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Glycolic acid protects neurons against ischemia in vitro and in two animal models of stroke

Alexandra Chovsepian, View ORCID ProfileDaniel Berchtold, View ORCID ProfileKatarzyna Winek, View ORCID ProfileUta Mamrak, Inés Ramírez Álvarez, Yanina Dening, View ORCID ProfileLuis Weitbrecht, Claudia Dames, Marine Aillery, View ORCID ProfileCelia Fernandez-Sanz, Marianne Dieterich, View ORCID ProfilePeter Falkai, View ORCID ProfileNikolaus Plesnila, View ORCID ProfileAndreas Meisel, View ORCID ProfileFrancisco Pan-Montojo
doi: https://doi.org/10.1101/2020.11.24.396051
Alexandra Chovsepian
1Department of Psychiatry, Ludwig-Maximilian University, Nußbaumstrasse. 7, 80336 Munich, Germany
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Daniel Berchtold
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Katarzyna Winek
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Uta Mamrak
3Laboratory of Experimental Stroke Research, Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Feodor-Lynen-Strasse 17, 81377 Munich, Germany
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Inés Ramírez Álvarez
4Department of Neurology, Ludwig-Maximilian University, Marchioninstrasse. 15, 81377 Munich
5Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilian University Munich, Germany
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Yanina Dening
1Department of Psychiatry, Ludwig-Maximilian University, Nußbaumstrasse. 7, 80336 Munich, Germany
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Luis Weitbrecht
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Claudia Dames
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Marine Aillery
1Department of Psychiatry, Ludwig-Maximilian University, Nußbaumstrasse. 7, 80336 Munich, Germany
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Celia Fernandez-Sanz
4Department of Neurology, Ludwig-Maximilian University, Marchioninstrasse. 15, 81377 Munich
5Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilian University Munich, Germany
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Marianne Dieterich
4Department of Neurology, Ludwig-Maximilian University, Marchioninstrasse. 15, 81377 Munich
5Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilian University Munich, Germany
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Peter Falkai
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Nikolaus Plesnila
3Laboratory of Experimental Stroke Research, Institute for Stroke and Dementia Research (ISD), University of Munich Medical Center, Feodor-Lynen-Strasse 17, 81377 Munich, Germany
5Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilian University Munich, Germany
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Andreas Meisel
2Department of Neurology, NeuroCure Clinical Research Center, Center for Stroke Research, Charité University Medicine, Charitéplatz 1, 10117 Berlin, Germany
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Francisco Pan-Montojo
1Department of Psychiatry, Ludwig-Maximilian University, Nußbaumstrasse. 7, 80336 Munich, Germany
4Department of Neurology, Ludwig-Maximilian University, Marchioninstrasse. 15, 81377 Munich
5Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilian University Munich, Germany
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  • For correspondence: Francisco.Pan-Montojo@med.uni-muenchen.de
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ABSTRACT

Stroke is the second leading cause of death and disability worldwide. Current treatments, like pharmacological thrombolysis or mechanical thrombectomy, re-open occluded arteries but do not protect against ischemia-induced damage caused before reperfusion or ischemia/reperfusion-induced neuronal damage. It has been shown that knocking out djr-1.1 and djr-1.2 or glod-4 results in a decreased tolerance to anhydrobiosis in C elegans dauer larva and that Glycolic Acid (GA) can rescue this phenotype. During the process of desiccation/rehydration, a metabolic stop/start similar to the one observed during ischemia/reperfusion occurs. In this study we tested the protective effect of GA against ischemia in three different models (oxygen-glucose deprivation in vitro and Global cerebral ischemia as well as Middle Cerebral Artery Occlusion in vivo). Our results show that GA, given during reperfusion, strongly protects against ischemia-induced neuronal death, reduces the mortality in mice with large infarcts, significantly reduces the ischemic area in the brain and improves the functional outcome. The effect of GA is stronger when the substance is applied near the damaged tissue (i.e. directly to the neurons in vitro or intra-arterially via the internal carotid artery in vivo). These results suggest that GA treatment has the potential to dramatically reduce the mortality and disability caused by stroke in patients.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted November 24, 2020.
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Glycolic acid protects neurons against ischemia in vitro and in two animal models of stroke
Alexandra Chovsepian, Daniel Berchtold, Katarzyna Winek, Uta Mamrak, Inés Ramírez Álvarez, Yanina Dening, Luis Weitbrecht, Claudia Dames, Marine Aillery, Celia Fernandez-Sanz, Marianne Dieterich, Peter Falkai, Nikolaus Plesnila, Andreas Meisel, Francisco Pan-Montojo
bioRxiv 2020.11.24.396051; doi: https://doi.org/10.1101/2020.11.24.396051
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Glycolic acid protects neurons against ischemia in vitro and in two animal models of stroke
Alexandra Chovsepian, Daniel Berchtold, Katarzyna Winek, Uta Mamrak, Inés Ramírez Álvarez, Yanina Dening, Luis Weitbrecht, Claudia Dames, Marine Aillery, Celia Fernandez-Sanz, Marianne Dieterich, Peter Falkai, Nikolaus Plesnila, Andreas Meisel, Francisco Pan-Montojo
bioRxiv 2020.11.24.396051; doi: https://doi.org/10.1101/2020.11.24.396051

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