PRIMARY FACULTY

Regina Armstrong, Ph.D.
Professor
Anatomy, Physiology, & Genetics
 
4301 Jones Bridge Road
Bethesda MD 20814
Office: 301-295-3205
Fax: 301-295-1996
rarmstrong@usuhs.mil

Developmental abnormalities and pathological processes involving glial cells can cause severe neurological dysfunction. Dr. Armstrong's current research activities focus on the cellular and molecular mechanisms that regulate glial cell development and regeneration. During development, one glial cell type, the oligodendrocyte, forms myelin which ensheaths axons to enable efficient neurotransmission in the CNS. Dr. Armstrong's lab group studies the growth factors and transcription factors that regulate the proliferation, migration, and differentiation of neural progenitor cells in development. Current experiments examine the role of fibroblast growth factor as an inhibitor of differentiation of precursors of oligodendrocytes into mature oligodendrocytes, and the role of platelet-derived growth factor in stimulating proliferation and migration of the progenitor cells. The proliferation, migration, and differentiation of oligodendrocytes are also being studied in adult animals after experimental myelin damage, or demyelination. Demyelination causes neurological dysfunction in several human diseases, the most common being multiple sclerosis. In multiple sclerosis myelin repair, or remyelination, is insufficient and recovery of function is incomplete. In the experimental model studied, demyelinated areas, with oligodendrocyte and myelin loss, are efficiently remyelinated. Dr. Armstrong is attempting to distinguish the roles of specific growth factors from lesioned areas that can induce cells around a lesion to proliferate and/or migrate into the lesion, and express myelin-specific genes, as required for myelination. It will be important to determine whether factors which control these processes during development will have the same roles in adult tissue during remyelination, and whether factors which are active in rodent experimental models of demyelination can also promote remyelination in human diseased tissues.

Selected Publications

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