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. 2020 Nov 19;10:20233. doi: 10.1038/s41598-020-75450-6

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Stroke induces long term neurodegeneration in hypertensive animals. Ischemic stroke causes a marked inflammation in stroked animals. In hypertensive animals, which already suffer from an increase in ROS production, the ischemic insult and the oxidative stress result in chronic increase in DNA damage and neuronal cell death, marked with an increase in PARP1 and HMGB1. PARP1 increase induces the transcription of MMP9, which triggers apoptosis. The result of these processes is chronic neuronal loss in the form of grey matter atrophy.