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GWAS Study

An atlas of genetic influences on osteoporosis in humans and mice.

Morris JA, Kemp JP, Youlten SE et al.

30598549 PubMed ID
GWAS Study Type
426824 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

MJ
Morris JA
KJ
Kemp JP
YS
Youlten SE
LL
Laurent L
LJ
Logan JG
CR
Chai RC
VN
Vulpescu NA
FV
Forgetta V
KA
Kleinman A
MS
Mohanty ST
SC
Sergio CM
QJ
Quinn J
NL
Nguyen-Yamamoto L
LA
Luco AL
VJ
Vijay J
SM
Simon MM
PA
Pramatarova A
MC
Medina-Gomez C
TK
Trajanoska K
GE
Ghirardello EJ
BN
Butterfield NC
CK
Curry KF
LV
Leitch VD
SP
Sparkes PC
AA
Adoum AT
MN
Mannan NS
KD
Komla-Ebri DSK
PA
Pollard AS
DH
Dewhurst HF
HT
Hassall TAD
BM
Beltejar MG
AD
Adams DJ
VS
Vaillancourt SM
KS
Kaptoge S
BP
Baldock P
CC
Cooper C
RJ
Reeve J
NE
Ntzani EE
EE
Evangelou E
OC
Ohlsson C
KD
Karasik D
RF
Rivadeneira F
KD
Kiel DP
TJ
Tobias JH
GC
Gregson CL
HN
Harvey NC
GE
Grundberg E
GD
Goltzman D
AD
Adams DJ
LC
Lelliott CJ
HD
Hinds DA
AC
Ackert-Bicknell CL
HY
Hsu YH
MM
Maurano MT
CP
Croucher PI
WG
Williams GR
BJ
Bassett JHD
ED
Evans DM
RJ
Richards JB
Chapter II

Abstract

Summary of the research findings

Osteoporosis is a common aging-related disease diagnosed primarily using bone mineral density (BMD). We assessed genetic determinants of BMD as estimated by heel quantitative ultrasound in 426,824 individuals, identifying 518 genome-wide significant loci (301 novel), explaining 20% of its variance. We identified 13 bone fracture loci, all associated with estimated BMD (eBMD), in ~1.2 million individuals. We then identified target genes enriched for genes known to influence bone density and strength (maximum odds ratio (OR) = 58, P = 1 × 10-75) from cell-specific features, including chromatin conformation and accessible chromatin sites. We next performed rapid-throughput skeletal phenotyping of 126 knockout mice with disruptions in predicted target genes and found an increased abnormal skeletal phenotype frequency compared to 526 unselected lines (P < 0.0001). In-depth analysis of one gene, DAAM2, showed a disproportionate decrease in bone strength relative to mineralization. This genetic atlas provides evidence linking associated SNPs to causal genes, offers new insight into osteoporosis pathophysiology, and highlights opportunities for drug development.

426,824 British ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

426824
Total Participants
GWAS
Study Type
Yes
Replicated
367,900 European ancestry cases, 363,919 European ancestry controls
Replication Participants
European
Ancestry
U.K.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

Important Disclaimer: This review has been performed semi-automatically and is provided for informational purposes only. While we strive for accuracy, this analysis may contain errors, omissions, or misinterpretations of the original research. DNA Genics disclaims all liability for any inaccuracies, errors, or consequences arising from the use of this information. Users should independently verify all information and consult original research publications before making any decisions based on this content. This analysis is not intended as a substitute for professional scientific review or medical advice.

Analysis In Progress

Our analysis of this publication is currently being prepared. Please check back soon for comprehensive insights into the health and genetic findings discussed in this research.