Experimental & Translational Stroke Medicine最新文献

{"title":"Platelet rich clots are resistant to lysis by thrombolytic therapy in a rat model of embolic stroke.","authors":"Amelia J Tomkins,&nbsp;Nadine Schleicher,&nbsp;Lucy Murtha,&nbsp;Manfred Kaps,&nbsp;Christopher R Levi,&nbsp;Max Nedelmann,&nbsp;Neil J Spratt","doi":"10.1186/s13231-014-0014-y","DOIUrl":"https://doi.org/10.1186/s13231-014-0014-y","url":null,"abstract":"<p><strong>Background: </strong>Early recanalization of occluded vessels in stroke is closely associated with improved clinical outcome. Microbubble-enhanced sonothrombolysis is a promising therapy to improve recanalization rates and reduce the time to recanalization. Testing any thrombolytic therapy requires a model of thromboembolic stroke, but to date these models have been highly variable with regards to clot stability. Here, we developed a model of thromboembolic stroke in rats with site-specific delivery of platelet-rich clots (PRC) to the main stem of the middle cerebral artery (MCA). This model was used in a subsequent study to test microbubble-enhanced sonothrombolysis.</p><p><strong>Methods: </strong>In Study 1 we investigated spontaneous recanalization rates of PRC in vivo over 4 hours and measured infarct volumes at 24 hours. In Study 2 we investigated tPA-mediated thrombolysis and microbubble-enhanced sonothrombolysis in this model.</p><p><strong>Results: </strong>Study 1 demonstrated stable occlusion out to 4 hours in 5 of 7 rats. Two rats spontaneously recanalized at 40 and 70 minutes post-embolism. Infarct volumes were not significantly different in recanalized rats, 43.93 ± 15.44% of the ischemic hemisphere, compared to 48.93 ± 3.9% in non-recanalized animals (p = 0.7). In Study 2, recanalization was not observed in any of the groups post-treatment.</p><p><strong>Conclusions: </strong>Site specific delivery of platelet rich clots to the MCA origin resulted in high rates of MCA occlusion, low rates of spontaneous clot lysis and large infarction. These platelet rich clots were highly resistant to tPA with or without microbubble-enhanced sonothrombolysis. This resistance of platelet rich clots to enhanced thrombolysis may explain recanalization failures clinically and should be an impetus to better clot-type identification and alternative recanalization methods.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"7 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2015-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13231-014-0014-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33033270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Report on the 6th scientific meeting of the \"Verein zur Förderung des Wissenschaftlichen Nachwuchses in der Neurologie\" (NEUROWIND e.V.) held in Motzen, Germany, Oct. 31th - Nov. 2nd, 2014.","authors":"Christoph Kleinschnitz,&nbsp;Ralf A Linker,&nbsp;Tim Magnus,&nbsp;Thomas Korn,&nbsp;Sven G Meuth","doi":"10.1186/s13231-014-0013-z","DOIUrl":"https://doi.org/10.1186/s13231-014-0013-z","url":null,"abstract":"<p><p>From October 31th - November 2nd, 2014, the 6th NEUROWIND e.V. meeting was held in Motzen, Brandenburg, Germany. 70 doctoral students and postdocs from over 25 different groups working in German and Swiss university hospitals or research institutes attended the meeting to discuss their latest experiments and findings in the fields of neuroimmunology, neurodegeneration and neurovascular research. The meeting was regarded as a very well organized platform to support research of young investigators in Germany and all participants enjoyed the stimulating environment for lively in depth discussions. According to the major aim of NEUROWIND e.V. to support younger researchers in Germany the 4th NEUROWIND YOUNG SCIENTIST AWARD for experimental neurology was awarded to Michael Breckwoldt on his work in the group of Thomas Misgeld (Institute of Neuronal Cell Biology, Technische Universität München, Germany). The successful project was published in Nature Medicine entitled \"Multiparametric optical analysis of mitochondrial redox signals during neuronal physiology and pathology in vivo\". This outstanding paper deals with a molecular imaging approach in living mice to optically analyze the role of mitochondrial redox signals in axons in health and disease. The award is endowed with 20.000 Euro sponsored by Merck Serono GmbH, Darmstadt, Germany (unrestricted educational grant). This year's keynote lecture was given by Bernhard Hemmer, Head of the Department of Neurology at the Klinikum rechts der Isar, Technische Universität München. Dr. Hemmer highlighted the particular role of B cells and (auto)antibodies in multiple sclerosis (MS). As a new highlight Dr. Urbahns, head of global discovery technologies at Merck research laboratories, gave insights from research practice in the pharmaceutical industry and introduced a shift in the view on present-day drug discovery paradigms. </p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"7 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2015-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s13231-014-0013-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33238025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flow cytometric characterization of brain dendritic cell subsets after murine stroke.","authors":"Claudia Pösel,&nbsp;Anna Uri,&nbsp;Isabell Schulz,&nbsp;Johannes Boltze,&nbsp;Gesa Weise,&nbsp;Daniel-Christoph Wagner","doi":"10.1186/2040-7378-6-11","DOIUrl":"https://doi.org/10.1186/2040-7378-6-11","url":null,"abstract":"<p><strong>Background: </strong>Sterile inflammation is a substantial element of post-stroke pathophysiology with the determination of autoimmunity versus tolerance being one of its most important aspects. It is believed that this determination is initiated relatively early after stroke onset by clearing macrophages and migratory dendritic cells (DC). However, the phenotypic differentiation of macrophages and DC is intricate particularly in the disease context. Here, we utilized a set of surface markers used in mucosal immunity research to investigate the involvement of macrophages and DC subpopulations in post-stroke inflammation in mice.</p><p><strong>Findings: </strong>Photothrombotic stroke induced a significant increase of lineage (CD3, B220, Ly6G and CD49b) negative CD11b+ cells in the brain primarily consisting of F4/80+ macrophages and, to a lesser extent, F4/80-/CD11c-/CD11b+ monocytes and F4/80-/CD11c+ DC. The latter could be differentiated into the classical migratory DC subpopulations (CD11b+ and CD103+), but no CD4 or CD8+ DC were found. Finally, stroke caused a significant increase of CD11b/CD103 double-positive DC in the affected brain hemisphere.</p><p><strong>Conclusions: </strong>The surface marker combination used in this study allowed a phenotypic differentiation of macrophages and DC subpopulations after stroke, thus providing an important prerequisite to study post-stroke immunity and tolerance.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 1","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2014-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-11","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32813678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A 2 × 2 factorial design for the combination therapy of minocycline and remote ischemic perconditioning: efficacy in a preclinical trial in murine thromboembolic stroke model.","authors":"Md Nasrul Hoda,&nbsp;Susan C Fagan,&nbsp;Mohammad B Khan,&nbsp;Kumar Vaibhav,&nbsp;Aizaz Chaudhary,&nbsp;Phillip Wang,&nbsp;Krishnan M Dhandapani,&nbsp;Jennifer L Waller,&nbsp;David C Hess","doi":"10.1186/2040-7378-6-10","DOIUrl":"https://doi.org/10.1186/2040-7378-6-10","url":null,"abstract":"<p><strong>Background: </strong>After the failure of so many drugs and therapies for acute ischemic stroke, innovative approaches are needed to develop new treatments. One promising strategy is to test combinations of agents in the pre-hospital setting prior to the administration of intravenous tissue plasminogen activator (IV-tPA) and/ or the use of mechanical reperfusion devices in the hospital.</p><p><strong>Methods: </strong>We performed a 2 × 2 factorial design preclinical trial where we tested minocycline (MINO), remote ischemic perconditioning (RIPerC) and their combination treatment in a thromboembolic clot model of stroke in mice, without IV-tPA or later treated with IV-tPA at 4 hours post-stroke. Cerebral blood flow (CBF) was measured by laser speckle contrast imaging (LSCI), behavioral outcomes as neurological deficit score (NDS) and adhesive tape removal test, and infarct size measurement were performed at 48 hours post-stroke. Mice within the experimental sets were randomized for the different treatments, and all outcome measures were blinded.</p><p><strong>Results: </strong>RIPerC significantly improved CBF as measured by LSCI in both with and without tPA treated mice (P < 0.001). MINO and RIPerC treatment were effective alone at reducing infarct size (p < 0.0001) and improving short-term functional outcomes (p < 0.001) in the tPA and non-tPA treated animals. The combination treatment of MINO and RIPerC significantly reduced the infarct size greater than either intervention alone (p < 0.05). There were trends in favor of improving functional outcomes after combination treatment of MINO and RIPerC; however combination treatment group was not significantly different than the individual treatments of MINO and RIPerC. There was no \"statistical\" interaction between minocycline and RIPerC treatments indicating that the effects of RIPerC and MINO were additive and not synergistic on the outcome measures.</p><p><strong>Conclusion: </strong>In the future, combining these two safe and low cost interventions in the ambulance has the potential to \"freeze\" the penumbra and improve outcomes in stroke patients. This pre-clinical 2 × 2 design can be easily translated into a pre-hospital clinical trial.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 ","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2014-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-10","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32764732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of functional electrical stimulation on hand motor recovery in stroke patients: a review.","authors":"Fanny Quandt,&nbsp;Friedhelm C Hummel","doi":"10.1186/2040-7378-6-9","DOIUrl":"https://doi.org/10.1186/2040-7378-6-9","url":null,"abstract":"<p><p>Neuromuscular stimulation has been used as one potential rehabilitative treatment option to restore motor function and improve recovery in patients with paresis. Especially stroke patients who often regain only limited hand function would greatly benefit from a therapy that enhances recovery and restores movement. Multiple studies investigated the effect of functional electrical stimulation on hand paresis, the results however are inconsistent. Here we review the current literature on functional electrical stimulation on hand motor recovery in stroke patients. We discuss the impact of different parameters such as stage after stoke, degree of impairment, spasticity and treatment protocols on the functional outcome. Importantly, we outline the results from recent studies investigating the cortical effects elicited by functional electrical stimulation giving insights into the underlying mechanisms responsible for long-term treatment effects. Bringing together the findings from present research it becomes clear that both, treatment outcomes as well as the neurophysiologic mechanisms causing functional recovery, vary depending on patient characteristics. In order to develop unified treatment guidelines it is essential to conduct homogenous studies assessing the impact of different parameters on rehabilitative success. </p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 ","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2014-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32713686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapamycin up-regulation of autophagy reduces infarct size and improves outcomes in both permanent MCAL, and embolic MCAO, murine models of stroke.","authors":"Kathleen M Buckley,&nbsp;Daniel L Hess,&nbsp;Irina Y Sazonova,&nbsp;Sudharsan Periyasamy-Thandavan,&nbsp;John R Barrett,&nbsp;Russell Kirks,&nbsp;Harrison Grace,&nbsp;Galina Kondrikova,&nbsp;Maribeth H Johnson,&nbsp;David C Hess,&nbsp;Patricia V Schoenlein,&nbsp;Md Nasrul Hoda,&nbsp;William D Hill","doi":"10.1186/2040-7378-6-8","DOIUrl":"https://doi.org/10.1186/2040-7378-6-8","url":null,"abstract":"<p><strong>Background and purpose: </strong>The role of autophagy in response to ischemic stroke has been confusing with reports that both enhancement and inhibition of autophagy decrease infarct size and improve post-stroke outcomes. We sought to clarify this by comparing pharmacologic modulation of autophagy in two clinically relevant murine models of stroke.</p><p><strong>Methods: </strong>We used rapamycin to induce autophagy, and chloroquine to block completion of autophagy, by treating mice immediately after stroke and at 24 hours post-stroke in two different models; permanent Middle Cerebral Artery Ligation (MCAL), which does not allow for reperfusion of distal trunk of middle cerebral artery, and Embolic Clot Middle Cerebral Artery Occlusion (eMCAO) which allows for a slow reperfusion similar to that seen in most human stroke patients. Outcome measures at 48 hours post-stroke included infarct size analysis, behavioral assessment using Bederson neurological scoring, and survival.</p><p><strong>Results: </strong>Chloroquine treatment reduced the lesion size by approximately 30% and was significant only in the eMCAO model, where it also improved the neurological score, but did not increase survival. Rapamycin reduced lesion size by 44% and 50% in the MCAL and eMCAO models, respectively. Rapamycin also improved the neurological score to a greater degree than chloroquine and improved survival.</p><p><strong>Conclusions: </strong>While both inhibition and enhancement of autophagy by pharmacological intervention decreased lesion size and improved neurological scores, the enhancement with rapamycin showed a greater degree of improvement in outcomes as well as in survival. The protective action seen with chloroquine may be in part due to off-target effects on apoptosis separate from blocking lysosomal activity in autophagy. We conclude pharmacologic induction of autophagy is more advantageous than its blockade in physiologically-relevant permanent and slow reperfusion stroke models.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 ","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2014-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32477628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intravenous immunoglobulin (IVIg) provides protection against endothelial cell dysfunction and death in ischemic stroke.","authors":"Alexander Widiapradja,&nbsp;Tomislav Santro,&nbsp;Milan Basta,&nbsp;Christopher G Sobey,&nbsp;Silvia Manzanero,&nbsp;Thiruma V Arumugam","doi":"10.1186/2040-7378-6-7","DOIUrl":"https://doi.org/10.1186/2040-7378-6-7","url":null,"abstract":"<p><strong>Background: </strong>The brain endothelium is a key component of the blood brain barrier which is compromised following ischemia, allowing infiltration of damaging immune cells and other inflammatory molecules into the brain. Intravenous immunoglobulin (IVIg) is known to reduce infarct size in a mouse model of experimental stroke.</p><p><strong>Findings: </strong>Flow cytometry analysis showed that the protective effect of IVIg in ischemia and reperfusion injury in vivo is associated with reduced leukocyte infiltration, suggesting an involvement of the endothelium. In an in vitro model of ischemia, permeability analysis of the mouse brain endothelial cell line bEnd.3 revealed that IVIg prevented the loss of permeability caused by oxygen and glucose deprivation (OGD). In addition, western blot analysis of these brain endothelial cells showed that IVIg prevented the down-regulation of tight junction proteins claudin 5 and occludin and the decline in anti-apoptotic proteins Bcl-2 and Bcl-XL caused by OGD.</p><p><strong>Conclusion: </strong>IVIg protects endothelial cells from ischemic insult. These studies support the use of IVIg as a pharmacological intervention for stroke therapy.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2014-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32476073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A microsurgical procedure for middle cerebral artery occlusion by intraluminal monofilament insertion technique in the rat: a special emphasis on the methodology.","authors":"Aslan Güzel,&nbsp;Roland Rölz,&nbsp;Guido Nikkhah,&nbsp;Ulf D Kahlert,&nbsp;Jaroslaw Maciaczyk","doi":"10.1186/2040-7378-6-6","DOIUrl":"https://doi.org/10.1186/2040-7378-6-6","url":null,"abstract":"<p><strong>Introduction: </strong>Although there are many experimental studies describing the methodology of the middle cerebral artery occlusion (MCAO) in the literature, only limited data on these distinct anatomical structures and the details of the surgical procedure in a step by step manner. The aim of the present study simply is to examine the surgical anatomy of MCAO model and its modifications in the rat.</p><p><strong>Materials and methods: </strong>Forty Sprague-Dawley rats were used; 20 during the training phase and 20 for the main study. The monofilament sutures were prepared as described in the literature. All surgical steps of the study were performed under the operating microscope, including insertion of monofilament into middle cerebral artery through the internal carotid artery.</p><p><strong>Results: </strong>After an extensive training period, we lost two rats in four weeks. The effects of MCAO were confirmed by the evidence of severe motor deficit during the recovery period, and histopathological findings of infarction were proved in all 18 surviving rats.</p><p><strong>Conclusion: </strong>In this study, a microsurgical guideline of the MCAO model in the rat is provided with the detailed description of all steps of the intraluminal monofilament insertion method with related figures.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2014-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32442437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and characterization of a Yucatan miniature biomedical pig permanent middle cerebral artery occlusion stroke model.","authors":"Simon R Platt,&nbsp;Shannon P Holmes,&nbsp;Elizabeth W Howerth,&nbsp;Kylee Jo J Duberstein,&nbsp;C Robert Dove,&nbsp;Holly A Kinder,&nbsp;Emily L Wyatt,&nbsp;Amie V Linville,&nbsp;Vivian W Lau,&nbsp;Steven L Stice,&nbsp;William D Hill,&nbsp;David C Hess,&nbsp;Franklin D West","doi":"10.1186/2040-7378-6-5","DOIUrl":"https://doi.org/10.1186/2040-7378-6-5","url":null,"abstract":"<p><strong>Background: </strong>Efforts to develop stroke treatments have met with limited success despite an intense need to produce novel treatments. The failed translation of many of these therapies in clinical trials has lead to a close examination of the therapeutic development process. One of the major factors believed to be limiting effective screening of these treatments is the absence of an animal model more predictive of human responses to treatments. The pig may potentially fill this gap with a gyrencephalic brain that is larger in size with a more similar gray-white matter composition to humans than traditional stroke animal models. In this study we develop and characterize a novel pig middle cerebral artery occlusion (MCAO) ischemic stroke model.</p><p><strong>Methods: </strong>Eleven male pigs underwent MCAO surgery with the first 4 landrace pigs utilized to optimize stroke procedure and 7 additional Yucatan stroked pigs studied over a 90 day period. MRI analysis was done at 24 hrs and 90 days and included T2w, T2w FLAIR, T1w FLAIR and DWI sequences and associated ADC maps. Pigs were sacrificed at 90 days and underwent gross and microscopic histological evaluation. Significance in quantitative changes was determined by two-way analysis of variance and post-hoc Tukey's Pair-Wise comparisons.</p><p><strong>Results: </strong>MRI analysis of animals that underwent MCAO surgery at 24 hrs had hyperintense regions in T2w and DWI images with corresponding ADC maps having hypointense regions indicating cytotoxic edema consistent with an ischemic stroke. At 90 days, region of interest analysis of T1 FLAIR and ADC maps had an average lesion size of 59.17 cc, a loss of 8% brain matter. Histological examination of pig brains showed atrophy and loss of tissue, consistent with MRI, as well as glial scar formation and macrophage infiltration.</p><p><strong>Conclusions: </strong>The MCAO procedure led to significant and consistent strokes with high survivability. These results suggest that the pig model is potentially a robust system for the study of stroke pathophysiology and potential diagnostics and therapeutics.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 1","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2014-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32197320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glatiramer acetate does not protect from acute ischemic stroke in mice.","authors":"Peter Kraft,&nbsp;Kerstin Göbel,&nbsp;Sven G Meuth,&nbsp;Christoph Kleinschnitz","doi":"10.1186/2040-7378-6-4","DOIUrl":"https://doi.org/10.1186/2040-7378-6-4","url":null,"abstract":"<p><strong>Background: </strong>The role of the immune system in the pathophysiology of acute ischemic stroke is increasingly recognized. However, targeted treatment strategies to modulate immunological pathways in stroke are still lacking. Glatiramer acetate is a multifaceted immunomodulator approved for the treatment of relapsing-remitting multiple sclerosis. Experimental studies suggest that glatiramer acetate might also work in other neuroinflammatory or neurodegenerative diseases apart from multiple sclerosis.</p><p><strong>Findings: </strong>We evaluated the efficacy of glatiramer acetate in a mouse model of brain ischemia/reperfusion injury. 60 min of transient middle cerebral artery occlusion was induced in male C57Bl/6 mice. Pretreatment with glatiramer acetate (3.5 mg/kg bodyweight) 30 min before the induction of stroke did not reduce lesion volumes or improve functional outcome on day 1.</p><p><strong>Conclusions: </strong>Glatiramer acetate failed to protect from acute ischemic stroke in our hands. Further studies are needed to assess the true therapeutic potential of glatiramer acetate and related immunomodulators in brain ischemia.</p>","PeriodicalId":12158,"journal":{"name":"Experimental & Translational Stroke Medicine","volume":"6 1","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2014-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2040-7378-6-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32117983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}