Amyloid Beta Peptide Plays an Immune Role in Alzheimer’s Disease Pathogenesis
Authors: Nguyen Le; Ashley Waring; Emma Hartness; Nathan Mortimer
Affiliation: Illinois State University, Normal, IL
Keywords: c. innate immunity; a. neural degeneration
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 have demonstrated that an increased level of Aβ protects the host against pathogen infections. Using Drosophila as a model organism, we find that the loss of the Drosophila APP homolog, APPL, leads to immune deficits against parasite infection, and that overexpression of Drosophila Aβ produces an inflammatory phenotype. These findings suggest that Aβ might be required for a successful immune response. We additionally aim to examine whether there is a correlation between Aβ aggregation and inflammatory responses and whether Aβ-mediated inflammation is associated with cognitive defects. We will produce flies that develop different levels of Aβ aggregation and examine the inflammation responses of these flies during a pathogen infection. In addition, a fly oviposition assay will be used to examine the cognitive functions of the Aβ-expressing flies. This study will help to shed light on how innate immunity and infection contribute to the development of AD.