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SUCLG2 identified as both a determinator of CSF Aβ1-42 levels and an attenuator of cognitive decline in Alzheimer's disease.

Ramirez A, van der Flier WM, Herold C et al.

25027320 PubMed ID
GWAS Study Type
878 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

RA
Ramirez A
VD
van der Flier WM
HC
Herold C
RD
Ramonet D
HS
Heilmann S
LP
Lewczuk P
PJ
Popp J
LA
Lacour A
DD
Drichel D
LE
Louwersheimer E
KM
Kummer MP
CC
Cruchaga C
HP
Hoffmann P
TC
Teunissen C
HH
Holstege H
KJ
Kornhuber J
PO
Peters O
NA
Naj AC
CV
Chouraki V
BC
Bellenguez C
GA
Gerrish A
HR
Heun R
FL
Frölich L
HM
Hüll M
BL
Buscemi L
HS
Herms S
KH
Kölsch H
SP
Scheltens P
BM
Breteler MM
RE
Rüther E
WJ
Wiltfang J
GA
Goate A
JF
Jessen F
MW
Maier W
HM
Heneka MT
BT
Becker T
NM
Nöthen MM
Chapter II

Abstract

Summary of the research findings

Cerebrospinal fluid amyloid-beta 1-42 (Aβ1-42) and phosphorylated Tau at position 181 (pTau181) are biomarkers of Alzheimer's disease (AD). We performed an analysis and meta-analysis of genome-wide association study data on Aβ1-42 and pTau181 in AD dementia patients followed by independent replication. An association was found between Aβ1-42 level and a single-nucleotide polymorphism in SUCLG2 (rs62256378) (P = 2.5×10(-12)). An interaction between APOE genotype and rs62256378 was detected (P = 9.5 × 10(-5)), with the strongest effect being observed in APOE-ε4 noncarriers. Clinically, rs62256378 was associated with rate of cognitive decline in AD dementia patients (P = 3.1 × 10(-3)). Functional microglia experiments showed that SUCLG2 was involved in clearance of Aβ1-42.

363 European ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

878
Total Participants
GWAS
Study Type
Yes
Replicated
515 individuals
Replication Participants
European
Ancestry
U.S., Canada, Germany, Netherlands
Recruitment Country
Chapter IV

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