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GWAS Study

Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer's disease risk.

Jansen IE, Savage JE, Watanabe K et al.

30617256 PubMed ID
GWAS Study Type
79145 Participants
410 Views
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

JI
Jansen IE
SJ
Savage JE
WK
Watanabe K
BJ
Bryois J
WD
Williams DM
SS
Steinberg S
SJ
Sealock J
KI
Karlsson IK
HS
Hägg S
AL
Athanasiu L
VN
Voyle N
PP
Proitsi P
WA
Witoelar A
SS
Stringer S
AD
Aarsland D
AI
Almdahl IS
AF
Andersen F
BS
Bergh S
BF
Bettella F
BS
Bjornsson S
BA
Brækhus A
BG
Bråthen G
DL
de Leeuw C
DR
Desikan RS
DS
Djurovic S
DL
Dumitrescu L
FT
Fladby T
HT
Hohman TJ
JP
Jonsson PV
KS
Kiddle SJ
RA
Rongve A
SI
Saltvedt I
SS
Sando SB
SG
Selbæk G
SM
Shoai M
SN
Skene NG
SJ
Snaedal J
SE
Stordal E
UI
Ulstein ID
WY
Wang Y
WL
White LR
HJ
Hardy J
HJ
Hjerling-Leffler J
SP
Sullivan PF
VD
van der Flier WM
DR
Dobson R
DL
Davis LK
SH
Stefansson H
SK
Stefansson K
PN
Pedersen NL
RS
Ripke S
AO
Andreassen OA
PD
Posthuma D
Chapter II

Abstract

Summary of the research findings

Alzheimer's disease (AD) is highly heritable and recent studies have identified over 20 disease-associated genomic loci. Yet these only explain a small proportion of the genetic variance, indicating that undiscovered loci remain. Here, we performed a large genome-wide association study of clinically diagnosed AD and AD-by-proxy (71,880 cases, 383,378 controls). AD-by-proxy, based on parental diagnoses, showed strong genetic correlation with AD (rg = 0.81). Meta-analysis identified 29 risk loci, implicating 215 potential causative genes. Associated genes are strongly expressed in immune-related tissues and cell types (spleen, liver, and microglia). Gene-set analyses indicate biological mechanisms involved in lipid-related processes and degradation of amyloid precursor proteins. We show strong genetic correlations with multiple health-related outcomes, and Mendelian randomization results suggest a protective effect of cognitive ability on AD risk. These results are a step forward in identifying the genetic factors that contribute to AD risk and add novel insights into the neurobiology of AD.

24,087 European ancestry cases, 55,058 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

79145
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
U.S., Norway, Sweden, U.K.
Recruitment Country
Chapter IV

AI-Generated Summary

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