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Article type: Short Communication
Authors: Pandey, Janardan P.a; * | Namboodiri, Aryan M.a | Nietert, Paul J.b | Barnes, Lisa L.c | Bennett, David A.c
Affiliations: [a] Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA | [b] Department of Public Health Sciences, Medical University of South Carolina, Charleston, SC, USA | [c] Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL, USA
Correspondence: [*] Correspondence to: Dr. J.P. Pandey, Department of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29425-2230, USA. Tel.: +1 843 792 4360; Fax: +1 843 792 4882; E-mail: pandeyj@musc.edu.
Abstract: We investigated whether FCGRIIB (rs1050501 C/T) and PILRA (rs1859788 A/G) genotypes contributed to the development of Alzheimer’s disease (AD). We genotyped 209 African American (AA) and 638 European American (EA) participants for the FCGRIIB and PILRA alleles. In the AA cohort, subjects homozygous for the C allele of FCGRIIB were more than 4 times as likely to develop AD as those homozygous for the alternative T allele. This SNP also interacted with PILRA: participants who were the carriers of the FCGRIIB C allele and PILRA A allele were 3 times as likely to develop AD as those who lacked these alleles.
Keywords: Amyloid-β, FCGRIIB, neurotoxicity, PILRA
DOI: 10.3233/JAD-215174
Journal: Journal of Alzheimer's Disease, vol. 84, no. 3, pp. 965-968, 2021
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