Chi Nai-Fang, Chao Shu-Ping, Huang Li-Kai, Chan Lung, Chen Yih-Ru, Chiou Hung-Yi, Hu Chaur-Jong
Department of Neurology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Department of Neurology, Stroke Center, Shuang Ho Hospital, Taipei Medical University, New Taipei, Taiwan.
Front Neurol. 2019 Jul 2;10:715. doi: 10.3389/fneur.2019.00715. eCollection 2019.
Post-stroke cognitive impairment (PSCI) is a common disease that may occur within 3 months after a stroke or even later. However, the mechanism of PSCI development is unclear. The present study investigated whether the levels of plasma amyloid beta-42 (Aβ42) and tau are associated with the onset of PSCI. Fifty-five patients admitted within 7 days of acute ischemic stroke were enrolled and followed up for 1 year. Montreal Cognitive Assessment (MoCA) was administered at 3 months and 1 year, and plasma Aβ42 and tau levels were determined using an ultrasensitive immunoassay (immunomagnetic reduction) within 7 days of the stroke event and 3 months later. In this study, 13 of 55 patients developed PSCI (MoCA score <23) at 3 months. Seven patients with PSCI at 3 months recovered to a cognitively normal state at 1 year, whereas seven cognitively normal patients developed PSCI at 1 year. The patients with PSCI at 1 year had a higher incidence of cognitive function deterioration between 3 months and 1 year compared with those without PSCI at 1 year. Plasma Aβ42 and tau levels at 3 months were lower in the patients with PSCI at 1 year than in those without PSCI (Aβ42: 15.1 vs. 17.2 pg/mL, = 0.013; tau: 16.7 vs. 19.9 pg/mL, = 0.018). Low education levels and pre-existing white matter disease were the most significant predictors of PSCI at 3 months, and poor cognitive performance at 3 months and low plasma Aβ42 and tau levels at 3 months were the most significant predictors of PSCI at 1 year. The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development.
卒中后认知障碍（PSCI）是一种常见疾病，可能在卒中后3个月内甚至更晚发生。然而，PSCI的发病机制尚不清楚。本研究调查了血浆淀粉样蛋白β-42（Aβ42）和tau水平是否与PSCI的发病有关。纳入55例急性缺血性卒中发病7天内入院的患者，并随访1年。在3个月和1年时进行蒙特利尔认知评估（MoCA），并在卒中事件发生7天内及3个月后使用超灵敏免疫测定法（免疫磁珠法）测定血浆Aβ42和tau水平。在本研究中，55例患者中有13例在3个月时发生PSCI（MoCA评分<23）。3个月时发生PSCI的7例患者在1年时恢复到认知正常状态，而7例认知正常的患者在1年时发生PSCI。与1年时无PSCI的患者相比，1年时发生PSCI的患者在3个月至1年期间认知功能恶化的发生率更高。1年时发生PSCI的患者3个月时的血浆Aβ42和tau水平低于无PSCI的患者（Aβ42：15.1 vs. 17.2 pg/mL，P = 0.013；tau：16.7 vs. 19.9 pg/mL，P = 0.018）。低教育水平和既往存在的白质病变是3个月时PSCI最显著的预测因素，3个月时认知表现差以及3个月时血浆Aβ42和tau水平低是1年时PSCI最显著的预测因素。PSCI的发病机制复杂且随时间变化。缺血诱导的Aβ42/tau病理可能参与了PSCI的发生发展。
