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201051 https://hdl.handle.net/2286/R.2.N.201051 http://rightsstatements.org/vocab/InC/1.0/ http://creativecommons.org/licenses/by-nc-sa/4.0 2025-05 33 pages Manzo III, Jose Lisenbee, Cayle Houtchens, Jason Barrett, The Honors College College of Health Solutions Alzheimer’s disease (AD) is a complex neurodegenerative disorder driven by genetic and epigenetic mechanisms, with increasing research efforts focused on understanding its multifactorial nature. Foundational literature on AD genetics has identified key risk factors, including mutations in APP, PSEN1, and PSEN2 for familial AD, while genone wide association studies (GWAS) have highlighted genetic variants such as APOE-ε4, TREM2, and BIN1 in late-onset AD. The integration of bioinformatics tools has advanced GWAS analyses, enabling researchers to decode gene-gene and gene-environment interactions that contribute to disease susceptibility. Physiological impacts of these interactions are profound, with environmental factors such as diet, lifestyle, and toxin exposure influencing epigenetic modifications, including DNA methylation and histone alterations, which regulate AD-related gene expression. Emerging gene therapy techniques aim to mitigate genetic and epigenetic effects through targeted interventions, including CRISPR-based editing, RNA interference, and epigenome modulation strategies. Advancing our understanding of these mechanisms is crucial for developing precision medicine approaches that could delay or prevent AD, ultimately improving cognitive health outcomes. This thesis will focus on the foundational literature on genetic and epigenetic mechanisms of AD, GWAS and advanced bioinformatic tools, and gene therapy techniques and modulating epigenetics to address AD. Alzheimer’s disease Gene Therapy Techniques Genetic Mechanisms in AD Epigenetic Mechanisms in AD Unraveling the Interplay of Epigenetic and Genetic Factors in Alzheimer's Disease