Genetic and multi-omic resources for Alzheimer disease and related dementia from the Knight Alzheimer Disease Research Center-Reference-Cited by-同舟云学术

Genetic and multi-omic resources for Alzheimer disease and related dementia from the Knight Alzheimer Disease Research Center

Published:2024-07-12 Issue:1 Volume:11 Page:
ISSN:2052-4463
Container-title:Scientific Data
language:en
Short-container-title:Sci Data

Author:

Fernandez Maria Victoria,Liu Menghan,Beric Aleksandra^ORCID,Johnson Matt,Cetin Arda^ORCID,Patel Maulik,Budde John^ORCID,Kohlfeld Pat^ORCID,Bergmann Kristy,Lowery Joseph,Flynn Allison,Brock William,Sanchez Montejo Brenda,Gentsch Jen,Sykora Nicholas,Norton Joanne,Gentsch Jen,Valdez Olga,Gorijala Priyanka,Sanford Jessie,Sun Yichen,Wang Ciyang,Western Dan^ORCID,Timsina Jigyasha,Mangetti Goncalves Tassia,Do Anh N.,Sung Yun Ju,Zhao Guoyan^ORCID,Morris John C.,Moulder Krista,Holtzman David M.^ORCID,Bateman Randall J.^ORCID,Karch Celeste^ORCID,Hassenstab Jason,Xiong Chengjie,Schindler Suzanne E.^ORCID,Balls-Berry Joyce,Benzinger Tammie L. S.,Perrin Richard J.^ORCID,Denny Andrea,Snider B. Joy,Stark Susan L.,Ibanez Laura,Cruchaga Carlos^ORCID

Abstract

AbstractThe Knight-Alzheimer Disease Research Center (Knight-ADRC) at Washington University in St. Louis has pioneered and led worldwide seminal studies that have expanded our clinical, social, pathological, and molecular understanding of Alzheimer Disease. Over more than 40 years, research volunteers have been recruited to participate in cognitive, neuropsychologic, imaging, fluid biomarkers, genomic and multi-omic studies. Tissue and longitudinal data collected to foster, facilitate, and support research on dementia and aging. The Genetics and high throughput -omics core (GHTO) have collected of more than 26,000 biological samples from 6,625 Knight-ADRC participants. Samples available include longitudinal DNA, RNA, non-fasted plasma, cerebrospinal fluid pellets, and peripheral blood mononuclear cells. The GHTO has performed deep molecular profiling (genomic, transcriptomic, epigenomic, proteomic, and metabolomic) from large number of brain (n = 2,117), CSF (n = 2,012) and blood/plasma (n = 8,265) samples with the goal of identifying novel risk and protective variants, identify novel molecular biomarkers and causal and druggable targets. Overall, the resources available at GHTO support the increase of our understanding of Alzheimer Disease.

Funder

U.S. Department of Health & Human Services | NIH | Center for Scientific Review

Publisher

Springer Science and Business Media LLC

Link

https://www.nature.com/articles/s41597-024-03485-9.pdf

Reference85 articles.

1. Nguyen, H. Q. et al. Dementia diagnosis and utilization patterns in a racially diverse population within an integrated health care delivery system. Alzheimers Dement (N Y) 8, e12279, https://doi.org/10.1002/trc2.12279 (2022).

2. LaFerla, F. M. & Oddo, S. Alzheimer’s disease: Abeta, tau and synaptic dysfunction. Trends Mol Med 11, 170–176, https://doi.org/10.1016/j.molmed.2005.02.009 (2005).

3. Ibanez, L., Cruchaga, C. & Fernandez, M. V. Advances in Genetic and Molecular Understanding of Alzheimer’s Disease. Genes 12, https://doi.org/10.3390/genes12081247 (2021).

4. Lin, Y. S., Cheng, C. Y., Liao, Y. C., Hong, C. J. & Fuh, J. L. Mutational analysis in familial Alzheimer’s disease of Han Chinese in Taiwan with a predominant mutation PSEN1 p.Met146Ile. Sci Rep 10, 19769, https://doi.org/10.1038/s41598-020-76794-9 (2020).

5. Bateman, R. J. et al. Autosomal-dominant Alzheimer’s disease: a review and proposal for the prevention of Alzheimer’s disease. Alzheimer’s research & therapy 3, 1, https://doi.org/10.1186/alzrt59 (2011).