SUCLG2 identified as both a determinator of CSF Aβ1-42 levels and an attenuator of cognitive decline in Alzheimer's disease.
Détails
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Accès restreint UNIL
Etat: Public
Version: de l'auteur⸱e
Accès restreint UNIL
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_05087FA7722D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
SUCLG2 identified as both a determinator of CSF Aβ1-42 levels and an attenuator of cognitive decline in Alzheimer's disease.
Périodique
Human Molecular Genetics
Collaborateur⸱rice⸱s
International Genomics of Alzheimer's Project (IGAP), Alzheimer's Disease Neuroimaging Initiative (ADNI)
ISSN
1460-2083 (Electronic)
ISSN-L
0964-6906
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
23
Numéro
24
Pages
6644-6658
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
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.
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/07/2014 18:41
Dernière modification de la notice
28/09/2019 6:08