School of Health Sciences
Alzheimer's Disease, Epigenetics, Methylation, Amyloid Beta
Genetic Processes | Nervous System Diseases
Baker, Matthew S., "Epigenetic Remodeling in an IMR-32 Cell Line and Transgenic Mouse Model of Alzheimer's Disease" (2014). Senior Honors Theses. 464.
The pathological features of Alzheimer’s disease (AD) have been researched and documented extensively, however the causes of these features are still unknown. The following studies sought to determine if epigenetic methylation alterations contribute to AD. Two studies were sequentially carried out, first using an IMR-32 model and then using a transgenic mouse model overexpressing beta-amyloid. A few assay and confirmation methods were carried out to determine the promoter regions in disease state models undergoing drastic change, and the genes linked to these promoter regions were analyzed to determine significant gene ontology being altered by this epigenetic modification. This data was further assessed in the transgenic mouse study by determining expression levels and transcription factor enrichment in the genes experiencing significant promoter methylation alterations. Both studies provided data supporting the idea that epigenetic methylation alterations are linked to genes having ontological functions associated with AD pathology. This conclusion supports the theory that epigenetics contributes to the development of AD.