Drivers of Chronic Pathology Following Ischemic Stroke: A Descriptive Review

IF 3.6 4区 医学 Q3 CELL BIOLOGY
Grant W. Goodman, Trang H. Do, Chunfeng Tan, Rodney M. Ritzel
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Abstract

Stroke is the third leading cause of death and long-term disability in the world. Considered largely a disease of aging, its global economic and healthcare burden is expected to rise as more people survive into advanced age. With recent advances in acute stroke management, including the expansion of time windows for treatment with intravenous thrombolysis and mechanical thrombectomy, we are likely to see an increase in survival rates. It is therefore critically important to understand the complete pathophysiology of ischemic stroke, both in the acute and subacute stages and during the chronic phase in the months and years following an ischemic event. One of the most clinically relevant aspects of the chronic sequelae of stroke is its extended negative effect on cognition. Cognitive impairment may be related to the deterioration and dysfunctional reorganization of white matter seen at later timepoints after stroke, as well as ongoing progressive neurodegeneration. The vasculature of the brain also undergoes significant insult and remodeling following stroke, undergoing changes which may further contribute to chronic stroke pathology. While inflammation and the immune response are well established drivers of acute stroke pathology, the chronicity and functional role of innate and adaptive immune responses in the post-ischemic brain and in the peripheral environment remain largely uncharacterized. In this review, we summarize the current literature on post-stroke injury progression, its chronic pathological features, and the putative secondary injury mechanisms underlying the development of cognitive impairment and dementia. We present findings from clinical and experimental studies and discuss the long-term effects of ischemic stroke on both brain anatomy and functional outcome. Identifying mechanisms that occur months to years after injury could lead to treatment strategies in the chronic phase of stroke to help mitigate stroke-associated cognitive decline in patients.

Abstract Image

缺血性脑卒中后慢性病变的驱动因素:描述性综述
中风是全球第三大死亡和长期残疾原因。脑卒中主要被认为是一种老龄化疾病,随着越来越多的人步入晚年,预计脑卒中对全球经济和医疗造成的负担将会增加。随着急性中风治疗的最新进展,包括静脉溶栓和机械取栓术治疗时间窗口的扩大,我们很可能会看到存活率的提高。因此,了解缺血性卒中的完整病理生理学至关重要,包括急性和亚急性阶段以及缺血性事件后数月和数年的慢性阶段。中风慢性后遗症与临床最相关的方面之一是其对认知的长期负面影响。认知障碍可能与中风后晚期出现的白质退化和功能障碍重组以及持续的进行性神经变性有关。脑血管在中风后也会受到严重损伤和重塑,其变化可能会进一步导致慢性中风病理。虽然炎症和免疫反应是急性中风病理的既定驱动因素,但缺血后大脑和外周环境中先天性和适应性免疫反应的慢性化和功能性作用在很大程度上仍未得到描述。在这篇综述中,我们总结了目前有关脑卒中后损伤进展、其慢性病理特征以及认知障碍和痴呆发生的潜在继发性损伤机制的文献。我们介绍了临床和实验研究的结果,并讨论了缺血性中风对大脑解剖和功能结果的长期影响。确定损伤后数月至数年内发生的机制可为中风慢性期的治疗策略提供依据,帮助减轻中风相关患者的认知功能下降。
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来源期刊
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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