Graduate Theses and Dissertations (2019 - present)
Date of Award
12-2025
Document Type
Thesis
Degree Name
M.S.
Department
Biological Sciences
Committee Chair
Ryan S. Littlefield, Ph.D.
Abstract
During Alzheimer's disease (AD), insoluble amyloid beta (AP) peptides accumulate to form extracellular aggregates (plaques). The direct cause of neuronal dysfunction observed in AD has been broadly investigated. The amyloid hypothesis states that AP plaques are neurotoxic, but recent studies support the AP oligomer hypothesis, which states that intracellular AP (iAP) is neurotoxic. To test this hypothesis, I used CRISPR-Cas9 gene editing to generate two transgenic Caenorhabditis elegans (C. elegans) strains. I generated a strain (RSLl 11) using the rab-3 promoter to co-express GFP in neurons, which showed no gross behavioral changes but had a 50% reduced egglaying rate. RSLl 11 males also express GFP in the vas deferens, suggesting this tissue may normally express a rab-3b isoform. I further modified RSLl 11 to express either AP and a split wrmScarlet or GFP stochastically in neurons using CRE recombinase, then mated it with a strain expressing CRE recombinase under a heat shock promoter, and visualized the hybrid by confocal microscopy.
Recommended Citation
Arditi, Jean-Pierre, "Improved Model for Neurodegeneration in C. elegans" (2025). Graduate Theses and Dissertations (2019 - present). 240.
https://jagworks.southalabama.edu/theses_diss/240
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Animal Experimentation and Research Commons, Cognitive Neuroscience Commons, Cognitive Science Commons, Molecular Genetics Commons, Neurology Commons, Neurosciences Commons, Other Genetics and Genomics Commons