Barbara M. Fenner, PhD
Associate Professor of Biology
Office: Parente 302
Phone: x5727

Educational Background

Ph.D, Cellular and Molecular Pathology, University of Pittsburgh School of Medicine, 2004

B.S., Neuroscience and Psychology, Allegheny College, 1998 

Courses Taught  
Bio 213 /L Intro Cell and Molec (+lab)
Bio 224/L Biochemistry (+lab)
Bio 229G Neuroscience Techniques
Bio 314 Microbiology
Bio 221/L Anatomy and Physiology (+ lab)
Bio 336/L Advanced Cell Biology (+lab)
Bio 370 Junior Seminar
Bio 380 Neuroendocrinology
Bio 420/L Botanical Pharmacology (+lab)
Bio 456 Molecular Neuroscience
Bio 490/491 Senior Research
Core 273 Biology of Stress
Core 100 Mind, Body, Soul

Research Interests    
Research Areas: Neurobiology, in vitro models of Parkinson’s Disease, Neurodegenerative diseases, Neuron regeneration, Inflammation, Oxidative Stress, Microscopy, Cellular and Molecular Biology

Techniques used: Tissue culture, Molecular Biology, Cell biology, Microscopy

Background: We study the cellular and molecular mechanisms underlying neurodegenerative diseases, such as Parkinson’s disease (PD).  Specifically, we are interested in understanding how the immune cells of the brain (microglia) are altered in PD and how those changes lead to neuronal death.  My lab uses in vitro models of a genetic variant of PD to understand the role of inflammation and phagocytosis in the process of neurodegeneration.  We use cellular, molecular, microscopy, and quantitative techniques to investigate the different environmental factors that can contribute to brain inflammation and neuronal distress.  At some point, the combination of genetic and environmental insults reach a tipping point, leading to extensive phagocytosis and neurotoxicity of neurons in PD.  

Brain-derived neurotrophic factor is a protein that is essential for neuronal health.  This protein binds to trkB, a receptor found in the plasma membrane of neurons.  These two proteins, and the intracellular signaling, are disrupted in many neurodegenerative diseases, including PD.  Therefore, my lab also investigates how these proteins get disrupted in PD and their relevance to neuroinflammation.  If we can understand how these proteins are disrupted in PD, we can identify potential therapeutic target in for neurodegenerative diseases.  

Microglial-neuronal interactions in two-hit in vivo and in vitro models of neurodegeneration

TrkB.t1-mediated intracellular sorting and translocation of BDNF and pro-BDNF in astrocytes and microglia

Role of early-life changes in trkB.t1 and expression in later neural-circuitry development in depression and anxiety

Recent Conference Presentations 

Fenner, BM, Fenner ME (2016). Research intensive courses: An alternative to faculty mentored independent research for undergraduate students. Mol Biol Cell 27, 3947 (M67).

Fenner, BM. Reciprocal paracrine signaling between SH-SY5Y and HUVEC cells alter cytokine and growth factor secretion in an in vitro model of the blood-brain barrier. Society for Neuroscience Meeting, New Orleans, LA (2013).

Fenner, BM. Neuroendocrinology for undergraduates: Implementation of popular science literature. Society for Neuroscience Meeting, New Orleans, LA (2013).

Fenner, BM. Cellular, molecular, computational, and microscopy approaches to neurodegenerative research. Northeastern Pennsylvania Biomedical Research-in-Progress Faculty Colloquium, Wilkes-Barre PA (2013).

Fenner, BM and Fenner, ME. Function-driven creation of protein families for phylogenomic
analysis. International Conference on Intelligent Systems for Molecular Biology and European Conference on Computation Biology, Stockholm, Sweden (2009).

Fenner, BM. Undergraduate biology research at Wheeling Jesuit University. PKAL, F21 Meeting, Chicago, Illinois (2006).

Fenner, BM, Achim, CL, and Stolz, DB. TrkB facilitates the endocytic sorting of internalized
BDNF in differentiated SH-SY5Y cells. American Society for Cell Biology meeting, San Francisco, California (2005).

Selected Student-Author Proceedings and Abstracts

Perez, Alexis, Stephanie Justice-Bitner and Fenner, Barbara. Glutamate exposure causes transposition of phosphatidylserine to the outer plasma membrane in SH-SY5Y cells. 2017 Annual Meeting of the Pennsylvania Academy of Science, Indiana, PA.

Cooney, Deirdre and Fenner, Barbara. Effects of Oxidative Stress on the Heteroplasmic Regions of Mitochondrial DNA in SHSY5Y cells. 2016 Annual Meeting of the Pennsylvania Academy of Science, Doylestown, PA.

Fisher, Andrew and Fenner, Barbara. Effects of Retinol on Neuronal Phenotype, Morphology, and trkB.T1 Expression in SH-SY5Y Cells. 2016 Annual Meeting of the Pennsylvania Academy of Science, Doylestown, PA.

Runner, Kaitlyn and Fenner, Barbara. The effects of trkB.t1, independent of, on neurite morphology in the presence of BDNF. 2015 Annual Meeting of the Pennsylvania Academy of Science, Labanon Valley, PA.

Erdmann, Cassie, Kimock, Matthew, and Fenner, Barbara. The effects of Aβ25-35-induced toxicity on SH-SY5Y cells. 2015 Annual Meeting of the Pennsylvania Academy of Science, Lebanon Valley, PA.

Rutkoski, Kayla, Daniel Simpson, Mara Olenick, and Barbara Fenner. The effects of brain-derived neurotrophic factor on neuronal injury in an oxidative stress model of Amyotrophic
Lateral Sclerosis. 2013 Annual Meeting of the Pennsylvania Academy of Science, Bradford, PA.

Fenner, ME, Achim, CL, and Fenner, BM. Expression of full-length and truncated trkB in human striatum and substantia nigra neurons: Implications for Parkinson’s Disease (2014). Journal of Molecular Histology, Volume 45, Issue 3, pp 349-361.

Fenner, ME and Fenner, BM. Automating quantitative confocal microscopy analysis (2013).
Proceedings of the 12th Python in Science Conference (SciPy2013), pp. 27-33.

Fenner, BM. Truncated TrkB: Beyond a dominant negative receptor (2012). Cytokine and Growth Factor Reviews, Volume 23, Issue 1-2, pp. 15-24.

Jordan-Sciutto, KL, Fenner, BAM, Wiley, CA, and Achim, CL (2001). Response of cell cycle proteins to neurotrophin and chemokine stimulation in human neuroglia. ExperimentalNeurobiology, Volume 167, pp. 205-214.