Department of Psychiatry and Behavioral Sciences, University of California San Francisco, San Francisco, CA, USA.
Department of Neurology, Mayo Clinic, Jacksonville, FL, USA.
J Alzheimers Dis. 2024;99(2):787-797. doi: 10.3233/JAD-240007.
Plasma amyloid-β (Aβ) has emerged as an important tool to detect risks of Alzheimer's disease and related dementias, although research in diverse populations is lacking.
We compared plasma Aβ42/40 by race with dementia risk over 15 years among Black and White older adults.
In a prospective cohort of 997 dementia-free participants (mean age 74±2.9 years, 55% women, 54% Black), incident dementia was identified based on hospital records, medication, and neurocognitive test over 15 years. Plasma Aβ42/40 was measured at Year 2 and categorized into low, medium, and high tertile. We used linear regression to estimate mean Aβ42/40 by race and race-stratified Cox proportional hazards models to assess the association between Aβ42/40 tertile and dementia risk.
Black participants had a lower age-adjusted mean Aβ 42/40 compared to White participants, primarily among APOE ɛ4 non-carriers (Black: 0.176, White: 0.185, p = 0.035). Among Black participants, lower Aβ 42/40 was associated with increased dementia risk: 33% in low (hazard ratios [HR] = 1.77, 95% confidence interval 1.09-2.88) and 27% in medium tertile (HR = 1.67, 1.01-2.78) compared with 18% in high Aβ 42/40 tertile; Increased risks were attenuated among White participants: 21% in low (HR = 1.43, 0.81-2.53) and 23% in medium tertile (HR = 1.27, 0.68-2.36) compared with 15% in high Aβ 42/40 tertile. The interaction by race was not statistically significant.
Among community-dwelling, non-demented older adults, especially APOE ɛ4 non-carriers, Black individuals had lower plasma Aβ 42/40 and demonstrated a higher dementia risk with low Aβ42/40 compared with White individuals.
血浆淀粉样蛋白-β（Aβ）已成为检测阿尔茨海默病和相关痴呆风险的重要工具，尽管在不同人群中的研究还很缺乏。
我们比较了不同种族的血浆 Aβ42/40 与黑人及白人老年人群中超过 15 年的痴呆风险。
在一项由 997 名无痴呆症的参与者组成的前瞻性队列研究中（平均年龄 74±2.9 岁，55%为女性，54%为黑人），通过 15 年的医院记录、药物和神经认知测试来确定痴呆的发病情况。在第 2 年测量了血浆 Aβ42/40，并将其分为低、中、高三分位数。我们使用线性回归来估计按种族划分的平均 Aβ42/40，并用种族分层的 Cox 比例风险模型来评估 Aβ42/40 三分位数与痴呆风险之间的关系。
与白人参与者相比，黑人参与者的年龄调整后平均 Aβ42/40 较低，主要是在 APOE ɛ4 非携带者中（黑人：0.176，白人：0.185，p=0.035）。在黑人参与者中，较低的 Aβ42/40 与痴呆风险增加有关：低三分位组的风险增加了 33%（风险比 [HR] = 1.77，95%置信区间 1.09-2.88），中三分位组的风险增加了 27%（HR = 1.67，1.01-2.78），而高 Aβ42/40 三分位组的风险增加了 18%；在白人参与者中，风险的增加幅度较小：低三分位组的风险增加了 21%（HR = 1.43，81-2.53），中三分位组的风险增加了 23%（HR = 1.27，68-2.36），而高 Aβ42/40 三分位组的风险增加了 15%。种族之间的交互作用没有统计学意义。
在居住在社区、无痴呆的老年人群中，尤其是 APOE ɛ4 非携带者中，与白人相比，黑人的血浆 Aβ42/40 水平较低，且低 Aβ42/40 水平与较高的痴呆风险相关。
