Huang Kuo-Lun, Hsiao Ing-Tsung, Chang Ting-Yu, Yang Shieh-Yueh, Chang Yeu-Jhy, Wu Hsiu-Chuan, Liu Chi-Hung, Wu Yi-Ming, Lin Kun-Ju, Ho Meng-Yang, Lee Tsong-Hai
Department of Neurology, Linkou Chang Gung Memorial Hospital, and College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Department of Nuclear Medicine and Molecular Imaging Center, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Front Hum Neurosci. 2021 Dec 14;15:735063. doi: 10.3389/fnhum.2021.735063. eCollection 2021.
: Neurodegeneration and vascular burden are the two most common causes of post-stroke cognitive impairment. However, the interrelationship between the plasma beta-amyloid (Aβ) and tau protein, cortical atrophy and brain amyloid accumulation on PET imaging in stroke patients is undetermined. We aimed to explore: (1) the relationships of cortical thickness and amyloid burden on PET with plasma Aβ40, Aβ42, tau protein and their composite scores in stroke patients; and (2) the associations of post-stroke cognitive presentations with these plasma and neuroimaging biomarkers. : The prospective project recruited first-ever ischemic stroke patients around 3 months after stroke onset. The plasma Aβ40, Aβ42, and total tau protein were measured with the immunomagnetic reduction method. Cortical thickness was evaluated on MRI, and cortical amyloid plaque deposition was evaluated by F-florbetapir PET. Cognition was evaluated with Mini-Mental State Examination (MMSE), Geriatric Depression Scale (GDS), Dementia Rating Scale-2 (DRS-2). : The study recruited 24 stroke patients and 13 normal controls. The plasma tau and tauAβ42 levels were correlated with mean cortical thickness after age adjustment. The Aβ42/Aβ40 ratio was correlated with global cortical F-florbetapir uptake value. The DRS-2 and GDS scores were associated with mean cortical thickness and plasma biomarkers, including Aβ42/Aβ40, tau, tauAβ42, tau/Aβ42, and tau/Aβ40 levels, in stroke patients. : Plasma Aβ, tau, and their composite scores were associated with cognitive performance 3 months after stroke, and these plasma biomarkers were correlated with corresponding imaging biomarkers of neurodegeneration. Further longitudinal studies with a larger sample size are warranted to replicate the study results.
神经退行性变和血管负担是中风后认知障碍最常见的两个原因。然而，中风患者血浆β淀粉样蛋白（Aβ）和tau蛋白、皮质萎缩与PET成像上脑淀粉样蛋白积累之间的相互关系尚未确定。我们旨在探讨：（1）中风患者PET上皮质厚度和淀粉样蛋白负担与血浆Aβ40、Aβ42、tau蛋白及其综合评分之间的关系；（2）中风后认知表现与这些血浆和神经影像学生物标志物之间的关联。：该前瞻性项目招募了首次发生缺血性中风且发病后约3个月的患者。采用免疫磁珠法测量血浆Aβ40、Aβ42和总tau蛋白。在MRI上评估皮质厚度，通过F-氟代贝他吡PET评估皮质淀粉样斑块沉积。使用简易精神状态检查表（MMSE）、老年抑郁量表（GDS）、痴呆评定量表-2（DRS-2）评估认知。：该研究招募了24名中风患者和13名正常对照。年龄校正后，血浆tau和tauAβ42水平与平均皮质厚度相关。Aβ42/Aβ40比值与全脑皮质F-氟代贝他吡摄取值相关。中风患者的DRS-2和GDS评分与平均皮质厚度和血浆生物标志物相关，包括Aβ42/Aβ40、tau、tauAβ42、tau/Aβ42和tau/Aβ40水平。：血浆Aβ、tau及其综合评分与中风后3个月的认知表现相关，这些血浆生物标志物与神经退行性变的相应影像学生物标志物相关。有必要进行更大样本量的进一步纵向研究以重复研究结果。
