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Intermediate filaments are a fundamental component of the cytoskeleton in neurons and astrocytes. The main intermediate filament in astrocytes is glial fibrillary acid protein (GFAP). Like other intermediate filaments, GFAP interacts with other components of the cytoskeleton, adhesion molecules, intracellular chaperones, and other proteins. GFAP is responsible for the cytoarchitecture and mechanical strength of astrocytes and their supporting functions on the physiology of neighboring neurons and maintenance of blood–brain barrier. GFAP is involved in the pathophysiology of several neurologic disorders. Alexander disease, due to mutations of the GFAP gene, is the prototypic primary astrocytopathy. Upregulation of GFAP expression is a marker of reactive astrogliosis in a wide range of acute and chronic neurologic disorders. GFAP is also a target of autoantibodies linked to autoimmune meningoencephalitis. There are several recent reviews on the composition, dynamics, and function of GFAP1–3; its involvement in neurologic disease2–10; and the potential uses and limitations of GFAP as a disease biomarker.11,12
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