Regina C. Armstrong, Ph.D.

Regina C. Armstrong, Ph.D.


Name: Regina C. Armstrong, Ph.D.

Department of Primary Appointment: Anatomy, Physiology & Genetics
Position: USU Faculty
Title: Professor

Affiliated Departments: Molecular & Cell Biology, Neuroscience

Research Interests:
Molecular and cellular mechanisms of glial cell development and regeneration

Email: (link sends e-mail)
Office Phone: (301) 295-9365

Department Website
PubMed Listing


Ph.D., University of North Carolina, 1987


Cellular and Molecular Mechanisms of Glial Cell

Dr. Armstrong's current research activities focus on the cellular and molecular mechanisms of 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 has studied the growth factors regulating the proliferation and migration of oligodendrocytes prior to myelin formation. Current experiments examine the differentiation of precursors of oligodendrocytes into mature oligodendrocytes, which express myelin-specific genes. This work is identifying proteins which bind to DNA and control transcription of genes expressed only in myelin-forming 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 identify factors from lesioned areas which 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 interesting 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 issues.