Mentor: Dr. Lucia Notterpek
College of Agricultural and Life Sciences
"I applied to the University Scholars Program to become more involved with research and gain the opportunity to work more independently in the lab. Through my current and future work in the University Scholars Program, I hope to develop practical research skills and garner a deep understanding of the research process that will undoubtedly carry over to a career in medicine. Among many other benefits of the University Scholars Program, the ability to present my research at the Undergraduate Research Conference is exciting and will motivate me to learn as much as possible during my time with the program."
Applied Physiology and Kinesiology
- Neuromuscular Junctions
UF Presidential Platinum Scholarship
Dr. Norma M. Leavitt Scholarship
Sigma Phi Epsilon Educational Foundation Scholarship
Florida Bright Futures
- Florida Diabetes Camp
- Footprints Buddy and Support Program
- Shands Hospital
Hobbies and Interests
- Acoustic Guitar, Vocals
Assessing the Effects of Rapamycin on Neuromuscular function in CMT1A Mice
Charcot-Marie-Tooth Disease type 1A (CMT1A) is a demyelinating peripheral neuropathy characterized by reduced nerve conduction velocity, decline in muscle strength, and progressive muscle atrophy. Caused by mis-expression of the gene coding for peripheral myelin protein 22 (PMP22), CMT1A can be studied in the TrJ mouse, which has a L16P mutation in PMP22. These mice exhibit the morphological and physiological traits of humans with the disease. Prior work in the Notterpek lab has shown altered trafficking of the PMP22 in CMT1A mice, affecting protein homeostasis leading to aggregation (Fortun et al., 2007). An intermittent fasting (IF) diet intervention study was performed, and showed that activation of autophagy improved the neuropathic phenotype of affected mice (Madorsky et al., 2009). Therefore, recent studies have focused on using rapamycin, an FDA approved drug, to activate autophagy. Rapamycin has already been shown to induce autophagy and improve myelination in vitro (Rangaraju et al., 2010). I hypothesize that rapamycin will have a positive effect on the neuropathic phenotype in TrJ mice. My hypothesis can be tested by examining locomotor performance, peripheral nerve morphology and neuromuscular junction integrity in CMT1A mice fed rapamycin or placebo. Starting at 2-4 months, mice will be fed a rapamycin-enriched diet for 3 months. At the end of 5-7 months, nerves and muscles will be collected for analysis. This animal use protocol is approved by IACUC and is being used by the Notterpek lab.