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St John-Williams, L.* ; MahmoudianDehkordi, S.* ; Arnold, M. ; Massaro, T.* ; Blach, C.* ; Kastenmüller, G. ; Louie, G.* ; Kueider-Paisley, A.* ; Han, X.* ; Baillie, R.* ; Motsinger-Reif, A.A.* ; Rotroff, D.* ; Nho, K.* ; Saykin, A.J.* ; Risacher, S.L.* ; Koal, T.* ; Moseley, M.A.* ; Tenenbaum, J.D.* ; Thompson, J.W.* ; Kaddurah-Daouk, R.* ; Alzheimer Disease Metabolomics Consortium*

Bile acids targeted metabolomics and medication classification data in the ADNI1 and ADNIGO/2 cohorts.

Sci. Data 6:212 (2019)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Alzheimer's disease (AD) is the most common cause of dementia. The mechanism of disease development and progression is not well understood, but increasing evidence suggests multifactorial etiology, with a number of genetic, environmental, and aging-related factors. There is a growing body of evidence that metabolic defects may contribute to this complex disease. To interrogate the relationship between system level metabolites and disease susceptibility and progression, the AD Metabolomics Consortium (ADMC) in partnership with AD Neuroimaging Initiative (ADNI) is creating a comprehensive biochemical database for patients in the ADNI1 cohort. We used the Biocrates Bile Acids platform to evaluate the association of metabolic levels with disease risk and progression. We detail the quantitative metabolomics data generated on the baseline samples from ADNI1 and ADNIGO/2 (370 cognitively normal, 887 mild cognitive impairment, and 305 AD). Similar to our previous reports on ADNI1, we present the tools for data quality control and initial analysis. This data descriptor represents the third in a series of comprehensive metabolomics datasets from the ADMC on the ADNI.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Global Biochemical Approach; Alzheimers-disease; Options
ISSN (print) / ISBN 2052-4463
e-ISSN 2052-4463
Journal Scientific Data
Quellenangaben Volume: 6, Issue: 1, Pages: , Article Number: 212 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Non-patent literature Publications
Reviewing status Peer reviewed