Alzheimer’s Disease is a deadly neurodegenerative disease that is increasing in prevalence as the population is aging and poses a significant health and economic threat. Most cases emerge from a combination of genetic and environmental factors, which is known as sporadic, but AD can also be familial. Genes of interest include the APP gene, presenilin 1 and 2, APOE genes, and genes on chromosomes 9, 10, and 12. Each of these genes in some way regulate Aβ production and degradation, so mutations lead to production of Aβ beyond what can be controlled. This overgrowth of Aβ forms plaques on neurons that lead to neuronal degradation. Aβ works with tau to form plaques and neurofibrillary tangles (NFTs) that further contribute to neurodegeneration. Aside from genetic factors, inflammation plays a significant role in neurodegeneration and AD pathology. Plaques and NFTs can trigger an autotoxic response in the brain that releases pro-inflammatory cytokines that inadvertently damage neurons. Systemic inflammation from outside of the brain can also lead to an increase in cytokines that eventually travel and affect the brain environment, such as in periodontitis. Oral infections can cause chronic inflammation of the oral structures, and this infection can become systemic, allowing bacteria and cytokines to reach the brain and cause neurodegenerative effects. For this reason, I propose a study of the effect of P. gingivalis on neuroinflammation, cytotoxicity, and Aβ production in neuronal cells. Information gathered from this experiment will aid in understanding the connection between oral health and AD and may give insight into future therapeutic approaches.