Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States; Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States.
Semin Immunol. 2022 Jan;59:101600. doi: 10.1016/j.smim.2022.101600. Epub 2022 Feb 25.
Myocardial infarction is associated with increased risk for vascular dementia. In both myocardial infarction and vascular dementia, there is evidence that elevated inflammatory biomarkers are associated with worsened clinical outcomes. Myocardial infarction leads to a systemic inflammatory response, which may contribute to recruitment or activation of myeloid cells, including monocytes, microglia, and perivascular macrophages, within the central nervous system. However, our understanding of the causative roles for these cells linking cardiac injury to the development and progression of dementia is incomplete. Herein, we provide an overview of inflammatory cellular and molecular links between myocardial infarction and vascular dementia and discuss strategies to resolve inflammation after myocardial infarction to limit neurovascular injury.
心肌梗死与血管性痴呆的风险增加有关。在心肌梗死和血管性痴呆中，有证据表明升高的炎症生物标志物与临床结局恶化相关。心肌梗死导致全身炎症反应，这可能导致中枢神经系统内髓样细胞（包括单核细胞、小胶质细胞和血管周巨噬细胞）的募集或激活。然而，我们对这些细胞将心脏损伤与痴呆的发生和进展联系起来的因果作用的理解并不完整。本文概述了心肌梗死与血管性痴呆之间炎症细胞和分子的联系，并讨论了在心肌梗死后解决炎症的策略，以限制神经血管损伤。
