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Myocardial ischemia/reperfusion impairs neurogenesis and hippocampal-dependent learning and memory
Kirsten S Evonuk1, Sumanth D Prabhu2, Martin E Young2
1Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, United States; Department of Physical Medicine Rehabilitation, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Insights
Acute myocardial infarction in mice impaired cognitive function and memory. This cardiac event triggered brain inflammation and reduced new neuron growth in the hippocampus, leading to long-term learning deficits.
Area of Science:
- Neuroscience
- Cardiology
- Pathology
Background:
- Cardiovascular disease (CVD) is linked to cognitive impairment, affecting patient quality of life and healthcare costs.
- Brain imaging in CVD patients reveals hippocampal changes, but the causal link between cardiac events and cognitive decline remains unclear.
Purpose of the Study:
- To investigate whether acute myocardial infarction triggers cognitive impairment.
- To explore the underlying mechanisms, including neuroinflammation and neurogenesis, in a murine model.
Main Methods:
- A murine model of acute myocardial ischemia/reperfusion (I/R) was used, involving coronary artery occlusion followed by reperfusion.
- Cognitive function was assessed using fear-conditioning and object location memory tests two months post-I/R.
- Hippocampal changes, including reactive gliosis and neurogenesis, were examined 72 hours and two months after cardiac I/R.
Main Results:
- Mice subjected to cardiac I/R exhibited significant deficits in hippocampal-dependent cognitive tasks compared to sham-operated controls.
- Reactive gliosis was observed in key hippocampal subregions (CA1, CA3, dentate gyrus) post-I/R.
- A decrease in doublecortin-positive newborn neurons was noted in the dentate gyrus at both 72 hours and two months post-I/R.
Conclusions:
- Acute myocardial infarction rapidly induces inflammatory responses in the brain.
- These inflammatory changes negatively impact hippocampal neurogenesis.
- Impaired neurogenesis following myocardial infarction may be the mechanism underlying long-term cognitive deficits in learning and memory.
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.
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