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缺血性脑卒中后的痴呆:从分子生物标志物到治疗选择。

Dementia after Ischemic Stroke, from Molecular Biomarkers to Therapeutic Options.

机构信息

Department of Neurology, Stony Brook University Hospital, Stony Brook, NY 11794, USA.

Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA.

出版信息

Int J Mol Sci. 2024 Jul 16;25(14):7772. doi: 10.3390/ijms25147772.

Abstract

Ischemic stroke is a leading cause of disability worldwide. While much of post-stroke recovery is focused on physical rehabilitation, post-stroke dementia (PSD) is also a significant contributor to poor functional outcomes. Predictive tools to identify stroke survivors at risk for the development of PSD are limited to brief screening cognitive tests. Emerging biochemical, genetic, and neuroimaging biomarkers are being investigated in an effort to unveil better indicators of PSD. Additionally, acetylcholinesterase inhibitors, NMDA receptor antagonists, dopamine receptor agonists, antidepressants, and cognitive rehabilitation are current therapeutic options for PSD. Focusing on the chronic sequelae of stroke that impair neuroplasticity highlights the need for continued investigative trials to better assess functional outcomes in treatments targeted for PSD.

摘要

缺血性脑卒中是全球范围内导致残疾的主要原因。虽然脑卒中后康复主要集中在身体康复方面,但脑卒中后痴呆(PSD)也是导致功能预后不良的重要因素。用于识别有 PSD 发展风险的脑卒中幸存者的预测工具仅限于简短的筛查认知测试。目前正在研究新兴的生化、遗传和神经影像学生物标志物,以试图揭示更好的 PSD 指标。此外,乙酰胆碱酯酶抑制剂、NMDA 受体拮抗剂、多巴胺受体激动剂、抗抑郁药和认知康复是 PSD 的当前治疗选择。关注脑卒中后损害神经可塑性的慢性后遗症,突出了需要继续进行试验研究,以更好地评估针对 PSD 的治疗的功能预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe9/11276729/6c3c496e1b92/ijms-25-07772-g001.jpg

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