Senior Honors Theses

Publication Date

Spring 5-2014

School

School of Health Sciences

Major

Biology: Pre-Med

Keywords

Alzheimer's Disease, Epigenetics, Methylation, Amyloid Beta

Disciplines

Genetic Processes | Nervous System Diseases

Abstract

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.

Comments

A portion of the methods and results in this thesis were also published in this article:

Journal of Alzheimer’s Disease, Volume 38, Number 4. Noor Taher, Courtney McKenzie, Rebecca Garrett, Matthew Baker, Nena Fox, and Gary D. Isaacs. “Amyloid-B Alters the DNA Methylation Status of Cell-fate Genes in an Alzheimer’s Disease Model.” Copyright 2013.

Reproduced here with permission from IOS Press.

IOS Press: www.iospress.nl

Journal of Alzheimer’s Disease: http://www.iospress.nl/journal/journal-of-alzheimers-disease/.

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