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Adaptive plasticity and recovery in preclinical models of stroke

机译:临床前中风模型的适应性可塑性和恢复

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Post-stroke recovery relies on neurobiological changes that modify the organization and function of the brain under pathophysiological conditions. The changes can be adaptive (i.e. restoration of function) or maladaptive (i.e. worsening of function). Preclinical models of stroke exhibit adaptive plasticity that leads to a "spontaneous recovery" of functions. This recovery can be modulated through external factors, such as rehabilitation, pharmacology or other adjuvant strategies. Nevertheless, current interventions only result in a limited improvement of deficits and there is also potential for maladaptation. Hence, a better understanding of the mechanisms underlying recovery is essential for the design of more efficient and targeted treatment strategies. Here, we review the main features of adaptive plasticity that are thought to underlie the spontaneous and induced recovery of function in animal models of stroke. Within this context, therapeutic interventions, used in isolation or synergistically to modulate recovery, are discussed. It is hoped that a focus on neurobiological principles and their manipulation will enhance interventional strategies to maximize therapeutic benefit. To ensure translation of these interventions into a clinical setting, a close interaction between basic and applied research is required.
机译:脑卒中后恢复依赖于在病理生理条件下改变大脑组织和功能的神经生物学变化。变化可以是适应性的(即功能恢复)或适应不良的(即功能恶化)。中风的临床前模型表现出适应性可塑性,导致功能“自发恢复”。可以通过外部因素来调节这种恢复,例如康复,药理学或其他辅助策略。但是,当前的干预措施只能有限地改善赤字,并且也存在适应不良的可能性。因此,更好地了解潜在的恢复机制对于设计更有效,更有针对性的治疗策略至关重要。在这里,我们回顾了自适应可塑性的主要特征,这些特征被认为是中风动物模型中自发和诱导功能恢复的基础。在这种情况下,讨论了单独或协同调节恢复的治疗干预措施。希望将重点放在神经生物学原理及其操纵上,以增强干预策略,以最大程度地提高治疗效果。为了确保将这些干预措施转化为临床环境,需要基础研究与应用研究之间的紧密互动。

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