Myocardial ischemia/reperfusion impairs neurogenesis and hippocampal-dependent learning and memory.

Academic Article

Abstract

  • The incidence of cognitive impairment in cardiovascular disease (CVD) patients has increased, adversely impacting quality of life and imposing a significant economic burden. Brain imaging of CVD patients has detected changes in the hippocampus, a brain region critical for normal learning and memory. However, it is not clear whether adverse cardiac events or other associated co-morbidities impair cognition. Here, using a murine model of acute myocardial ischemia/reperfusion (I/R), where the coronary artery was occluded for 30min followed by reperfusion, we tested the hypothesis that acute myocardial infarction triggers impairment in cognitive function. Two months following cardiac I/R, behavioral assessments specific for hippocampal cognitive function were performed. Mice subjected to cardiac I/R performed worse in the fear-conditioning paradigm as well as the object location memory behavioral test compared to sham-operated mice. Reactive gliosis was apparent in the hippocampal subregions CA1, CA3, and dentate gyrus 72h post-cardiac I/R as compared with sham, which was sustained two months post-cardiac I/R. Consistent with the inflammatory response, the abundance of doublecortin positive newborn neurons was decreased in the dentate gyrus 72h and 2months post-cardiac I/R as compared with sham. Therefore, we conclude that following acute myocardial infarction, rapid inflammatory responses negatively affect neurogenesis, which may underlie long-term changes in learning and memory.
  • Authors

    Published In

    Keywords

  • Cognition, Myocardial infarction, Neuroinflammation, Reactive gliosis, Animals, Cognition, Conditioning, Classical, Fear, Hippocampus, Learning, Male, Memory, Mice, Myocardial Ischemia, Myocardial Reperfusion Injury, Neurogenesis, Neurons
  • Digital Object Identifier (doi)

    Author List

  • Evonuk KS; Prabhu SD; Young ME; DeSilva TM
  • Start Page

  • 266
  • End Page

  • 273
  • Volume

  • 61