Survivability of Transgenic Zebrafish (Danio rerio) with the ApoE4 1-151 Fragment
Additional Funding Sources
The Bridges to Baccalaureate program is supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award No. R25GM123927. This project was further supported by the Center of Excellence in Biomedical Research through the Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under Grant Nos. P20GM109095 and P20GM103408 and the National Science Foundation S-STEM Gateway Scholarships in Biological Sciences under Grant Award No. DUE-1644233. Additional support was received from the National Institutes of Health Grant No. 2R15AG042781-02A1 and the KO Alzheimer's Dementia Foundation in Boise, ID. We also acknowledge support from an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under Grant Nos. P20GM103408 and P20GM109095.
Presentation Date
7-2022
Abstract
Alzheimer’s is a fatal disorder that causes neuronal cell loss in brain regions crucial for thinking and memory. While the inheritance risk of the APOE4 allele has been well documented, the molecular basis for how ApoE4 leads to enhanced dementia risk is not yet understood. Previous work in the Rohn lab has shown that proteolysis and formation of an amino-terminal fragment (ApoE41-151) may contribute to toxicity in vitro. Using Zebrafish as an in vivo model organism, mutants expressing this fragment were generated to examine any deleterious effects. As an initial approach, this study seeks to determine the lethality of these transgenic F1 mosaic zebrafish.
Survivability of Transgenic Zebrafish (Danio rerio) with the ApoE4 1-151 Fragment
Alzheimer’s is a fatal disorder that causes neuronal cell loss in brain regions crucial for thinking and memory. While the inheritance risk of the APOE4 allele has been well documented, the molecular basis for how ApoE4 leads to enhanced dementia risk is not yet understood. Previous work in the Rohn lab has shown that proteolysis and formation of an amino-terminal fragment (ApoE41-151) may contribute to toxicity in vitro. Using Zebrafish as an in vivo model organism, mutants expressing this fragment were generated to examine any deleterious effects. As an initial approach, this study seeks to determine the lethality of these transgenic F1 mosaic zebrafish.