Risk of Alzheimer's disease and genetically predicted levels of 1400 plasma metabolites: a Mendelian randomization study.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
30 10 2024
Historique:
received: 29 03 2024
accepted: 28 10 2024
medline: 31 10 2024
pubmed: 31 10 2024
entrez: 31 10 2024
Statut: epublish

Résumé

Alzheimer's disease (AD) is a metabolic disorder. Discovering the metabolic products involved in the development of AD may help not only in the early detection and prevention of AD but also in understanding its pathogenesis and treatment. This study investigated the causal association between the latest large-scale plasma metabolites (1091 metabolites and 309 metabolite ratios) and AD. Through the application of Mendelian randomization analysis methods such as inverse-variance weighted (IVW), MR-Egger, and weighted median models, 66 metabolites and metabolite ratios were identified as potentially having a causal association with AD, with 13 showing significant causal associations. During the replication validation phase, six metabolites and metabolite ratios were confirmed for their roles in AD: N-lactoyl tyrosine, argininate, and the adenosine 5'-monophosphate to flavin adenine dinucleotide ratio were found to exhibit protective effects against AD. In contrast, ergothioneine, piperine, and 1,7-dimethyluric acid were identified as contributing to an increased risk of AD. Among them, argininate showed a significant effect against AD. Replication and sensitivity analyses confirmed the robustness of these findings. Metabolic pathway analysis linked "Vitamin B6 metabolism" to AD risk. No genetic correlations were found, but colocalization analysis indicated potential AD risk elevation through top SNPs in APOE and PSEN2 genes. This provides novel insights into AD's etiology from a metabolomic viewpoint, suggesting both protective and risk metabolites.

Identifiants

pubmed: 39478193
doi: 10.1038/s41598-024-77921-6
pii: 10.1038/s41598-024-77921-6
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

26078

Subventions

Organisme : Key Research and Development Project of the Jilin Provincial Department of Science and Technology
ID : 20220203153SF
Organisme : Qihuang scholar in the National Support Program for Leading Talents of Traditional Chinese Medicine
ID : [2018] No. 12
Organisme : Key Project of National Natural Science Foundation of China
ID : 82130119

Informations de copyright

© 2024. The Author(s).

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Auteurs

Di Cao (D)

Hubei University of Chinese Medicine, Wuhan, 430070, Hubei, China.
Engineering Research Center of TCM Protection Technology and New Product Development for the Elderly Brain Health, Ministry of Education, Wuhan, 430070, Hubei, China.
Hubei Shizhen Laboratory, Wuhan, 430070, Hubei, China.

Yini Zhang (Y)

Hubei University of Chinese Medicine, Wuhan, 430070, Hubei, China.
Engineering Research Center of TCM Protection Technology and New Product Development for the Elderly Brain Health, Ministry of Education, Wuhan, 430070, Hubei, China.
Hubei Shizhen Laboratory, Wuhan, 430070, Hubei, China.

Shaobo Zhang (S)

Changchun University of Chinese Medicine, Changchun, 130000, Jilin, China.

Jun Li (J)

Department of Rehabilitation Medicine, the First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.

Qiguang Yang (Q)

The Second Affiliated Hospital of Changchun University of Chinese Medicine (Changchun Hospital of Chinese Medicine), Changchun, 130000, Jilin, China.

Ping Wang (P)

Hubei University of Chinese Medicine, Wuhan, 430070, Hubei, China. pwang54@hbucm.edu.cn.
Engineering Research Center of TCM Protection Technology and New Product Development for the Elderly Brain Health, Ministry of Education, Wuhan, 430070, Hubei, China. pwang54@hbucm.edu.cn.
Hubei Shizhen Laboratory, Wuhan, 430070, Hubei, China. pwang54@hbucm.edu.cn.

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