Departments of Neurosurgery and Neurology, University of Colorado Anschutz Medical Campus, Rocky Mountain Alzheimer's Disease Center, Aurora, CO, USA.
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
J Alzheimers Dis. 2018;62(1):385-397. doi: 10.3233/JAD-170602.
Inflammatory markers have been shown to predict neurocognitive outcomes in aging adults; however, the degree to which peripheral markers mirror the central nervous system remains unknown. We investigated the association between plasma and cerebrospinal fluid (CSF) markers of inflammation, and explored whether these markers independently predict CSF indicators of Alzheimer's disease (AD) pathology or neuronal damage. Plasma and CSF samples were analyzed for inflammatory markers in a cohort of asymptomatic older adults (n = 173). CSF samples were analyzed for markers of AD pathology (Aβ42, phosphorylated tau [p-tau], sAβPPβ) or neuronal damage (total tau; neurofilament light chain) (n = 147). Separate linear models for each analyte were conducted with CSF and plasma levels entered simultaneously as predictors and markers of AD pathology or neuronal damage as outcome measures. Strong associations were noted between CSF and plasma MIP-1β levels, and modest associations were observed for remaining analytes. With respect to AD pathology, higher levels of plasma and CSF IL-8, CSF MIP-1β, and CSF IP-10 were associated with higher levels of p-tau. Higher levels of CSF IL-8 were associated with higher levels of CSF Aβ42. Higher CSF sAβPPβ levels were associated with higher plasma markers only (IL-8; MCP-1). In terms of neuronal injury, higher levels of plasma and CSF IL-8, CSF IP-10, and CSF MIP-1β were associated with higher levels of CSF total tau. Exploratory analyses indicated that CSF Aβ42 modifies the relationship between plasma inflammatory levels and CSF tau levels. Results suggest that both plasma and CSF inflammatory markers independently relay integral information about AD pathology and neuronal damage.
炎症标志物已被证明可预测老年人群的神经认知结局;然而,外周标志物与中枢神经系统的吻合程度尚不清楚。我们研究了血浆和脑脊液 (CSF) 炎症标志物之间的相关性,并探讨了这些标志物是否可独立预测 CSF 中阿尔茨海默病 (AD) 病理或神经元损伤的标志物。我们分析了一组无症状老年人群 (n = 173) 的血浆和 CSF 炎症标志物。对 CSF 样本进行了 AD 病理标志物 (Aβ42、磷酸化 tau [p-tau]、sAβPPβ) 或神经元损伤标志物 (总 tau;神经丝轻链) (n = 147) 的分析。对于每个分析物,我们分别进行了线性模型,将 CSF 和血浆水平同时作为预测因子输入,并将 AD 病理或神经元损伤标志物作为结果指标。我们注意到 CSF 和血浆 MIP-1β 水平之间存在很强的相关性,而对于其余分析物则观察到适度的相关性。就 AD 病理而言,较高的血浆和 CSF IL-8、CSF MIP-1β 和 CSF IP-10 水平与较高的 p-tau 水平相关。较高的 CSF IL-8 水平与较高的 CSF Aβ42 水平相关。较高的 CSF sAβPPβ 水平仅与较高的血浆标志物相关 (IL-8;MCP-1)。就神经元损伤而言,较高的血浆和 CSF IL-8、CSF IP-10 和 CSF MIP-1β 水平与较高的 CSF 总 tau 水平相关。探索性分析表明,CSF Aβ42 改变了血浆炎症水平与 CSF tau 水平之间的关系。结果表明,血浆和 CSF 炎症标志物均可独立传递 AD 病理和神经元损伤的重要信息。