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Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats

BACKGROUND: Post-stroke dementia (PSD) is one of the major consequences after stroke. Chronic cerebral hypoperfusion (CCH) can induce vascular cognitive impairment and potentiate amyloid pathology. We investigated how CCH contributes to the development of PSD after stroke in the context of neuroinfl...

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Autores principales: Back, Dong Bin, Kwon, Kyoung Ja, Choi, Dong-Hee, Shin, Chan Young, Lee, Jongmin, Han, Seol-Heui, Kim, Hahn Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5679180/
https://www.ncbi.nlm.nih.gov/pubmed/29121965
http://dx.doi.org/10.1186/s12974-017-0992-5
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author Back, Dong Bin
Kwon, Kyoung Ja
Choi, Dong-Hee
Shin, Chan Young
Lee, Jongmin
Han, Seol-Heui
Kim, Hahn Young
author_facet Back, Dong Bin
Kwon, Kyoung Ja
Choi, Dong-Hee
Shin, Chan Young
Lee, Jongmin
Han, Seol-Heui
Kim, Hahn Young
author_sort Back, Dong Bin
collection PubMed
description BACKGROUND: Post-stroke dementia (PSD) is one of the major consequences after stroke. Chronic cerebral hypoperfusion (CCH) can induce vascular cognitive impairment and potentiate amyloid pathology. We investigated how CCH contributes to the development of PSD after stroke in the context of neuroinflammation and amyloid pathology. METHODS: We designed a unique animal model for PSD. We performed middle cerebral artery occlusion (MCAO) surgery in rats mimicking acute territorial infarct, which was followed by bilateral common carotid artery occlusion (BCCAo) surgery mimicking CCH. We performed behavioral tests including neurologic function test and water maze task and histological investigations including neuroinflammation, neuronal cell death, amyloid pathology, and aquaporin 4 (AQP4) distribution. RESULTS: Spatial memory was synergistically impaired when BCCAo was superimposed on MCAO. Neuroinflammation with astroglial or microglial activation and amyloid pathology were enhanced in the ipsilateral cortex, thalamus, and hippocampus when BCCAo was superimposed on MCAO. Glymphatic pathway-related AQP4 distribution changed from perivascular to parenchymal pattern. CONCLUSIONS: Our experimental results suggest that CCH may contribute to the development of PSD by interfering with amyloid clearance through the glymphatic pathway and concomitant neuroinflammation. Therapeutic strategy to clear brain metabolic waste through the glymphatic pathway may be a promising approach to prevent PSD after stroke.
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spelling pubmed-56791802017-11-17 Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats Back, Dong Bin Kwon, Kyoung Ja Choi, Dong-Hee Shin, Chan Young Lee, Jongmin Han, Seol-Heui Kim, Hahn Young J Neuroinflammation Research BACKGROUND: Post-stroke dementia (PSD) is one of the major consequences after stroke. Chronic cerebral hypoperfusion (CCH) can induce vascular cognitive impairment and potentiate amyloid pathology. We investigated how CCH contributes to the development of PSD after stroke in the context of neuroinflammation and amyloid pathology. METHODS: We designed a unique animal model for PSD. We performed middle cerebral artery occlusion (MCAO) surgery in rats mimicking acute territorial infarct, which was followed by bilateral common carotid artery occlusion (BCCAo) surgery mimicking CCH. We performed behavioral tests including neurologic function test and water maze task and histological investigations including neuroinflammation, neuronal cell death, amyloid pathology, and aquaporin 4 (AQP4) distribution. RESULTS: Spatial memory was synergistically impaired when BCCAo was superimposed on MCAO. Neuroinflammation with astroglial or microglial activation and amyloid pathology were enhanced in the ipsilateral cortex, thalamus, and hippocampus when BCCAo was superimposed on MCAO. Glymphatic pathway-related AQP4 distribution changed from perivascular to parenchymal pattern. CONCLUSIONS: Our experimental results suggest that CCH may contribute to the development of PSD by interfering with amyloid clearance through the glymphatic pathway and concomitant neuroinflammation. Therapeutic strategy to clear brain metabolic waste through the glymphatic pathway may be a promising approach to prevent PSD after stroke. BioMed Central 2017-11-09 /pmc/articles/PMC5679180/ /pubmed/29121965 http://dx.doi.org/10.1186/s12974-017-0992-5 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Back, Dong Bin
Kwon, Kyoung Ja
Choi, Dong-Hee
Shin, Chan Young
Lee, Jongmin
Han, Seol-Heui
Kim, Hahn Young
Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title_full Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title_fullStr Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title_full_unstemmed Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title_short Chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
title_sort chronic cerebral hypoperfusion induces post-stroke dementia following acute ischemic stroke in rats
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5679180/
https://www.ncbi.nlm.nih.gov/pubmed/29121965
http://dx.doi.org/10.1186/s12974-017-0992-5
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