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Molecular genetic evidence for overlap between general cognitive ability and risk for schizophrenia: a report from the Cognitive Genomics consorTium (COGENT).

Lencz T, Knowles E, Davies G et al.

24342994 PubMed ID
GWAS Study Type
4896 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

LT
Lencz T
KE
Knowles E
DG
Davies G
GS
Guha S
LD
Liewald DC
SJ
Starr JM
DS
Djurovic S
MI
Melle I
SK
Sundet K
CA
Christoforou A
RI
Reinvang I
MS
Mukherjee S
DP
DeRosse P
LA
Lundervold A
SV
Steen VM
JM
John M
ET
Espeseth T
RK
Räikkönen K
WE
Widen E
PA
Palotie A
EJ
Eriksson JG
GI
Giegling I
KB
Konte B
IM
Ikeda M
RP
Roussos P
GS
Giakoumaki S
BK
Burdick KE
PA
Payton A
OW
Ollier W
HM
Horan M
DG
Donohoe G
MD
Morris D
CA
Corvin A
GM
Gill M
PN
Pendleton N
IN
Iwata N
DA
Darvasi A
BP
Bitsios P
RD
Rujescu D
LJ
Lahti J
HS
Hellard SL
KM
Keller MC
AO
Andreassen OA
DI
Deary IJ
GD
Glahn DC
MA
Malhotra AK
Chapter II

Abstract

Summary of the research findings

It has long been recognized that generalized deficits in cognitive ability represent a core component of schizophrenia (SCZ), evident before full illness onset and independent of medication. The possibility of genetic overlap between risk for SCZ and cognitive phenotypes has been suggested by the presence of cognitive deficits in first-degree relatives of patients with SCZ; however, until recently, molecular genetic approaches to test this overlap have been lacking. Within the last few years, large-scale genome-wide association studies (GWAS) of SCZ have demonstrated that a substantial proportion of the heritability of the disorder is explained by a polygenic component consisting of many common single-nucleotide polymorphisms (SNPs) of extremely small effect. Similar results have been reported in GWAS of general cognitive ability. The primary aim of the present study is to provide the first molecular genetic test of the classic endophenotype hypothesis, which states that alleles associated with reduced cognitive ability should also serve to increase risk for SCZ. We tested the endophenotype hypothesis by applying polygenic SNP scores derived from a large-scale cognitive GWAS meta-analysis (~5000 individuals from nine nonclinical cohorts comprising the Cognitive Genomics consorTium (COGENT)) to four SCZ case-control cohorts. As predicted, cases had significantly lower cognitive polygenic scores compared to controls. In parallel, polygenic risk scores for SCZ were associated with lower general cognitive ability. In addition, using our large cognitive meta-analytic data set, we identified nominally significant cognitive associations for several SNPs that have previously been robustly associated with SCZ susceptibility. Results provide molecular confirmation of the genetic overlap between SCZ and general cognitive ability, and may provide additional insight into pathophysiology of the disorder.

4,896 European ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

4896
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
U.S., Germany, Finland, Norway, U.K., Greece
Recruitment Country
Chapter IV

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