Beta-Amyloid Instigates Dysfunction of Mitochondria in Cardiac Cells

Alzheimer’s disease (AD) includes the formation of extracellular deposits comprising aggregated β-amyloid (Aβ) fibers associated with oxidative stress, inflammation, mitochondrial abnormalities, and neuronal loss. There is an associative link between AD and cardiac diseases; however, the mechanisms underlying the potential role of AD, particularly Aβ in cardiac cells, remain unknown. Here, we investigated the role of mitochondria in mediating the effects of Aβ(1-40) and Aβ(1-42) in cultured cardiomyocytes and primary coronary endothelial cells. Our results demonstrated that Aβ(1-40) and Aβ(1-42) are differently accumulated in cardiomyocytes and coronary endothelial cells. Aβ(1-42) had more adverse effects than Aβ(1-40) on cell viability and mitochondrial function in both types of cells. Mitochondrial and cellular ROS were significantly increased, whereas mitochondrial membrane potential and calcium retention capacity decreased in both types of cells in response to Aβ(1-42). Mitochondrial dysfunction induced by Aβ was associated with apoptosis of the cells. The effects of Aβ(1-42) on mitochondria and cell death were more evident in coronary endothelial cells. In addition, Aβ(1-40) and Aβ(1-42) significantly increased Ca(2+) -induced swelling in mitochondria isolated from the intact rat hearts. In conclusion, this study demonstrates the toxic effects of Aβ on cell survival and mitochondria function in cardiac cells.