Abstract Title

DNA Methylation as a Potential Molecular Mechanism Underlying Exercise-Induced Rescue of Alzheimer’s Disease Memory Deficit

Additional Funding Sources

This project is supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award No. R25GM123927.

Abstract

Alzheimer’s disease is a neurodegenerative disorder that affects people 65 and older. This disease is the sixth leading cause of death in the United States and currently has no cure. We explore the potential that epigenetics plays in finding the connection between exercise and slowing down the progression of AD. Using a transgenic rat model allowed us to study the effects of gene regulation through DNA methylation when exposed to exercise.

We found Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1a) as a candidate gene of interest that may exhibit hypomethylation within the gene promoter after exercise. By designing two sets of primers, we aim to target CpG sites within the promoter region of PGC1a and hope to amplify during PCR using our parent study samples. Targeted pyrosequencing will follow for quantification of methylation at specific CpG sites in the promoter, identifying any significant differences that would allow for further experimentation.

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DNA Methylation as a Potential Molecular Mechanism Underlying Exercise-Induced Rescue of Alzheimer’s Disease Memory Deficit

Alzheimer’s disease is a neurodegenerative disorder that affects people 65 and older. This disease is the sixth leading cause of death in the United States and currently has no cure. We explore the potential that epigenetics plays in finding the connection between exercise and slowing down the progression of AD. Using a transgenic rat model allowed us to study the effects of gene regulation through DNA methylation when exposed to exercise.

We found Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1a) as a candidate gene of interest that may exhibit hypomethylation within the gene promoter after exercise. By designing two sets of primers, we aim to target CpG sites within the promoter region of PGC1a and hope to amplify during PCR using our parent study samples. Targeted pyrosequencing will follow for quantification of methylation at specific CpG sites in the promoter, identifying any significant differences that would allow for further experimentation.