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Description

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder with many biological processes, and molecular changes. The etiology of AD is complex and not specific to a single genetic factor. Epigenetic changes could help explain the missing heritability not capture in GWAS chips and determine functional variants in genome-wide significant loci. DNA methylation data from 431 parietal lobe of AD and neuropath-free controls was generated from the Knight-ADRC. The Illumina Infinium MethylationEPIC interrogates the methylation over 850,000 CpG and non-CpG sites, open chromatin, enhancers, DNase hypersensitive sites and promoters.

Sample Summary per Data Type

Sample SetAccessionData TypeNumber of Samples
Harari Methylation snd10025Methylation446

Available Filesets

NameAccessionLatest ReleaseDescription
Harari Methylationfsa000018NG00114.v1Methylation Data, Phenotypes, etc.

View the File Manifest for a full list of files released in this dataset.

DNA methylation data from 431 parietal lobe of AD and neuropath-free controls was generated from the Knight-ADRC. The Illumina Infinium MethylationEPIC interrogates the methylation over 850,000 CpG and non-CpG sites, open chromatin, enhancers, DNase hypersensitive sites and promoters.

Sample SetAccession NumberNumber of Subjects
Harari Methylation snd10025431
Consent LevelNumber of Subjects
DS-ADRD-IRB-PUB431

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 NG00114.

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