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GWAS Study

Multi-ancestry GWAS reveals excitotoxicity associated with outcome after ischaemic stroke.

Ibanez L, Heitsch L, Carrera C et al.

35213696 PubMed ID
GWAS Study Type
5063 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

IL
Ibanez L
HL
Heitsch L
CC
Carrera C
FF
Farias FHG
DA
Del Aguila JL
DR
Dhar R
BJ
Budde J
BK
Bergmann K
BJ
Bradley J
HO
Harari O
PC
Phuah CL
LR
Lemmens R
VO
Viana Oliveira Souza AA
MF
Moniche F
CA
Cabezas-Juan A
AJ
Arenillas JF
KJ
Krupinksi J
CN
Cullell N
TN
Torres-Aguila N
ME
Muiño E
CJ
Cárcel-Márquez J
MJ
Marti-Fabregas J
DR
Delgado-Mederos R
MR
Marin-Bueno R
HA
Hornick A
VC
Vives-Bauza C
NR
Navarro RD
TS
Tur S
JC
Jimenez C
OV
Obach V
ST
Segura T
SG
Serrano-Heras G
CJ
Chung JW
RJ
Roquer J
SC
Soriano-Tarraga C
GE
Giralt-Steinhauer E
MM
Mola-Caminal M
PJ
Pera J
LK
Lapicka-Bodzioch K
DJ
Derbisz J
DA
Davalos A
LE
Lopez-Cancio E
ML
Muñoz L
TT
Tatlisumak T
MC
Molina C
RM
Ribo M
BA
Bustamante A
ST
Sobrino T
CJ
Castillo-Sanchez J
CF
Campos F
RE
Rodriguez-Castro E
AS
Arias-Rivas S
RM
Rodríguez-Yáñez M
HC
Herbosa C
FA
Ford AL
GA
Gutierrez-Romero A
UR
Uribe-Pacheco R
AA
Arauz A
LI
Lopes-Cendes I
LT
Lowenkopf T
BM
Barboza MA
AH
Amini H
SB
Stamova B
AB
Ander BP
SF
Sharp FR
KG
Kim GM
BO
Bang OY
JJ
Jimenez-Conde J
SA
Slowik A
SD
Stribian D
TE
Tsai EA
BL
Burkly LC
MJ
Montaner J
FI
Fernandez-Cadenas I
LJ
Lee JM
CC
Cruchaga C
Chapter II

Abstract

Summary of the research findings

During the first hours after stroke onset, neurological deficits can be highly unstable: some patients rapidly improve, while others deteriorate. This early neurological instability has a major impact on long-term outcome. Here, we aimed to determine the genetic architecture of early neurological instability measured by the difference between the National Institutes of Health Stroke Scale (NIHSS) within 6 h of stroke onset and NIHSS at 24 h. A total of 5876 individuals from seven countries (Spain, Finland, Poland, USA, Costa Rica, Mexico and Korea) were studied using a multi-ancestry meta-analyses. We found that 8.7% of NIHSS at 24 h of variance was explained by common genetic variations, and also that early neurological instability has a different genetic architecture from that of stroke risk. Eight loci (1p21.1, 1q42.2, 2p25.1, 2q31.2, 2q33.3, 5q33.2, 7p21.2 and 13q31.1) were genome-wide significant and explained 1.8% of the variability suggesting that additional variants influence early change in neurological deficits. We used functional genomics and bioinformatic annotation to identify the genes driving the association from each locus. Expression quantitative trait loci mapping and summary data-based Mendelian randomization indicate that ADAM23 (log Bayes factor = 5.41) was driving the association for 2q33.3. Gene-based analyses suggested that GRIA1 (log Bayes factor = 5.19), which is predominantly expressed in the brain, is the gene driving the association for the 5q33.2 locus. These analyses also nominated GNPAT (log Bayes factor = 7.64) ABCB5 (log Bayes factor = 5.97) for the 1p21.1 and 7p21.1 loci. Human brain single-nuclei RNA-sequencing indicates that the gene expression of ADAM23 and GRIA1 is enriched in neurons. ADAM23, a presynaptic protein and GRIA1, a protein subunit of the AMPA receptor, are part of a synaptic protein complex that modulates neuronal excitability. These data provide the first genetic evidence in humans that excitotoxicity may contribute to early neurological instability after acute ischaemic stroke.

5,063 European ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

5063
Total Participants
GWAS
Study Type
No
Replicated
European, African American or Afro-Caribbean, Hispanic or Latin American, East Asian
Ancestry
U.S., Finland, Poland, Spain, Mexico, Costa Rica, Republic of Korea
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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