In Professor Roger Sher's lab, I work on a research project investigating the role of TDP-43 pathology in ALS. Our team focuses on whether focal induction of TDP-43 abnormalities in neurons leads to inappropriate retrotransposon expression in nearby glial cells, a process potentially linked to ALS progression. My contributions involve assisting in experiments that explore cellular interactions and protein expression within neural tissue samples. Through this work, we aim to better understand the molecular mechanisms behind ALS, with the long-term goal of identifying therapeutic targets to mitigate the spread and impact of TDP-43-related pathology in neurodegenerative diseases.
In the neurobiology lab course, we explored the physiology and neurobiology of action, examining how nerve and muscle cells generate and control movements fundamental to animal behavior. We began with experiments on nerve impulse conduction, studying how sensory information travels to the central nervous system. My contributions included investigating neural-to-muscle communication through electrical impulses that initiate muscular excitation and contraction, as well as studying the regulation of the vertebrate heartbeat.
In the Afshar Lab, our project focused on developing an optimized topical delivery system for dapsone to treat acne vulgaris. This study aimed to address the physicochemical challenges of formulating dapsone as a topical treatment by creating a hydrogel-thickened microemulsion. My contributions involved preparing microemulsions composed of dapsone (5%) with a mix of isopropyl myristate, tween 80, diethylene glycol monoethyl ether, ethanol, and water. We optimized this formulation by incorporating carbomer 940 to enhance skin permeation and evaluated properties such as droplet size, pH, conductivity, and skin permeation through rat skin. This work demonstrated a novel approach to enhancing the efficacy of dapsone treatments, potentially benefiting those affected by chronic acne.