Vascular Cellular Adhesion Molecule-1 (VCAM-1) and Memory Impairment in African-Americans after Small Vessel-Type Stroke
Vascular Cellular Adhesion Molecule-1 (VCAM-1) and Memory Impairment in African-Americans after Small Vessel-Type Stroke
复制标题
DOI：
10.1016/j.jstrokecerebrovasdis.2020.104646
复制
发表时间：
2020-04-01
影响因子：
2.5
通讯作者：
Goldstein, Larry B.
中科院分区：
文献类型：
--
作者：
El Husseini, Nada;Bushnell, Cheryl;Goldstein, Larry B.
背景：非裔美国人（AA）发生小血管型缺血性卒中（SVS）的可能性是白人的3倍。小血管卒中与认知障碍相关，白色物质高信号（WMH）负荷不能完全解释这种关系。我们研究了炎症/内皮功能障碍生物标志物是否与AAs中SVS后的认知相关。方法：在24名受试者中获得生物标志物（中位年龄56.5岁，54%为女性，中位教育年限12年）。卒中后6周以上，使用记忆综合评分（MCS）评估认知功能，MCS是使用霍普金斯言语学习测试II和简明视觉空间记忆测试修订版的回忆产生的。使用半自动体积方案来量化临床MRI扫描上的WMH体积（WMHv）。对包括血管细胞粘附分子-1（VCAM-1）、白细胞介素-1受体拮抗剂、白细胞介素6、白细胞介素-8、白细胞介素-10、干扰素γ和凝血酶-抗凝血酶（达特）在内的潜在生物标志物进行对数转换，并与MCS相关，调整潜在混杂因素。结果：在血清生物标志物中，只有VCAM-1与基于MCS的记忆力较差相关（r = -.659; P = .0006）。VCAM-1（r = .554; P = .005）和年龄（r = .479; P = .018）与WMHv相关;在校正WMHv、年龄和教育后，VCAM-1与MCS独立相关（P = .023）。结论：这项探索性分析的结果表明，血管内皮细胞粘附分子-1水平反映的内皮功能障碍和炎症可能在卒中后认知功能障碍中发挥作用。需要更多的研究来验证这一观察结果，并评估非AA和其他卒中类型的这种关系，并将这一发现与非卒中人群的认知障碍进行比较。
Background: African-Americans (AA) are 3 times more likely to have small-vessel-type ischemic strokes (SVS) than Whites. Small vessel strokes are associated with cognitive impairment, a relationship incompletely explained by white matter hyperintensity (WMH) burden. We examined whether inflammatory/endothelial dysfunction biomarkers are associated with cognition after SVS in AAs. Methods: Biomarkers were obtained in 24 subjects (median age 56.5 years, 54% women, median 12 years education). Cognition was assessed more than 6 weeks poststroke using the memory composite score (MCS), which was generated using recall from the Hopkins Verbal Learning Test-II and Brief Visuospatial Memory Test-Revised. A semi-automated, volumetric protocol was used to quantify WMH volume (WMHv) on clinical MRI scans. Potential biomarkers including vascular cell adhesion molecule-1 (VCAM-1), interleukin-1 receptor antagonist, interleukin6, interleukin-8, interleukin-10, interferon gamma, and thrombin-antithrombin (TAT) were log-transformed and correlated with MCS with adjustment for potential confounders. Results: Among serum biomarkers, only VCAM-1-correlated with poorer memory based on the MCS (r = -.659; P = .0006). VCAM-1 (r = .554; P = .005) and age (r = .479; P = .018) correlated with WMHv; VCAM-1 was independently associated with MCS after adjustment for WMHv, age, and education (P = .023). Conclusions: The findings of this exploratory analysis suggest that endothelial dysfunction and inflammation as reflected by VCAM-1 levels may play a role in post-stroke cognitive impairment. Additional studies are needed to validate this observation and to evaluate this relationship in non-AAs and with other stroke types and compare this finding to cognitive impairment in nonstroke populations.