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Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury
At present, predicting the severity of brain injury caused by global cerebral ischemia/reperfusion injury (GCI/RI) is a clinical problem. After such an injury, clinical indicators that can directly reflect neurological dysfunction are lacking. The change in hippocampal microstructure is the key to m...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8530111/ https://www.ncbi.nlm.nih.gov/pubmed/34472484 http://dx.doi.org/10.4103/1673-5374.322468 |
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author | Wang, Wen-Zhu Liu, Xu Yang, Zheng-Yi Wang, Yi-Zheng Lu, Hai-Tao |
author_facet | Wang, Wen-Zhu Liu, Xu Yang, Zheng-Yi Wang, Yi-Zheng Lu, Hai-Tao |
author_sort | Wang, Wen-Zhu |
collection | PubMed |
description | At present, predicting the severity of brain injury caused by global cerebral ischemia/reperfusion injury (GCI/RI) is a clinical problem. After such an injury, clinical indicators that can directly reflect neurological dysfunction are lacking. The change in hippocampal microstructure is the key to memory formation and consolidation. Diffusion tensor imaging is a highly sensitive tool for visualizing injury to hippocampal microstructure. Although hippocampal microstructure, brain-derived neurotrophic factor (BDNF), and tropomyosin-related kinase B (TrkB) levels are closely related to nerve injury and the repair process after GCI/RI, whether these indicators can reflect the severity of such hippocampal injury remains unknown. To address this issue, we established rat models of GCI/RI using the four-vessel occlusion method. Diffusion tensor imaging parameters, BDNF, and TrkB levels were correlated with modified neurological severity scores. The results revealed that after GCI/RI, while neurological function was not related to BDNF and TrkB levels, it was related to hippocampal fractional anisotropy. These findings suggest that hippocampal fractional anisotropy can reflect the severity of hippocampal injury after global GCI/RI. The study was approved by the Institutional Animal Care and Use Committee of Capital Medical University, China (approval No. AEEI-2015-139) on November 9, 2015. |
format | Online Article Text |
id | pubmed-8530111 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-85301112021-11-09 Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury Wang, Wen-Zhu Liu, Xu Yang, Zheng-Yi Wang, Yi-Zheng Lu, Hai-Tao Neural Regen Res Research Article At present, predicting the severity of brain injury caused by global cerebral ischemia/reperfusion injury (GCI/RI) is a clinical problem. After such an injury, clinical indicators that can directly reflect neurological dysfunction are lacking. The change in hippocampal microstructure is the key to memory formation and consolidation. Diffusion tensor imaging is a highly sensitive tool for visualizing injury to hippocampal microstructure. Although hippocampal microstructure, brain-derived neurotrophic factor (BDNF), and tropomyosin-related kinase B (TrkB) levels are closely related to nerve injury and the repair process after GCI/RI, whether these indicators can reflect the severity of such hippocampal injury remains unknown. To address this issue, we established rat models of GCI/RI using the four-vessel occlusion method. Diffusion tensor imaging parameters, BDNF, and TrkB levels were correlated with modified neurological severity scores. The results revealed that after GCI/RI, while neurological function was not related to BDNF and TrkB levels, it was related to hippocampal fractional anisotropy. These findings suggest that hippocampal fractional anisotropy can reflect the severity of hippocampal injury after global GCI/RI. The study was approved by the Institutional Animal Care and Use Committee of Capital Medical University, China (approval No. AEEI-2015-139) on November 9, 2015. Wolters Kluwer - Medknow 2021-08-30 /pmc/articles/PMC8530111/ /pubmed/34472484 http://dx.doi.org/10.4103/1673-5374.322468 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Research Article Wang, Wen-Zhu Liu, Xu Yang, Zheng-Yi Wang, Yi-Zheng Lu, Hai-Tao Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title | Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title_full | Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title_fullStr | Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title_full_unstemmed | Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title_short | Diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
title_sort | diffusion tensor imaging of the hippocampus reflects the severity of hippocampal injury induced by global cerebral ischemia/reperfusion injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8530111/ https://www.ncbi.nlm.nih.gov/pubmed/34472484 http://dx.doi.org/10.4103/1673-5374.322468 |
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