Current advisor: Erik S. Musiek, MD, PhD
Undergraduate university: Washington University
I worked in the lab of Dr. Gregory Wu investigating the role of a specific calcium channel in the pathophysiology of a mouse model of multiple sclerosis (MS). This channel is highly expressed on microglia, the tissue-resident macrophages of the central nervous system (CNS). Microglial activation exacerbates the inflammatory demyelination characteristic of MS, and calcium flux through this channel polarizes the microglia into a pro-inflammatory phenotype. Previous studies have shown that pharmacological inhibition of this channel attenuates the microglial activation and decreases the pathology in various demyelination models. My specific project was helping to develop a plan to completely and specifically ablate this channel in microglia using an inducible Cre recombinase system and to create ways to analyze its pathology using various immunohistochemical and gene transcription based methods. Furthermore, we sought to characterize whether the microglia change their expression profile upon ablation of this channel and were planning to use flow cytometry, RT-qPCR, and calcium flux imaging to analyze any phenotypic shifts.
lt of non-circadian molecular signaling disruption or from arrhythmicity of the circadian system.
Basak JM, Ferreiro A, Cohen LS, Sheehan PW, Nadarajah CJ, Kanan MF, Sukhum KV, Dantas G, Musiek E. 2021 Bacterial sepsis increases hippocampal fibrillar amyloid plaque load and neuroinflammation in a mouse model of Alzheimer’s disease. Neurobiol Dis, 152():105292.