Fardo David W, Gibbons Laura E, Mukherjee Shubhabrata, Glymour M Maria, McCormick Wayne, McCurry Susan M, Bowen James D, Larson Eric B, Crane Paul K
Department of Biostatistics and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Department of Medicine, University of Washington, Seattle, WA, USA.
Alzheimers Dement. 2017 Aug;13(8):933-939. doi: 10.1016/j.jalz.2017.01.012. Epub 2017 Feb 21.
Findings for genetic correlates of late-onset Alzheimer's disease (LOAD) in studies that rely solely on clinic visits may differ from those with capacity to follow participants unable to attend clinic visits.
We evaluated previously identified LOAD-risk single nucleotide variants in the prospective Adult Changes in Thought study, comparing hazard ratios (HRs) estimated using the full data set of both in-home and clinic visits (n = 1697) to HRs estimated using only data that were obtained from clinic visits (n = 1308). Models were adjusted for age, sex, principal components to account for ancestry, and additional health indicators.
LOAD associations nominally differed for 4 of 21 variants; CR1 and APOE variants were significant after Bonferroni correction.
Estimates of genetic associations may differ for studies limited to clinic-only designs. Home visit capacity should be explored as a possible source of heterogeneity and potential bias in genetic studies.
在仅依赖门诊就诊的研究中,晚发性阿尔茨海默病(LOAD)的遗传相关性研究结果可能与那些有能力跟踪无法前往门诊就诊参与者的研究结果有所不同。
我们在前瞻性的“成人思维变化”研究中评估了先前确定的LOAD风险单核苷酸变异,将使用家庭访视和门诊就诊的完整数据集估计的风险比(HRs)(n = 1697)与仅使用门诊就诊获得的数据估计的HRs(n = 1308)进行比较。模型针对年龄、性别、用于解释祖先的主成分以及其他健康指标进行了调整。
21个变异中的4个变异的LOAD关联名义上有所不同;CR1和APOE变异在Bonferroni校正后具有显著性。
对于仅限于门诊设计的研究,遗传关联的估计可能会有所不同。家庭访视能力应作为遗传研究中异质性和潜在偏差的一个可能来源进行探索。