Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Cassidy, Jessica M.; Cramer, Steven C.

doi:10.1007/s12975-016-0467-5

Cited by 214 publications

(152 citation statements)

References 203 publications

(235 reference statements)

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“…Although the principal events leading to post-stroke recovery are widely concordant in humans and animals, the kinetics differ considerably. While recovery processes in rodents are almost completed 4 weeks post-stroke, in humans they primarily occur within about 3 months but may even continue for years (for review, see [17, 138]). The exact reason for this difference is not known up so far [74].…”

Section: Animal Models Of Post-stroke Recovery and Long-term Post-strmentioning

confidence: 99%

Ischemic stroke: experimental models and reality

2017

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The vast majority of cerebral stroke cases are caused by transient or permanent occlusion of a cerebral blood vessel (“ischemic stroke”) eventually leading to brain infarction. The final infarct size and the neurological outcome depend on a multitude of factors such as the duration and severity of ischemia, the existence of collateral systems and an adequate systemic blood pressure, etiology and localization of the infarct, but also on age, sex, comorbidities with the respective multimedication and genetic background. Thus, ischemic stroke is a highly complex and heterogeneous disorder. It is immediately obvious that experimental models of stroke can cover only individual specific aspects of this multifaceted disease. A basic understanding of the principal molecular pathways induced by ischemia-like conditions comes already from in vitro studies. One of the most frequently used in vivo models in stroke research is the endovascular suture or filament model in rodents with occlusion of the middle cerebral artery (MCA), which causes reproducible infarcts in the MCA territory. It does not require craniectomy and allows reperfusion by withdrawal of the occluding filament. Although promptly restored blood flow is far from the pathophysiology of spontaneous human stroke, it more closely mimics the therapeutic situation of mechanical thrombectomy which is expected to be increasingly applied to stroke patients. Direct transient or permanent occlusion of cerebral arteries represents an alternative approach but requires craniectomy. Application of endothelin-1, a potent vasoconstrictor, allows induction of transient focal ischemia in nearly any brain region and is frequently used to model lacunar stroke. Circumscribed and highly reproducible cortical lesions are characteristic of photothrombotic stroke where infarcts are induced by photoactivation of a systemically given dye through the intact skull. The major shortcoming of this model is near complete lack of a penumbra. The two models mimicking human stroke most closely are various embolic stroke models and spontaneous stroke models. Closeness to reality has its price and goes along with higher variability of infarct size and location as well as unpredictable stroke onset in spontaneous models versus unpredictable reperfusion in embolic clot models.

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Section: Animal Models Of Post-stroke Recovery and Long-term Post-strmentioning

confidence: 99%

Ischemic stroke: experimental models and reality

2017

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“…The recovery from neurological impairments or deficits is called neurological recovery, which is the result of brain recovery, brain repair or brain reorganization (Robert Teasell et al, 2014). However, spontaneous recovery after stroke is generally incomplete (Cassidy and Cramer, 2016; Yozbatiran and Cramer, 2006). …”

Section: The Intrinsic Capability Of Brain Self-repair In Stroke Recomentioning

confidence: 99%

Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

Zhao

Willing

2018

Progress in Neurobiology

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Stroke represents a severe medical condition that causes stroke survivors to suffer from long-term and even lifelong disability. Over the past several decades, a vast majority of stroke research targets neuroprotection in the acute phase, while little work has been done to enhance stroke recovery at the later stage. Through reviewing current understanding of brain plasticity, stroke pathology, and emerging preclinical and clinical restorative approaches, this review aims to provide new insights to advance the research field for stroke recovery. Lifelong brain plasticity offers the long-lasting possibility to repair a stroke-damaged brain. Stroke impairs the structural and functional integrity of entire brain networks; the restorative approaches containing multi-components have great potential to maximize stroke recovery by rebuilding and normalizing the stroke-disrupted entire brain networks and brain functioning. The restorative window for stroke recovery is much longer than previously thought. The optimal time for brain repair appears to be at later stage of stroke rather than the earlier stage. It is expected that these new insights will advance our understanding of stroke recovery and assist in developing the next generation of restorative approaches for enhancing brain repair after stroke.

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“…Stroke is a prominent cause of mortality and long-term disability and is accompanied by unusually high social and medical costs [1, 2]. The major causes of death in stroke-related mortalities are a consequence of neurological damage and/or cardiovascular complications [3].…”

Section: Introductionmentioning

confidence: 99%

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

Chen

Cui

Yang

et al. 2017

Transl. Stroke Res.

126

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Cardiovascular diseases are approximately three times higher in patients with neurological deficits than in patients without neurological deficits. MicroRNA-126 (MiR-126) facilitates vascular remodeling and decreases fibrosis and is emerging as an important factor in the pathogenesis of cardiovascular diseases and cerebral stroke. In this study, we tested the hypothesis that decreased miR-126 after ischemic stroke may play an important role in regulating cardiac function. Wild-type (WT), specific conditional-knockout endothelial cell miR-126 (miR-126EC−/−), and miR-126 knockout control (miR-126fl/fl) mice were subjected to distal middle cerebral artery occlusion (dMCAo) (n = 10/group). Cardiac hemodynamics and function were measured using transthoracic Doppler echocardiography. Mice were sacrificed at 28 days after dMCAo. WT mice subjected to stroke exhibited significantly decreased cardiac ejection fraction and increased myocyte hypertrophy, fibrosis as well as increased heart inflammation, infiltrating macrophages, and oxidative stress compared to non-stroke animals. Stroke significantly decreased serum and heart miR-126 expression and increased miR-126 target genes, vascular cell adhesion protein-1, and monocyte chemotactic protein-1 gene, and protein expression in the heart compared to non-stroke mice. MiR-126EC−/− mice exhibited significantly decreased cardiac function and increased cardiomyocyte hypertrophy, fibrosis, and inflammatory factor expression after stroke compared to miR-126fl/fl stroke mice. Exosomes derived from endothelial cells of miR-126EC−/− (miR-126EC−/−EC-Exo) mice exhibited significantly decreased miR-126 expression than exosomes derived from miR-126fl/fl (miR-126fl/fl-EC-Exo) mice. Treatment of cardiomyocytes subjected to oxygen glucose deprivation with miR-126fl/fl-EC-Exo exhibited significantly decreased hypertrophy than with miR-126EC−/−EC-Exo treatment. Ischemic stroke directly induces cardiac dysfunction. Decreasing miR-126 expression may contribute to cardiac dysfunction after stroke in mice.

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Spontaneous and Therapeutic-Induced Mechanisms of Functional Recovery After Stroke

Cited by 214 publications

References 203 publications

Ischemic stroke: experimental models and reality

Ischemic stroke: experimental models and reality

Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

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