Date of Award
Master of Science (MS)
School of Biological Sciences
Nathan N.T.M Mortimer
Alzheimer’s Disease (AD) is a neurodegenerative disease characterized by severe memory decline and cognitive impairments. In AD patients’ brains, aggregates of amyloid beta (Aβ) peptides, called amyloid plaques, are hypothesized to trigger innate immune responses that contribute to AD pathogenesis. Interestingly, recent studies demonstrated that an increased level of Aβ protected the host against pathogen infections. Using Drosophila as a model organism, our preliminary data showed that the loss of the Drosophila APP homolog, APPL, led to immune deficits against parasite infection, and that overexpression of Drosophila Aβ produced an inflammatory phenotype. These findings suggested that Aβ might be required for a successful immune response. Additionally, we produced flies that develop different levels of Aβ aggregation and examine the inflammation responses of these flies during a pathogen infection. We also optimized fly cognition assay to examine the cognitive functions of the Aβ-expressing flies. Our data suggested that there was a correlation between Aβ aggregation and inflammatory responses, and that Aβ-mediated inflammation was associated with cognitive defects. This study helped us to gain a deeper insight on how innate immunity and infection contribute to the development of AD.
Le, Nguyen, "Investigating the Role of Amyloid Beta Peptides in Inflammation and Alzheimer’s Disease Pathogenesis" (2022). Theses and Dissertations. 1607.