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A role for hypertrophic astrocytes and astrocyte precursors in a case of rapidly progressive multiple sclerosis

Department of Neurology, University of Tennessee Health Sciences Center, Memphis, TN, USA, Center for the Neurobiology of Brain Disease, University of Tennessee Health Sciences Center, Memphis, TN, USA, ymorcos{at}utmem.edu

Sang Min Lee

Department of Neurology, University of Tennessee Health Sciences Center, Memphis, TN, USA, Center for the Neurobiology of Brain Disease, University of Tennessee Health Sciences Center, Memphis, TN, USA

Michael C Levin

Department of Neurology, University of Tennessee Health Sciences Center, Memphis, TN, USA, Center for the Neurobiology of Brain Disease, University of Tennessee Health Sciences Center, Memphis, TN, USA, Research Service, Veterans Affairs Medical Center, Memphis, TN, USA

The purpose of this study was to examine the roles played by astrocytes in a case of rapidly progressive multiple sclerosis (MS). Within early-active and active lesions, hypertrophic astrocytes played an important role in lesion patho logy through the phagocytosis of myelin and axonal debris and through the internalization of other glial cells, including astrocytes. In addition to this critical role, hypertrophic astrocytes, in areas that lack significant inflammation (within the adjacent normal appearing white matter and within late remyelinating lesions) were found to be active in myelin and axonal debris phagocytosis with no evidence of cellular internalization. Hypertrophic astrocytes therefore not only play an important role in the patho genesis of MS lesions but also exert a continued deleterio us effect upon tissue in the absence of significant inflammation. In addition, we found evidence for a significant population of vimentin-positive, glial fibrillary acidic protein (GFA P)-negative, bipolar, astrocyte precursors within the late remyelinating lesions. Their significance is not known but a possible role may include their participatio n in the successful remyelination of the lesion.

Key Words: Axon • demyelination • lesion • myelin • plaque • remyelination

Multiple Sclerosis, Vol. 9, No. 4, 332-341 (2003)
DOI: 10.1191/1352458503ms931oa


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