Date of Submission
Spring 2014
Academic Programs and Concentrations
Biology
Project Advisor 1
Michael Tibbetts
Abstract/Artist's Statement
Current models suggest that Alzheimer’s disease is caused by the self-aggregation of Aβ peptide fragments in the brain, resulting from the cleavage of Amyloid Precursor Protein (APP). In humans, α-secretase proteolytically cleaves APP precluding the formation of Aβ, thus inhibiting Alzheimer’s disease. Zebrafish was shown to posses a homolog to the human α-secretase, ADAM10a. This study shows that ADAM10a is crucial for embryogenesis. My results show that knocking down ADAM10a leads to mortality during gastrulation. In addition, ADAM10a knockdown leads to a decrease in the number and length of axons and dendrites, consistent with an increase in neuronal apoptosis. I propose zebrafish ADAM10a as a potential target to study the role of Aβ peptides in Alzheimer’s disease pathogenicity.
Open Access Agreement
On-Campus only
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
Recommended Citation
Blanco, Ismary C., "Zebrafish as a model organism for studying Alzheimer's disease–focusing on the role of ADAM10a" (2014). Senior Projects Spring 2014. 25.
https://digitalcommons.bard.edu/senproj_s2014/25
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