BACKGROUND/AIM: HLA-A is a locus of the major histocompatibility complex situated on chromosome 6p21.3. Several genome-wide linkage analyses suggested that a putative locus predisposition for Alzheimer's disease (AD) is found on chromosome 6p21. In this study, we investigated the association between HLA-A alleles and AD in a Chinese community. METHODS: Fine genotyping of 160 Chinese AD and 167 age-matched nondemented subjects was performed for the first time by sequence-based typing of the HLA-A locus. RESULTS: We found that HLA-A2 carriers (including prevalent alleles, 0201, 0203 and 0207) were more prevalent in the AD group; the frequency of HLA-A2 was increased in AD patients versus controls, but the difference was not significant after Bonferroni correction for the number of alleles tested (p = 0.075). A gene-gene interaction was observed between ApoE and HLA-A, the presence of HLA-A24 (particularly the prevalent allele 2402) might act as another independent risk factor of developing AD for subjects not carrying the ApoE epsilon4 allele (relative risk = 2.98, 95% CI = 1.14-8.24). Carriers of HLA-A2 had an earlier onset of AD by 2.4 years (p = 0.030) and HLA-A2 interacted with ApoE epsilon4 in modulating the age at onset in AD. CONCLUSIONS: This study suggested that HLA-A may be involved in the pathogenesis of AD. Copyright 2008 S. Karger AG, Basel.
BACKGROUND/AIM: HLA-A is a locus of the major histocompatibility complex situated on chromosome 6p21.3. Several genome-wide linkage analyses suggested that a putative locus predisposition for Alzheimer's disease (AD) is found on chromosome 6p21. In this study, we investigated the association between HLA-A alleles and AD in a Chinese community. METHODS: Fine genotyping of 160 Chinese AD and 167 age-matched nondemented subjects was performed for the first time by sequence-based typing of the HLA-A locus. RESULTS: We found that HLA-A2 carriers (including prevalent alleles, 0201, 0203 and 0207) were more prevalent in the AD group; the frequency of HLA-A2 was increased in ADpatients versus controls, but the difference was not significant after Bonferroni correction for the number of alleles tested (p = 0.075). A gene-gene interaction was observed between ApoE and HLA-A, the presence of HLA-A24 (particularly the prevalent allele 2402) might act as another independent risk factor of developing AD for subjects not carrying the ApoE epsilon4 allele (relative risk = 2.98, 95% CI = 1.14-8.24). Carriers of HLA-A2 had an earlier onset of AD by 2.4 years (p = 0.030) and HLA-A2 interacted with ApoE epsilon4 in modulating the age at onset in AD. CONCLUSIONS: This study suggested that HLA-A may be involved in the pathogenesis of AD. Copyright 2008 S. Karger AG, Basel.
Authors: Shanker Swaminathan; Li Shen; Sungeun Kim; Mark Inlow; John D West; Kelley M Faber; Tatiana Foroud; Richard Mayeux; Andrew J Saykin Journal: Curr Alzheimer Res Date: 2012-09 Impact factor: 3.498
Authors: Shanker Swaminathan; Matthew J Huentelman; Jason J Corneveaux; Amanda J Myers; Kelley M Faber; Tatiana Foroud; Richard Mayeux; Li Shen; Sungeun Kim; Mari Turk; John Hardy; Eric M Reiman; Andrew J Saykin Journal: PLoS One Date: 2012-12-05 Impact factor: 3.240
Authors: Maciej J Lazarczyk; Julia E Kemmler; Brett A Eyford; Jennifer A Short; Merina Varghese; Allison Sowa; Daniel R Dickstein; Frank J Yuk; Rishi Puri; Kaan E Biron; Marcel Leist; Wilfred A Jefferies; Dara L Dickstein Journal: Sci Rep Date: 2016-05-27 Impact factor: 4.379