Plasma GFAP

The Plasma GFAP protein assay quantifies glial fibrillary acidic protein, a cytoskeletal protein of astrocytes released into circulation when astrocytes become reactive in response to brain injury or neurodegeneration. Using an ultra-sensitive single-molecule array, plasma levels can be measured at sub-picogram/mL concentrations. Plasma GFAP rises during the preclinical phase of Alzheimer's disease, correlates with amyloid-β pathology, and has established clinical utility in acute evaluation of mild traumatic brain injury.

1. Screening and research use as an early plasma biomarker of Alzheimer's disease pathology, particularly amyloid-β burden.
2. Risk stratification for future cognitive decline in individuals with subjective cognitive decline or mild cognitive impairment.
3. Aiding triage of mild traumatic brain injury, where an elevated plasma GFAP and UCH-L1 combination supports FDA-cleared rule-in of intracranial injury.
4. Monitoring astrocyte activation in neuroinflammatory and demyelinating disease.

Use 2x EDTA vacuum blood collection tubes (purple cap) to draw 4 mL of venous blood.

Transfer to 4°C for immediate storage and arrange shipment to Codex Genetics Laboratory (within 6 hours)

Available through Codex Genetics as part of the Neurodegenerative Biomarker panel.

Reported in pg/mL. Age-stratified reference ranges apply. Elevation indicates active neurodegeneration.

Elevated plasma GFAP indicates neurodegeneration/astrocytosis. In combination with amyloid and tau biomarkers (p-tau217, Aβ42/40), GFAP contributes to full AT(N) staging per NIA-AA 2024 framework.

GFAP is a brain-enriched cytoskeletal protein of astrocytes that becomes elevated in blood when astrocytes are activated by neurodegeneration, demyelination, or acute injury. Single-molecule ultra-sensitive immunoassay technologies reliably quantify plasma GFAP at the low pg/mL range, making it a minimally invasive biomarker. In Alzheimer's disease, plasma GFAP rises during the preclinical phase, tracks amyloid-β positivity more closely than tau pathology, and is associated with increased risk of future cognitive decline. In traumatic brain injury, a combined plasma GFAP and UCH-L1 assay received FDA clearance in 2018 for ruling in CT-visible intracranial injury in mild TBI, with reported sensitivity exceeding 97%. GFAP is also investigated in multiple sclerosis and neuromyelitis optica spectrum disorder. It is non-disease-specific and must be interpreted alongside clinical assessment.

Per the NIA-AA 2024 revised criteria (Jack CR Jr et al., Alzheimer's & Dementia 2024; DOI: 10.1002/alz.13859), GFAP is classified as an (N) neurodegeneration biomarker — non-specific but informative for staging disease severity. Studies show that plasma GFAP begins to rise years before symptom onset in AD, making it one of the earliest detectable blood signals of AD neurodegeneration. GFAP levels correlate with amyloid PET burden and track cognitive decline longitudinally. It is also elevated in TBI, stroke, ALS, and MS.