The search for novel risk factors and genetic modifiers for Alzheimer disease relies on the access to accurate and deeply phenotyped datasets. The Memory and Aging Project (MAP) at the Knight-ADRC (Washington University in St. Louis) collects cognitive data, CSF and imaging longitudinally. This clinical information combined with deep molecular phenotyping (i.e. genetic, proteomics, transcriptomics, metabolomics and lipidomics among others) will lead to the identification of novel genetic modifiers, protective variants, molecular biomarkers and the novel targets. Participants were recruited by the Knight-ADRC at Washington University in St. Louis (MO). Knight-ADRC participants have to be at least 65 years old and have no memory problems or mild dementia at the time of enrollment.
The cohort consists of individuals who are non-Hispanic white from North America (95%) or African American (5%). Individuals carrying known mutations in the Mendelian genes for AD (APP, PSEN1, PSEN2) or Frontotemporal Dementia (GRN, MAPT, C9ORF72) were excluded. AD definition is based on a combination of both clinical and pathological information if available. Pathologic diagnosis will overrule clinical diagnosis. Autopsy information is provided if available, but is not a requirement for enrollment.
Knight ADRC Datasets Available in DSS
The datasets listed here are available for request through NIAGADS DSS.
Knight ADRC Datasets Available in Archive NIAGADS
The datasets listed here are currently available for request through the NIAGADS archive website. All datasets are in the process of being moved over to DSS.
| Dataset | Name | Type | Cases/Controls | Total Subjects |
|---|---|---|---|---|
| NG00030 | WashU1 GWAS | GWAS Imputation | 208 / 350 | 678 |
| NG00035 | GWAS of CSF tau levels identifies risk variants for AD | GWAS Imputation | NA | 1934 |
| NG00049 | CSF Summary Statistics- Cruchaga et al. (2013) | Summary Statistics | NA | NA |
| NG00050 | GWAS of CLU, A potential endophenotype for Alzheimer’s disease | GWAS Imputation | NA | 673 |
| NG00051 | SORL1 coding variants and risk for AD | Targeted Genotyping Targeted Sequencing | sEOAD- 212/167 sLOAD- 134/266 fLOAD- 866/324 | sEOAD- 379 sLOAD- 400 fLOAD- 1190 |
| NG00052 | CLU, A potential endophenotype for AD: Summary Statistics- Deming et al. (2016) | Summary Statistics | NA | NA |
| NG00055 | CSF Aβ/ptau Summary Statistics – Deming Y et al. (2017) | Summary Statistics | NA | NA |
| NG00083 | Circular RNAs in Alzheimer Disease Brains – RNA-seq Data | Summary Statistics/RNA-Seq | NA | NA |
| NG00085 | ExomeChip – WashU | GWAS | 519 / 349 | 868 |
| NG00087 | WashU2 GWAS | GWAS Imputation | 38 / 94 | 235 |
| NG00089 | CSF TREM2 Summary Statistics | Summary Statistics | NA | NA |
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.