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This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.
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This test This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample. |
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This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sam> This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample. |
Expected Turnaround Time
1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Related Documents
Specimen Requirements
Specimen
Plasma (EDTA)
Volume
1 mL
Minimum Volume
0.7 mL (Note: This volume does not allow for repeat testing.)
Container
Lavender-top (EDTA) tube
Collection
Draw blood in lavender-top (EDTA) tube. Invert to mix with preservatives. Centrifuge and transfer to a labeled plastic transport tube.
Storage Instructions
Room temperature
Stability Requirements
| Temperature | Period |
|---|---|
| Room temperature | 14 days |
| Refrigerated | 14 days |
| Frozen | 14 days |
| Freeze/thaw cycles | Stable x3 |
Test Details
Use
This test is used for measurement of glial fibrillary acidic protein (GFAP) in EDTA plasma.
Limitations
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.
There are significant variations in measured GFAP levels among different methods and labs. Care must be taken when interpreting results obtained in different studies.
Given the frequent occurrence of mixed brain pathologies in dementia,1 the assessment of biomarker accuracy should account for the effect of overlapping comorbidities.
GFAP levels have low specificity for differentiating among stroke subtypes.2
Along with neural astrocytes, small amounts of GFAP are expressed in the periphery by Schwann cells, mature glial cells in the gut, hepatic stellate cells and other non-neural cells.3,4
Methodology
Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA)
Reference Interval
See table.
| Age | Range (pg/mL) |
|---|---|
| 0 to 39 y | 0.00−57.40 |
| 40 to 49 y | 0.00−65.80 |
| 50 to 59 y | 0.00−87.10 |
| ≥60 y | 0.00−186.00 |
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See table.
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See table.
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Additional Information
GFAP is a 50 k-Da intermediate filament protein that forms the structural backbone of astrocytes.2,5-7 Astrocytes represent approximately 35 percent of the cells in the central nervous system8,9 and serve as an integral part of the blood-brain barrier. These cells facilitate numerous interactions with other cells in the nervous system, including neurons. Astrocytes are central to the normal function of synapses and contribute to axonal metabolic maintenance through the regulation of ion homeostasis.10 Growing research supports the fundamental role of reactive astrocytosis in neurodegenerative disease with elevated GFAP expression as a primary marker.11 Following plasma membrane damage secondary to neurotrauma, GFAP is released into the interstitial fluid and enters the blood stream by crossing the blood-brain barrier, which is compromised following trauma12-14 or via the lymphatic system.13,15 There is a large body of published data on the utility of measuring CSF levels of GFAP.16-19 With the development of more sensitive assays, accurate measurement of serum levels of GFAP is now available. Increased levels of serum GFAP have been associated with cognitive decline and dementia status due to a number of pathologies.2,20-24
The formation of pathological GFAP aggregates in vivo can accompany lethal neurological disorders such as Alexander disease.5 Alexander disease is caused by various dominant heterozygous mutations in the gene encoding GFAP.25 The pathological hallmark of the disease is the formation of cytoplasmic aggregations in astrocytes.5 Owing to the rarity of the disease, studies investigating GFAP levels in the blood of individuals with Alexander disease are limited. One study found a modest elevation of GFAP levels in the serum of participants with infantile and juvenile Alexander disease, but not in adult participants with the disease compared with levels in healthy controls.26
A number of studies have reported that blood GFAP levels are elevated in individuals with brain tumors.27-34 Some studies have found blood GFAP levels to be higher in participants with glioblastoma multiforme (GBM) than in healthy control participants, patients with other non-glial primary tumors and patients with brain metastasis.27-30 In patients with GBM, blood GFAP concentration correlated with preoperative tumor volume,27,28,30,33,34 volume of necrosis27,34 and GFAP expression levels in tumor tissue.27-34 In one study, individuals with systemic metastasis of myxopapillary ependymoma, a brain tumor with high GFAP expression, had very high blood GFAP concentrations compared with those in healthy controls.32
Glial fibrillary acidic protein (GFAP) concentration is increased following a traumatic brain injury (TBI) in studies of patients with predominantly mild to moderate injuries.2,5,35-49 There is some evidence that GFAP is associated with and may be able to predict unfavorable outcomes following TBI.50-52 GFAP has been shown to be detectable within one hour of injury,37,53,54 continues to rise and appears to peak within 20-24 hours37,54 and then declines over 72 hours,37 with a biological half-life of 24-48 hours.55 Many studies have examined the utility of GFAP for identifying patients with intracranial abnormalities following TBI.56 GFAP is considered useful for this purpose given that it is specific to brain injury57-59 and has a relatively long half-life compared to other biomarkers.55
The results of several studies suggest that serum GFAP could be employed as a biomarker of glial injury indicative of intracerebral hemorrhage in patients presenting with acute stroke symptoms.60-64 Studies have found serum levels of GFAP to be substantially higher in patients with intracerebral hemorrhage than in patients with ischemic stroke.60,64 A number of studies investigated the role of GFAP as a predictor of functional outcomes after acute ischemic stroke.65,66 Like ischemic stroke, blood GFAP concentration at admission could significantly predict poor outcomes after subarachnoid hemorrhage at six months after the event.67,68
GFAP levels have been shown to be higher in patients with multiple sclerosis (MS) than in healthy controls and individuals with non-inflammatory neurological diseases.69-72 Higher serum GFAP levels have been reported in patients with progressive MS, whereas the results for the relapsing-remitting MS phenotype differed between studies.17,69,70 Multiple studies have found a correlation between blood GFAP concentration and severity of disability inpatients with MS.17,69-73 Increased levels of GFAP have also been reported in patients with neuromyelitis optica spectrum disorder.73-75
Reactive astrogliosis is a hallmark of frontotemporal dementia (FTD).76-80 The most common genes linked to familial FTD are MAPT, progranulin (GRN) and chromosome 9 open reading frame 72 (C9orf72).80 Plasma GFAP is raised in symptomatic progranulin-associated frontotemporal dementia but not in those with C9orf72 expansions or MAPT mutations.24
Elevation of GFAP levels has been shown to occur in Alzheimer's disease (AD) and predict future conversion to Alzheimer's dementia in patients with mild cognitive impairment.18,59,81-84 Histological data have shown a close spatial relationship between reactive astrocytes and amyloid plaques in brain tissue of patients with AD.85 While the combination of elevated cerebral amyloid beta and tau is considered specific for AD, glial dysfunction and neuroinflammation manifest across dementia subtypes.86 GFAP expression is increased in the brains of individuals with AD, often co-localizing with plaques and tangles.87,88 Increased GFAP concentrations have been detected in CSF and blood of AD patients, with rising levels observed at the preclinical phase of the disease, as well as an association between GFAP levels and cerebral amyloid pathology, brain atrophy, cognitive decline and future conversion to dementia.82,89-94 CSF levels have been shown to differentiate individuals with dementia from cognitively unimpaired adults.95,96 Some recent studies have reported that increased blood levels of GFAP are associate with poorer cognition and AD status.82,89,97-99 Several studies have observed that plasma GFAP performed better than the CSF GFAP in detecting AD pathology,82,92,100 even in the preclinical or mild cognitive impairment AD stages.20,21,92,94,100,101
Relevant to secondary prevention efforts, plasma GFAP levels have also been found to predict amyloid positivity among cognitively unimpaired adults.85,93,94,100 Several studies have reported negative associations between blood derived GFAP levels and cognition.20,97,98,100 Studies have found that plasma GFAP has utility in discriminating healthy controls from patients with AD but also in distinguishing Ab+ from Ab- individuals.85,90 In the AIBL cohort, elevated GFAP was observed in A(beta)-PET (positron emission tomography) positive participants across the Alzheimer's disease continuum.93 In addition, higher GFAP levels were associated with prospective cognitive decline, lower plasma A(beta)1-42/A(beta)1-40 ratio and increased A(beta)-PET load prospectively.93 Plasma GFAP concentrations were higher in A(beta)-CU.102 Furthermore, higher GFAP levels have been associated with an increased risk for future progression to dementia and a steeper cognitive decline.91,94
Footnotes
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2. Abdelhak A, Foschi M, Abu-Rumeileh S, et al. Blood GFAP as an emerging biomarker in brain and spinal cord disorders. Nat Rev Neurol. 2022 Mar;18(3):158-172.35115728
3. Middeldorp J, Hol EM. GFAP in health and disease. Prog Neurobiol. 2011 Mar;93(3):421-443.21219963
4. Clairembault T, Kamphuis W, Leclair-Visonneau L, et al. Enteric GFAP expression and phosphorylation in Parkinson's disease. J Neurochem. 2014 Sep;130(6):805-815.24749759
5. Messing A, Brenner M. GFAP at 50. ASN Neuro. 2020 Jan-Dec:12:1759091420949680.32811163
6. Eng LF, Vanderhaeghen JJ, Bignami A, Gerstl B. An acidic protein isolated from fibrous astrocytes. Brain Res. 1971 May 7;28(2):351-354.5113526
7. Eng LF. Glial fibrillary acidic protein (GFAP): the major protein of glial intermediate filaments in differentiated astrocytes. J Neuroimmunol. 1985 Jun;8(4-6):203-214.2409105
8. Escartin C, Galea E, Lakatos A, et al. Reactive astrocyte nomenclature, definitions, and future directions. Nat Neurosci. 2021 Mar;24(3):312-325.33589835
9. Cohen-Salmon M, Slaoui L, Mazaré N, et al. Astrocytes in the regulation of cerebrovascular functions. Glia. 2021 Apr;69(4):817-841.33058289
10. Sofroniew MV, Vinters HV. Astrocytes: biology and pathology. Acta Neuropathol. 2010 Jan;119(1):7-35.20012068
11. Carter SF, Herholz K, Rosa-Neto P, Pellerin L, Nordberg A , Zimmer ER. Astrocyte Biomarkers in Alzheimer's Disease. Trends Mol Med. 2019 Feb;25(2):77-95.30611668
12. Hay JR, Johnson VE, Young AMH, Smith DH, Stewart W. Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans. J Neuropathol Exp Neurol. 2015 Dec;74(12):1147-1157.26574669
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76. Bolsewig K, Hok-A-Hin YS, Sepe FN, et al. A Combination of Neurofilament Light, Glial Fibrillary Acidic Protein, and Neuronal Pentraxin-2 Discriminates Between Frontotemporal Dementia and Other Dementias. J Alzheimers Dis. 2022;90(1):363-380.36120776
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78. Benussi A, Ashton NJ, Karikari TK, et al. Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration. J Alzheimers Dis. 2020;77(3):1129-1141.32804092
79. Del Campo M, Zetterberg H, Gandy S, et al. New developments of biofluid-based biomarkers for routine diagnosis and disease trajectories in frontotemporal dementia. Alzheimers Dement. 2022 Nov;18(11):2292-2307.35235699
80. Ntymenou S, Tsantzali I, Kalamatianos T, et al. Blood Biomarkers in Frontotemporal Dementia: Review and Meta-Analysis. Brain Sci. 2021 Feb 15;11(2):244.33672008
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85. Verberk IMW, Laarhuis MB, van den Bosch KA, et al. Serum markers glial fibrillary acidic protein and neurofilament light for prognosis and monitoring in cognitively normal older people: a prospective memory clinic-based cohort study. Lancet Healthy Longev. 2021 Feb;2(2):e87-e95.36098162
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