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Updated: May 2, 2026

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
Published on: July 25, 2011
Glatiramer acetate does not protect from acute ischemic stroke in mice
Peter Kraft1,2, Kerstin Göbel3, Sven G Meuth3,4
1Department of Neurology, University Hospital Würzburg, Josef-Schneider-Str. 11, 97080 Würzburg, Germany.
Glatiramer acetate did not reduce brain lesion size or improve outcomes in a mouse model of acute ischemic stroke. Further research is needed to explore its therapeutic potential in brain ischemia.
Area of Science:
- Neuroscience
- Immunology
- Neurology
Background:
- The immune system's role in acute ischemic stroke pathophysiology is recognized, yet targeted immunomodulatory treatments are absent.
- Glatiramer acetate, an approved immunomodulator for multiple sclerosis, shows potential for other neuroinflammatory conditions.
- This study investigates glatiramer acetate's efficacy in a preclinical model of stroke.
Purpose of the Study:
- To evaluate the neuroprotective effects of glatiramer acetate in a mouse model of ischemic stroke.
- To determine if glatiramer acetate reduces infarct volume and improves functional recovery after middle cerebral artery occlusion.
Main Methods:
- Transient middle cerebral artery occlusion (60 minutes) was induced in male C57Bl/6 mice.
- Mice received glatiramer acetate (3.5 mg/kg) 30 minutes before stroke induction.
- Lesion volumes and functional outcomes were assessed on day 1 post-stroke.
Main Results:
- Glatiramer acetate pretreatment did not significantly reduce lesion volumes.
- No improvement in functional outcomes was observed on day 1 after stroke.
- The drug failed to demonstrate efficacy in this acute ischemic stroke model.
Conclusions:
- Glatiramer acetate did not provide protection against acute ischemic stroke in this experimental setting.
- Further investigation is required to ascertain the therapeutic potential of glatiramer acetate and similar immunomodulators in brain ischemia.
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