Affiliations: [a] Department of Physiology, University of Puerto Rico School of Medicine, San Juan, PR, USA
| [b] Department of Biochemistry, University of Puerto Rico School of Medicine, San Juan, PR, USA
| [c] Department of Physiology, School of Medicine, Universidad Central del Caribe, Bayamon, PR, USA
| [d] Alzheimer’s Center at Temple, Department of Neural Sciences, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA
Correspondence:
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Correspondence to: Sabzali Javadov, MD, PhD, Department of Physiology, University of Puerto Rico School of Medicine, San Juan, PR 00936-5067, USA. Tel.: +1 787 758 2525; Fax: +1 787 753 0120; E-mail: sabzali.javadov@upr.edu.
Abstract: Background: An increasing number of experimental and clinical studies show a link between Alzheimer’s disease and heart diseases such as heart failure, ischemic heart disease, and atrial fibrillation. However, the mechanisms underlying the potential role of amyloid-β (Aβ) in the pathogenesis of cardiac dysfunction in Alzheimer’s disease remain unknown. We have recently shown the effects of Aβ1 - 40 and Aβ1 - 42 on cell viability and mitochondrial function in cardiomyocytes and coronary artery endothelial cells. Objective: In this study, we investigated the effects of Aβ1 - 40 and Aβ1 - 42 on the metabolism of cardiomyocytes and coronary artery endothelial cells. Methods: Gas chromatography-mass spectrometry was used to analyze metabolomic profiles of cardiomyocytes and coronary artery endothelial cells treated with Aβ1 - 40 and Aβ1 - 42. In addition, we determined mitochondrial respiration and lipid peroxidation in these cells. Results: We found that the metabolism of different amino acids was affected by Aβ1 - 42 in each cell type, whereas the fatty acid metabolism is consistently disrupted in both types of cells. Lipid peroxidation was significantly increased, whereas mitochondrial respiration was reduced in both cell types in response to Aβ1 - 42. Conclusion: This study revealed the disruptive effects of Aβ on lipid metabolism and mitochondria function in cardiac cells.
