San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA.
Department of Psychiatry, University of California San Diego, La Jolla, CA, USA.
J Alzheimers Dis. 2022;89(2):633-640. doi: 10.3233/JAD-220026.
Studies have demonstrated that both tau and cardiovascular risk are associated with cognitive decline, but the possible synergistic effects of these pathologic markers remain unclear.
To explore the interaction of AD biomarkers with a specific vascular risk marker (pulse pressure) on longitudinal cognition.
Participants included 139 older adults from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Biomarkers of tau, amyloid-β (Aβ), and vascular risk (pulse pressure) were assessed. Neuropsychological assessment provided memory, language, and executive function domain composite scores at baseline and 1-year follow-up. Multiple linear regression examined interactive effects of pulse pressure with tau PET independent of Aβ PET and Aβ PET independent of tau PET on baseline and 1-year cognitive outcomes.
The interaction between pulse pressure and tau PET significantly predicted 1-year memory performance such that the combined effect of high pulse pressure and high tau PET levels was associated with lower memory at follow-up but not at baseline. In contrast, Aβ PET did not significantly interact with pulse pressure to predict baseline or 1-year outcomes in any cognitive domain. Main effects revealed a significant effect of tau PET on memory, and no significant effects of Aβ PET or pulse pressure on any cognitive domain.
Results indicate that tau and an indirect marker of arterial stiffening (pulse pressure) may synergistically contribute to memory decline, whereas Aβ may have a lesser role in predicting cognitive progression. Tau and vascular pathology (particularly in combination) may represent valuable targets for interventions intended to slow cognitive decline.
研究表明,tau 蛋白和心血管风险都与认知能力下降有关,但这些病理标志物的可能协同作用尚不清楚。
探讨 AD 生物标志物与特定血管风险标志物(脉压)对纵向认知的相互作用。
参与者包括来自阿尔茨海默病神经影像学倡议(ADNI)的 139 名老年人。评估了 tau、淀粉样蛋白-β(Aβ)和血管风险(脉压)的生物标志物。神经心理学评估在基线和 1 年随访时提供了记忆、语言和执行功能域复合评分。多元线性回归检查了脉压与 tau PET 的交互作用,tau PET 独立于 Aβ PET,Aβ PET 独立于 tau PET,对基线和 1 年认知结果的影响。
脉压与 tau PET 的相互作用显著预测了 1 年的记忆表现,即高脉压和高 tau PET 水平的联合作用与随访时的记忆降低相关,但与基线时无关。相比之下,Aβ PET 与脉压之间的相互作用在任何认知域中均未显著预测基线或 1 年的结果。主要效应显示 tau PET 对记忆有显著影响,而 Aβ PET 或脉压对任何认知域均无显著影响。
结果表明,tau 和动脉僵硬的间接标志物(脉压)可能协同导致记忆下降,而 Aβ 可能在预测认知进展方面作用较小。tau 和血管病理学(特别是联合作用)可能是减缓认知能力下降的干预措施的有价值的靶点。