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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.
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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.
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