CNUP Training Faculty

Sharyl L. Fyffe-Maricich, Ph.D.

Assistant Professor, Pediatrics

Ph.D. Baylor College of Medicine (2008)

Office: 3512 Rangos Research Center
Telephone:412-692-6400
Fax:412-692-5723
E-mail: sharyl.fyffemaricich@chp.edu
Website:

Cellular and molecular signaling processes important for central nervous system myelination and myelin repair.

Research Summary:

Sharyl Fyffe-Maricich discusses her work in myelin repair

Central nervous system (CNS) function depends critically on the effective and timely communication between neurons in distant regions of the brain and spinal cord. This communication is achieved through axonally-transmitted action potentials whose ability to be efficiently propagated over long distances relies upon myelination. The importance of myelination becomes obvious in diseases such as multiple sclerosis (MS) where autoimmune-mediated demyelination throughout the CNS results in devastating functional disability. MS is the most prevalent neurodegenerative disease in young adults, affecting more than 2 million people worldwide. Myelin sheaths can be restored by newly generated oligodendrocytes (the myelin forming cells of the CNS), although this process ultimately fails in patients with MS despite the fact that oligodendrocyte progenitor cells can be found at lesion sites. My lab is interested in understanding the molecules and signaling pathways that are essential for controlling the onset of myelination and for determining the thickness of the myelin sheaths that are generated. We are interested in learning more about these processes both during development and after demyelinating injuries in the adult. To investigate these questions we use a variety of techniques including rodent behavioral analysis, immunohistochemistry, electron microscopy, cell culture, and biochemistry to analyze various genetic mouse mutants. The ultimate goal of our work is to develop new treatment approaches for patients with MS.

Selected Publications:

Fyffe-Maricich, S.L., Schott, A., Karl, M., Krasno, J., Miller, R.H. Signaling through ERK1/2 Controls Myelin Thickness during Myelin Repair in the Adult Central Nervous System. J Neurosci. Nov 20; 33(47): 18402-18408, 2013.

R.H. Miller, S.L., Fyffe-Maricich, A.V. and Caprariello, “Animal Models for the Study of Multiple Sclerosis”, in Animal Models for the Study of Human Disease, P.M. Conn, Ed. London: Elsevier Inc., pp. 1037-1057, 2013.

*Ishii, A., *Fyffe-Maricich, S.L., Furusho, M., Miller, R.H. and Bansal, R. ERK1/ERK2 MAPK signaling is required to increase myelin thickness independent of oligodendrocyte differentiation and initiation of myelination. J Neurosci. Jun 27;32(26): 8855-64, 2012.

Fyffe-Maricich, S.L., Karlo, J.C., Landreth, G.E. and Miller, R.H. The ERK2 mitogen-activated protein kinase regulates the timing of oligodendrocyte differentiation. J Neurosci. Jan 19;31(3): 843-50, 2011.

Miller, R.H. and Fyffe-Maricich, S.L. Restoring the balance between disease and repair in Multiple Sclerosis: Insights from Mouse models. Dis Model Mech. Sep-Oct;3(9-10): 535-9, 2010.