Tejera César Higgins, Ware Erin, Hicken Margaret, Kobayashi Lindsay, Wang Herong, Adkins-Jackson Paris, Blostein Freida, Zawistowski Matthew, Mukherjee Bhramar, Bakulski Kelly
University of Michigan.
Res Sq. 2023 Apr 5:rs.3.rs-2753483. doi: 10.21203/rs.3.rs-2753483/v1.
Exposure to systemic racism is linked to increased dementia burden. To assess systemic inflammation as a potential pathway linking exposure to racism and dementia disparities, we investigated the mediating role of C-reactive protein (CRP), a systemic inflammation marker, and the moderating role of race/ethnicity on racialized disparities in incident dementia.
In the US Health and Retirement Study (n=5,143), serum CRP was measured at baseline (2006, 2008 waves). Incident dementia was classified by cognitive tests over a six-year follow-up. Self-reported racialized categories were a proxy for exposure to the racialization process. We decomposed racialized disparities in dementia incidence (non-Hispanic Black and/or Hispanic vs. non-Hispanic White) into 1) the mediated effect of CRP, 2) the moderated portion attributable to the interaction between racialized group membership and CRP, and 3) the controlled direct effect (other pathways through which racism operates).
The 6-year cumulative incidence of dementia was 15.5%. Among minoritized participants (i.e., non-Hispanic Black and/or Hispanic), high CRP levels (> 75th percentile or 4.57mcg/mL) was associated with 1.27 (95%CI: 1.01,1.59) times greater risk of incident dementia than low CRP (<4.57mcg/mL). Decomposition analysis comparing minoritized versus non-Hispanic White participants showed that the mediating effect of CRP accounted for 2% (95% CI: 0%, 6%) of the racial disparity, while the interaction effect between minoritized group status and high CRP accounted for 12% (95% CI: 2%, 22%) of the disparity. Findings were robust to potential violations of causal mediation assumptions.
Systemic inflammation mediates racialized disparities in incident dementia.
暴露于系统性种族主义与痴呆症负担增加有关。为了评估全身炎症作为连接种族主义暴露和痴呆症差异的潜在途径，我们研究了系统性炎症标志物C反应蛋白（CRP）的中介作用，以及种族/族裔对新发痴呆症种族化差异的调节作用。
在美国健康与退休研究（n = 5143）中，在基线（2006年、2008年波次）测量血清CRP。通过六年随访期间的认知测试对新发痴呆症进行分类。自我报告的种族化类别是暴露于种族化过程的替代指标。我们将痴呆症发病率的种族化差异（非西班牙裔黑人或西班牙裔与非西班牙裔白人）分解为：1）CRP的中介效应；2）归因于种族化群体成员身份与CRP之间相互作用的调节部分；3）受控直接效应（种族主义运作的其他途径）。
痴呆症的6年累积发病率为15.5%。在少数族裔参与者（即非西班牙裔黑人或西班牙裔）中，高CRP水平（>第75百分位数或4.57mcg/mL）与新发痴呆症风险比低CRP（<4.57mcg/mL）高1.27倍（95%CI：1.01，1.59）相关。比较少数族裔与非西班牙裔白人参与者的分解分析表明，CRP的中介效应占种族差异的2%（95%CI：0%，6%），而少数族裔群体状态与高CRP之间的相互作用效应占差异的12%（95%CI：2%，22%）。研究结果对因果中介假设的潜在违反具有稳健性。
全身炎症介导了新发痴呆症的种族化差异。
