Overview

My lab studies basic subcellular mechanisms that govern neuroinflammation and cell death in neurodegenerative disorders, with a focus on mitochondria, the primary energy-generating organelles of the cell. Past investigations have centered on two key pathways of injury, caspase-dependent apoptotic cell death regulated by Bcl-2 family proteins and caspase-independent cell death mediated by calcium overload and mitochondrial dysfunction.

Current projects focus on the role of mitochondrial structural and functional remodeling in inflammatory microglial activation, how microglial activation exacerbates neuronal injury through nitric oxide production, and how oxygen availability influences the mechanisms of injury. The lab has pioneered the development of novel applications of Seahorse Extracellular Flux Technology, such as real-time assessment of mitochondrial respiration within permeabilized primary neurons and from whole brain tissue slices, expanding the ways in which mitochondrial function can be studied in cells of the central nervous system. The lab is also one of the few in the world conducting real-time bioenergetic measurements and live cell imaging experiments at brain physiological oxygen (15-40 mm Hg, 2-5% oxygen). The ultimate goal is to establish mitochondrial bioenergetics as a druggable target by taking rational, mechanism-based approaches to neuroprotective therapy.

Team Members:

Hyehyun Hwang -Research Assistant
Naibo Zhang -Ph.D. Student Neuroscience Program
Ryan Mayers -Ph.D. Student Neuroscience Program
Daniel Freeman -Ph.D. Student Neuroscience Program
Nathan Tran- Lab Helper- Volunteer
Shahana Wilson -Lab Helper P/T
Michele Robinson -Program Specialist

Research Interests:

Limiting damage to mitochondria, the primary energy-generating organelles of the cell, is crucial for neuroprotection. My laboratory studies basic subcellular mechanisms that govern neuroinflammation and cell death in neurodegenerative disorders, with a focus on mitochondrial bioenergetics. My active projects study the roles of mitochondrial structural and functional remodeling in pro-inflammatory microglial activation, how this neuroinflammatory response exacerbates neuronal injury, and translational strategies for targeting metabolism to promote brain recovery following traumatic brain injury, neonatal hypoxic-ischemic encephalopathy and in Alzheimer’s disease-related dementias. We have pioneered the development and implementation of two novel applications of Seahorse Bioscience Extracellular Flux Technology, a real-time assessment of mitochondrial respiration within permeabilized brain cells and from whole brain tissue slices, expanding how mitochondrial function can be studied in cells of the central nervous system. 

Publications:

Samaddar S, Rolandelli A, O'Neal AJ, Laukaitis-Yousey HJ, Marnin L, Singh N, Wang X, Butler LR, Rangghran P, Kitsou C, Cabrera Paz FE, Valencia L, R Ferraz C, Munderloh UG, Khoo B, Cull B, Rosche KL, Shaw DK, Oliver J, Narasimhan S, Fikrig E, Pal U, Fiskum GM, Polster BM, Pedra JHF.Nat Microbiol. (2024). Sep;9(9):2278-2291. doi: 10.1038/s41564-024-01756-0. Epub 2024 Jul 12.PMID: 38997520

Walker, R. V., Yao, Q., Xu, H., Maranto, A., Swaney, K. F., Ramachandran, S., Li, R., Cassina, L., Polster, B. M., Outeda, P., Boletta, A., Watnick, T., & Qian, F. (2023). Fibrocystin/Polyductin releases a C-terminal fragment that translocates into mitochondria and suppresses cystogenesis. Nature communications, 14(1), 6513. https://doi.org/10.1038/s41467-023-42196-4. PMID: 37845212

Interests

Subcellular mechanisms that govern neuroinflammation and cell death in neurodegenerative disorders.

Please see Dr. Polster's faculty profile for a complete list of his publications.

You can also see his publications on PubMed.

Contact

Office: (410) 706-3418
Email: bpolster@som.umaryland.edu