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Novel Alzheimer Disease Risk Loci and Pathways in African American Individuals Using the African Genome Resources Panel
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JAMA Neurology | October 19, 2020 | Volume: 78 | Issue: 1 | Pages: 102
Two novel loci, COBL and SLC10A2, for Alzheimer's disease in African Americans
Chung, Jaeyoon , Jun, Gyungah , Kriegel, Joshua, Bourlas, Alexandra P., Sherva, Richard , Barnes, Lisa L. , Bennett, David A. , Buxbaum, Joseph D. , Byrd, Goldie S. , Crane, Paul K. , Ertekin‐Taner, Nilüfer , Evans, Denis A., Fallin, M. Daniele , Goate, Alison , Graff‐Radford, Neill R. , Hall, Kathleen, Kukull, Walter A. , Larson, Eric B., Haines, Jonathan L. , Mayeux, Richard , Pericak‐Vance, Margaret A. , Schellenberg, Gerard D. , Lunetta, Kathryn L. , Farrer, Lindsay A. , Bennett, David A. , Mez, Jesse , Sherva, Richard , Logue, Mark W. , Foroud, Tatiana , Kamboh, M. Ilyas , Manly, Jennifer J. , Goate, Alison M , Barnes, Lisa L
Alzheimer's & Dementia | October 20, 2016 | Volume: 13 | Issue: 2 | Pages: 119-129
AbstractIntroductionAfrican Americans' (AAs) late‐onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power.MethodsWe conducted a genome‐wide association study (GWAS) in AAs employing informed conditioning in 1825 LOAD cases and 3784 cognitively normal controls. We derived a posterior liability conditioned on age, sex, diabetes status, current smoking status, educational attainment, and affection status, with parameters informed by external prevalence information. We assessed association between the posterior liability and a genome‐wide set of single‐nucleotide polymorphisms (SNPs), controlling for APOE and ABCA7, identified previously in a LOAD GWAS of AAs.ResultsTwo SNPs at novel loci, rs112404845 (P = 3.8 × 10−8), upstream of COBL, and rs16961023 (P = 4.6 × 10−8), downstream of SLC10A2, obtained genome‐wide significant evidence of association with the posterior liability.DiscussionAn informed conditioning approach can detect LOAD genetic associations in AAs not identified by traditional GWAS.
Association of Long Runs of Homozygosity With Alzheimer Disease Among African American Individuals
Reitz, Christiane , Cheng, Rong , Jun, Gyungah , Sato, Christine , Rajbhandary, Ruchita, Wang, Li San, Lin, Chiao‐Feng , Larson, Eric B., Graff‐Radford, Neill R. , Evans, Denis A., Jager, Philip L. De , Crane, Paul K. , Buxbaum, Joseph D. , Murrell, Jill R. , Raj, Towfique , Ertekin‐Taner, Nilüfer , Logue, Mark, Baldwin, Clinton T., Green, Robert C. , Barnes, Lisa L. , Cantwell, Laura B., Fallin, M. Daniele , Go, Rodney C.P., Griffith, Patrick , Obisesan, Thomas O. , Bennett, David A. , Hendrie, Hugh C. , Hall, Kathleen, Byrd, Goldie S. , Kukull, Walter A. , Foroud, Tatiana M., Haines, Jonathan L. , Farrer, Lindsay A. , Pericak‐Vance, Margaret A. , Schellenberg, Gerard D. , Mayeux, Richard , Morris, John C. , Leverenz, James B. , DeKosky, Steven T. , Håkonarson, Håkon , Jarvik, Gail P. , Albin, Roger L. , Lyketsos, Constantine G. , Jicha, Gregory A. , Demirci, F. Yesim , Burke, James R. , Cao, Chuanhai , Carroll, Steven L. , Cribbs, David H. , Mack, Wendy J. , Sonnen, Joshua A. , Bennett, David A. , Ghani, Mahdi , Vardarajan, Badri Narayan , Naj, Adam Christian , Valladares, Otto , Manly, Jennifer J. , Lunetta, Kathryn L. , Kamboh, M. Ilyas , López, Oscar L. , Goate, Alison , Lee, Joseph H. , George‐Hyslop, Peter St , Rogaeva, Ekaterina A. , Hakonarson, Hakon , Leverenz, James B , Jarvik, Gail P , Morris, John C , Jicha, Gregory A , Sonnen, Joshua , Barnes, Lisa L
JAMA Neurology | September 14, 2015 | Volume: 72 | Issue: 11 | Pages: 1313
Global and local ancestry in African‐Americans: Implications for Alzheimer's disease risk
Hohman, Timothy J. , Bailey, Jessica N. Cooke , Reitz, Christiane , Jun, Gyungah , Beecham, Gary W. , Carney, Regina M., Vance, Jeffery M. , Rajbhandary, Ruchita, Lin, Chiao‐Feng , Larson, Eric B., Graff‐Radford, Neill R. , Evans, Denis A., Jager, Philip L. De , Crane, Paul K. , Buxbaum, Joseph D. , Murrell, Jill R. , Raj, Towfique , Ertekin‐Taner, Nilüfer , Baldwin, Clinton T., Green, Robert C. , Barnes, Lisa L. , Cantwell, Laura B., Fallin, M. Daniele , Go, Rodney C.P., Griffith, Patrick , Obisesan, Thomas O. , Lunetta, Kathryn L. , Kamboh, M. Ilyas , Bennett, David A. , Hardy, John , Hendrie, Hugh C. , Hall, Kathleen, Goate, Alison , Lang, Rosalyn, Byrd, Goldie S. , Kukull, Walter A. , Farrer, Lindsay A. , Martin, Eden R. , Pericak‐Vance, Margaret A. , Schellenberg, Gerard D. , Mayeux, Richard , Haines, Jonathan L. , Thornton‐Wells, Tricia A., Carroll, Steven L. , Bennett, David A. , Naj, Adam Christian , Liu, Zhi , Cuccaro, Michael L. , Vardarajan, Badri Narayan , Wang, Weixin , Valladares, Otto , Logue, Mark W. , Manly, Jennifer J. , López, Oscar L. , Foroud, Tatiana , Seto, Mabel , Hardy, John , Goate, Alison M , Barnes, Lisa L
Alzheimer's & Dementia | June 16, 2015 | Volume: 12 | Issue: 3 | Pages: 233-243
AbstractIntroductionAfrican‐American (AA) individuals have a higher risk for late‐onset Alzheimer's disease (LOAD) than Americans of primarily European ancestry (EA). Recently, the largest genome‐wide association study in AAs to date confirmed that six of the Alzheimer's disease (AD)‐related genetic variants originally discovered in EA cohorts are also risk variants in AA; however, the risk attributable to many of the loci (e.g., APOE, ABCA7) differed substantially from previous studies in EA. There likely are risk variants of higher frequency in AAs that have not been discovered.MethodsWe performed a comprehensive analysis of genetically determined local and global ancestry in AAs with regard to LOAD status.ResultsCompared to controls, LOAD cases showed higher levels of African ancestry, both globally and at several LOAD relevant loci, which explained risk for AD beyond global differences.DiscussionExploratory post hoc analyses highlight regions with greatest differences in ancestry as potential candidate regions for future genetic analyses.
Two rare AKAP9 variants are associated with Alzheimer's disease in African Americans
Schu, Matthew , Farrell, John J. , Bennett, David A. , Buxbaum, Joseph D. , Byrd, Goldie S. , Ertekin‐Taner, Nilüfer , Evans, Denis A., Goate, Alison , Graff‐Radford, Neill R. , Kamboh, M. Ilyas , Kukull, Walter A. , Haines, Jonathan L. , Mayeux, Richard , Pericak‐Vance, Margaret A. , Schellenberg, Gerard D. , Baldwin, Clinton T., Fallin, M. Daniele , Farrer, Lindsay A. , Tsuang, Debby W. , Carroll, Steven L. , Logue, Mark W. , Vardarajan, Badri Narayan , Foroud, Tatiana , Manly, Jennifer J. , Lunetta, Kathryn L. , Bennett, David A. , Goate, Alison M
Alzheimer's & Dementia | August 26, 2014 | Volume: 10 | Issue: 6 | Pages: 609
AbstractBackgroundLess is known about the genetic basis of Alzheimer's disease (AD) in African Americans (AAs) than in non‐Hispanic whites.MethodsWhole exome sequencing (WES) was performed on seven AA AD cases. Disease association with potentially AD‐related variants from WES was assessed in an AA discovery cohort of 422 cases and 394 controls. Replication was sought in an AA sample of 1037 cases and 1869 controls from the Alzheimer Disease Genetics Consortium (ADGC).ResultsForty‐four single nucleotide polymorphisms (SNPs) from WES passed filtering criteria and were successfully genotyped. Nominally significant (P < .05) association to AD was observed with two African‐descent specific AKAP9 SNPs in tight linkage disequilibrium: rs144662445 (P = .014) and rs149979685 (P = .037). These associations were replicated in the ADGC sample (rs144662445: P = .0022, odds ratio [OR] = 2.75; rs149979685: P = .0022, OR = 3.61).ConclusionsBecause AKAP9 was not previously linked to AD risk, this study indicates a potential new disease mechanism.