GB
XX
Xu X
SK
Stefansson K
GD
Geschwind DH
NM
Nordentoft M
HD
Hougaard DM
WT
Werge T
MO
Mors O
MP
Mortensen PB
NB
Neale BM
DM
Daly MJ
BA
Børglum AD
Chapter II

Abstract

Summary of the research findings

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD.

18,381 European ancestry cases, 27,969 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

190848
Total Participants
GWAS
Study Type
Yes
Replicated
2,119 European ancestry cases, 142,379 European ancestry controls
Replication Participants
European
Ancestry
Denmark, Ukraine, Georgia, Finland, Iceland, Norway, Sweden, Serbia
Recruitment Country
Chapter IV

AI-Generated Summary

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