Mentor
Dr. John Starbuck
Abstract
Down syndrome (DS) is caused by the trisomy 21 genetic disorder, which produces a unique craniofacial phenotype. The purpose of this research is to better understand how Epigallocatechin-3-gallate (ECGC) influences the development of DS craniofacial phenotypes. Ts65Dn DS mouse models have been genetically modified to have 3 copies of numerous genes found on human chromosome 21, including DYRK1A, which plays a role in bone and brain development. EGCG is a known inhibitor of Dyrk1a activity. For this study, pregnant Ts65Dn mice were treated with 200 mg/kg of ECGC twice daily on days 7 and 8 of pregnancy. It was hypothesized that EGCG treatment will reduce Dyrk1a overexpression during development resulting in a measurable improvement in craniofacial morphology. To test this hypothesis, three mouse samples were analyzed: Ts65Dn, Ts65Dn + EGCG, and euploid. Skulls were imaged using high-resolution μCT at 6 weeks after birth. Anatomical landmark coordinates were measured from μCT images using Amira software. Euclidean Distance Matrix Analysis was used to assess craniofacial shape variation among samples. Results show that EGCG improves craniofacial morphology in treated Ts65Dn mice relative to untreated baselines, but improvements vary by region for the cranial vault, face, base, and mandible. Being able to understand how EGCG influences craniofacial development on a trisomic background is the first step in finding a way to improve phenotypic development to potentially avoid health issues of the craniofacial complex associated with DS. These results suggest that EGCG could be a useful therapeutic option.
Recommended Citation
Santana, Nicole
(2019)
"The Impact of Epigallocatechin-3-Gallate (EGCG) on Ts65Dn Down Syndrome Mouse Models,"
The Pegasus Review: UCF Undergraduate Research Journal: Vol. 10:
Iss.
2, Article 2.
Available at:
https://stars.library.ucf.edu/urj/vol10/iss2/2
