GFAP and Astrogliosis

Authors

  • Lawrence F. Eng,

    Corresponding author
    1. Pathology Research, Veterans Affairs Medical Center, Palo Alto, CA 94304, U.S.A.
    2. Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, U.S.A.
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  • Roopa S. Ghirnikar

    1. Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, U.S.A.
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Pathology Research (113R), Veterans Affairs Medical Center, 3801 Miranda Avenue, Palo Alto, CA 94304, U.S.A. Tel. +1 (415) 493 5000 ext. 5758; Fax +1 (415) 725 7023

Abstract

One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species. The astroglial response occurs rapidly and can be detected within one hour of a focal mechanical trauma (Mucke et al., 1991). Prominent reactive astrogliosis is seen; in AIDS dementia; a variety of other viral infections; prion associated spongiform encephalopathies; inflammatory demyelinating diseases; acute traumatic brain injury; neurodegenerative diseases such as Alzheimer's disease. The prominence of astroglial reactions in various diseases, the rapidity of the astroglial response and the evolutionary conservation of reactive astrogliosis indicate that reactive astrocytes fulfill important functions of the central nervous system (CNS). Yet, the exact role reactive astrocytes play in the injured CNS has so far remained elusive. This chapter summaries the various experimental models and diseases that exhibit astrogliosis and increase in glial fibrillary acidic protein (GFAP). Recent in vitro studies to inhibit GFAP synthesis are also presented.

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