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The identification of genetic risk factors for Alzheimer’s Disease (AD) provides additional to support that multiple pathways contribute to its onset and progression. However, the metabolomic and lipidomic profiles altered among carriers of distinct genetic risk factors is not fully understood. The study of the metabolome can provide a direct image of dysregulated patterns in an organism, providing information on direct targets for therapeutic treatments. High-throughput metabolomic and lipidomic data for 880 analytes was generated from parietal brain tissue from 423 AD donors and neuropathology free controls using the Metabolon Precision Metabolomics platform.
Sample Summary per Data Type
|Sample Set||Accession||Data Type||Number of Samples|
|Harari Metabolomics||fsa000017||NG00113.v1||Metabolomics Data, Phenotypes, etc.|
View the File Manifest for a full list of files released in this dataset.
High-throughput metabolomic and lipidomic data for 880 analytes was generated from parietal brain tissue from 423 AD donors and neuropathology free controls using the Metabolon Precision Metabolomics platform.
|Sample Set||Accession Number||Number of Subjects|
|Consent Level||Number of Subjects|
Visit the Data Use Limitations page for definitions of the consent levels above.
Acknowledgment statement for any data distributed by NIAGADS:
Data for this study were prepared, archived, and distributed by the National Institute on Aging Alzheimer’s Disease Data Storage Site (NIAGADS) at the University of Pennsylvania (U24-AG041689), funded by the National Institute on Aging.
Use the study-specific acknowledgement statements below (as applicable):
For investigators using any data from this dataset:
Please cite/reference the use of NIAGADS data by including the accession NG00113.
For investigators using KnightADRC (sa000008) data:
This work was supported by grants from the National Institutes of Health (R01AG044546, P01AG003991, RF1AG053303, R01AG058501, U01AG058922, RF1AG058501 and R01AG057777). The recruitment and clinical characterization of research participants at Washington University were supported by NIH P50 AG05681, P01 AG03991, and P01 AG026276. This work was supported by access to equipment made possible by the Hope Center for Neurological Disorders, and the Departments of Neurology and Psychiatry at Washington University School of Medicine.
We thank the contributors who collected samples used in this study, as well as patients and their families, whose help and participation made this work possible. This work was supported by access to equipment made possible by the Hope Center for Neurological Disorders, and the Departments of Neurology and Psychiatry at Washington University School of Medicine