Carsyn Snagg


Summer Research Description: Atrial fibrillation (AF) is an “abnormal heart rhythm characterized by rapid and irregular beating” according to the CDC. AF is the most common sustained heart arrhythmia, and increases risk of stroke and death. Currently, treatments are largely unsuccessful due to a lack of understanding of the factors that cause AF. Recently, a family was reported in which AF was linked to a mutation in the gene encoding atrial natriuretic peptide (ANP), a hormone that regulates blood volume. ANP is a protein that tends to misfold, causing it to coalesce, forming oligomers and ultimately fibrils in a specific disease-causing pattern known as amyloid. Pre-amyloid oligomers (PAOs) are currently believed to cause the brain damage that causes Alzheimer’s disease. We recently showed that the mutant ANP (mANP) implicated in familial AF, forms oligomers much more readily than wild-type ANP. In addition, we found that a mouse model of mANP contains oligomers in the atria. Therefore, given that oligomers in the brain cause cell damage, we hypothesized that oligomers are cytotoxic in atrial cardiomyocytes.