Publication Date

Spring 2026

Degree Type

Master's Project

Degree Name

Master of Science in Bioinformatics (MSBI)

Department

Computer Science

First Advisor

Dr. Leonard Wesley

Second Advisor

Dr. Philip Heller

Third Advisor

Dr. Cleber Ouverney

Keywords

Amyloid-Beta, Tau, Alzheimer's Disease, epigenetics, glutathione, plaque buildup

Abstract

Alzheimer’s disease (AD) has been interpreted as a profuse buildup of the proteins beta amyloid (Aβ) and tau. Recent studies have reported that 30%-40% of cognitively normal individuals display high levels of Aβ and tau so they are not substantial enough to diagnose or explain all occurrences of AD. Glutathione is an antioxidant in the brain that works to neutralize reactive oxygen species. The depletion of glutathione has been linked to neurodegeneration. This research involves finding potential biomarkers for AD that are epigenetically associated with the glutathione pathway that may allow for the onset and progression of AD. The GWAS data of 76 Alzheimer’s Disease Neuroimaging Initiative (ADNI) control subjects to see if there are any significant single nucleotide polymorphisms (SNPs) interacting with glutathione that can be a potential distinguishing factor between the two groups. Chi-square and hypothesis tests were carried out to identify possible epigenetic relationships between the SNPs and glutathione. The NCBI Variation Viewer and database was used to identify interactions between mutated genes and the glutathione gene. There were inconclusive results due to lack of ADNI GWAS data.

Download

Available for download on Saturday, May 15, 2027

Share

COinS