Plasma amyloid beta and tau levels are predictors of post-stroke cognitive impairment: A longitudinal study

研究成果: 雜誌貢獻文章

摘要

Objectives: 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. Methods: 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. Results: 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, P = 0.013; tau: 16.7 vs. 19.9 pg/mL, P = 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. Conclusion: The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development.

原文英語
文章編號715
期刊Frontiers in Neurology
10
發行號JUL
DOIs
出版狀態已發佈 - 一月 1 2019

指紋

Amyloid
Longitudinal Studies
Stroke
Cognitive Dysfunction
Leukoencephalopathies
Immunoassay
Cognition

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

引用此文

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title = "Plasma amyloid beta and tau levels are predictors of post-stroke cognitive impairment: A longitudinal study",
abstract = "Objectives: 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. Methods: 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. Results: 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, P = 0.013; tau: 16.7 vs. 19.9 pg/mL, P = 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. Conclusion: The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development.",
keywords = "Amyloid (A) 42, Montreal Cognitive Assessment (MoCA), Post-stroke cognitive impairment, Tau, Vascular cognition impairment",
author = "Chi, {Nai Fang} and Chao, {Shu Ping} and Huang, {Li Kai} and Lung Chan and Chen, {Yih Ru} and Chiou, {Hung Yi} and Hu, {Chaur Jong}",
year = "2019",
month = "1",
day = "1",
doi = "10.3389/fneur.2019.00715",
language = "English",
volume = "10",
journal = "Frontiers in Neurology",
issn = "1664-2295",
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number = "JUL",

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TY - JOUR

T1 - Plasma amyloid beta and tau levels are predictors of post-stroke cognitive impairment

T2 - A longitudinal study

AU - Chi, Nai Fang

AU - Chao, Shu Ping

AU - Huang, Li Kai

AU - Chan, Lung

AU - Chen, Yih Ru

AU - Chiou, Hung Yi

AU - Hu, Chaur Jong

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Objectives: 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. Methods: 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. Results: 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, P = 0.013; tau: 16.7 vs. 19.9 pg/mL, P = 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. Conclusion: The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development.

AB - Objectives: 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. Methods: 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. Results: 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, P = 0.013; tau: 16.7 vs. 19.9 pg/mL, P = 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. Conclusion: The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development.

KW - Amyloid (A) 42

KW - Montreal Cognitive Assessment (MoCA)

KW - Post-stroke cognitive impairment

KW - Tau

KW - Vascular cognition impairment

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