Clinical Information

Glial fibrillary acidic protein (GFAP) functions as the primary intermediate filament protein within the astrocyte cytoskeleton. Under pathological conditions such as inflammation, neurodegeneration or traumatic brain injury, GFAP expression is upregulated resulting in morphological alterations of astrocytes through reorganization of intermediate filaments. Increased GFAP concentrations correlate with the severity of neural damage, leading to structural hypertrophy of reactive astrocytes. In cases of severe and widespread brain injuries, astrocytes undergo extensive proliferation and form physical and chemical barriers surrounding lesion sites. This response is critical for containing damage and preventing its propagation to healthy tissues. The upregulation of GFAP acts as a marker of astrocyte activation following neural injury. GFAP is primarily localized intracellularly, but various mechanisms can induce its release into the cerebrospinal fluid (CSF) and subsequent entry to the bloodstream. The mechanism leading to release of GFAP into biofluids is not fully understood. Mechanisms such as astrocyte damage or death and neuroinflammation have been proposed to contribute to the release GFAP into the CSF and subsequently into the bloodstream. GFAP is a brain-specific protein with limited secretion into biofluids under physiological conditions, reinforcing its relevance as a neurodegenerative brain disease biomarker.