"I applied to the Scholars program because I wanted the opportunity to work on my own research project, but to also have the guidance and support that USP offers. I plan on successfully completely my project and being able to present my findings clearly and concisely."
I am interested in biology, particularly neuroscience and potential treatments for peripheral demyelination caused by a genetic mutation.
- Florida Academic Scholars
- Collegiate Health Service Corps
- Director of the Advisory Committee Florida Alternative Breaks
- Site Leader for Winter Break 2010 UF Club Sailing Team
- Mobile Outreach Clinic, a traveling clinic that offers free healthcare to Alachua County residents Arts in Medicine at Shands Hospital, I work with patients in different wards creating art projects with them. Mentoring and tutoring elementary students
- UF English Language Institute Conversation Partner Program
Hobbies and Interests
- Dancing, sailing and reading
Pharmacological Activation of Autophagy
Pharmacological Activation of Autophagy through Rapamycin in a CMT1A Mouse Model: Mutations of peripheral myelin protein 22 (PMP22), a membrane glycoprotein expressed by Schwann cells of the peripheral nervous system can lead to disease states including Charcot-Marie-Tooth disease type 1A (CMT1A). CMT1A is the most commonly inherited neuromuscular disorder with muscle wasting and weakness due to demyelination. A spontaneous L16P mutant mouse model, the Trembler J (TrJ), contains the same point mutation as seen in human CMT1A. TrJ mice have reduced motor capabilities and a reduced percentage of intact neuromuscular junctions when age-matched to wild-type (Wt) mice. Mutant (L16P) PMP22 results in misfolded protein, which is tagged and sent to be degraded by the ubiquitin-protease system. However, there is an overload of misfolded protein, which overloads the UPS, creating aggregrates of misfolded protein. Previous studies have shown that stimulating autophagy, thus clearing protein aggregates, in TrJ mice through intermittent fasting results in improved motor capabilities. An intermittent fasting diet is not practical for human treatment, so other mechanisms to induce autophagy were studied in vitro of the TrJ mouse, including pharmacological modulation by rapamycin (RM). RM treatment results in inhibition of the mTOR pathway, which induces autophagy and leads to a reduction of poly-ubiquitinated substrates (aggregates). I am working on an in vivo study of TrJ mice by injecting RM or control solution and measuring the motor behavior through accelerating rotarod, rearing and forepaw grip strength over a six month period. I will then sacrifice the mice and through sectioning and immunocytochemistry determine the percentage of intact neuromuscular junctions. This research will show if stimulating autophagy through RM will alleviate some of the disease state phenotypes commonly seen in CMT1A. From this information, potentially, a future therapy for human CMT1A can be tested.