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Evolving Clinical-Translational Investigations of Cerebroprotection in Ischemic Stroke
Yinghui Li1, Laurel E Schappell1,2, Claire Polizu1
1Department of Neurology, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794-8651, USA.
Insights
Despite advanced treatments, many ischemic stroke patients face disability. This review explores neuroprotection and cerebroprotection strategies to improve stroke outcomes and promote brain repair.
Area of Science:
- Neurology
- Translational Science
- Neuroprotection Research
Background:
- Ischemic stroke causes significant disability, even with reperfusion therapies like thrombolysis and thrombectomy.
- The concept of the ischemic penumbra highlights a salvageable brain area after stroke.
- Neuroprotection aims to minimize infarct expansion, reduce secondary injury, and promote repair, but clinical translation remains challenging.
Purpose of the Study:
- To review the translational science of past, current, and emerging cerebroprotection strategies.
- To propose a novel paradigm for optimizing stroke outcomes by considering the whole brain.
Main Methods:
- Literature review of preclinical and clinical studies on neuroprotection and cerebroprotection.
- Analysis of translational gaps in stroke research.
- Synthesis of existing knowledge to propose a new approach.
Main Results:
- Despite extensive research, no neuroprotective agent has significantly improved outcomes beyond reperfusion therapies.
- The concept of cerebroprotection broadens the focus to the entire brain's response to stroke.
Conclusions:
- Significant translational gaps persist in developing effective neuroprotective agents for ischemic stroke.
- A novel cerebroprotection paradigm is needed to optimize stroke outcomes by considering the whole brain.
- Continued investigation into neuroprotective and cerebroprotective strategies is crucial for advancing stroke care.
Abstract:
Ischemic stroke is a highly morbid disease, with over 50% of large vessel stroke (middle cerebral artery or internal carotid artery terminus occlusion) patients suffering disability despite maximal acute reperfusion therapy with thrombolysis and thrombectomy. The discovery of the ischemic penumbra in the 1980s laid the foundation for a salvageable territory in ischemic stroke. Since then, the concept of neuroprotection has been a focus of post-stroke care to (1) minimize the conversion from penumbra to core irreversible infarct, (2) limit secondary damage from ischemia-reperfusion injury, inflammation, and excitotoxicity and (3) to encourage tissue repair. However, despite multiple studies, the preclinical-clinical research enterprise has not yet created an agent that mitigates post-stroke outcomes beyond thrombolysis and mechanical clot retrieval. These translational gaps have not deterred the scientific community as agents are under continuous investigation. The NIH has recently promoted the concept of cerebroprotection to consider the whole brain post-stroke rather than just the neurons. This review will briefly outline the translational science of past, current, and emerging breakthroughs in cerebroprotection and use of these foundational ideas to develop a novel paradigm for optimizing stroke outcomes.
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