Department of Pharmacology, Bengbu Medical College, Bengbu, Anhui, China.
Department of Neurology, University of Pittsburgh, S-598 South Biomedical Science Tower, 3500 Terrace St., Pittsburgh, PA, 15213, USA.
Transl Stroke Res. 2018 Jun;9(3):238-250. doi: 10.1007/s12975-017-0570-2. Epub 2017 Oct 2.
Newly emerged evidence reveals that ischemic stroke and Alzheimer's disease (AD) share pathophysiological changes in brain tissue including hypoperfusion, oxidative stress, immune exhaustion, and inflammation. A mechanistic link between hypoperfusion and amyloid β accumulation can lead to cell damage as well as to motor and cognitive deficits. This review will discuss decreased cerebral perfusion and other related pathophysiological changes common to both ischemic stroke and AD, such as vascular damages, cerebral blood flow alteration, abnormal expression of amyloid β and tau proteins, as well as behavioral and cognitive deficits. Furthermore, this review highlights current treatment options and potential therapeutic targets that warrant further investigation.
新出现的证据表明,缺血性脑卒中与阿尔茨海默病(AD)在脑组织中存在共同的病理生理改变,包括低灌注、氧化应激、免疫耗竭和炎症。低灌注与β-淀粉样蛋白(Aβ)聚集之间的机制联系可导致细胞损伤,以及运动和认知功能缺陷。本综述将讨论缺血性脑卒中与 AD 共有的脑灌注减少和其他相关病理生理改变,如血管损伤、脑血流改变、Aβ和tau 蛋白的异常表达,以及行为和认知缺陷。此外,本综述还强调了目前的治疗选择和潜在的治疗靶点,这些都需要进一步研究。