Find Locations
For hours, walk-ins and appointments.Special Instructions
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.
|
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. |
|
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 | 0.0−57.4 |
| 40 to 49 y | 0.0−65.8 |
| 50 to 59 y | 0.0−87.1 |
| ≥60 y | 0.0−186.0 |
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
1. Kovacs GG, Alafuzoff I, Al-Sarraj S, et al. Mixed brain pathologies in dementia: the BrainNet Europe consortium experience. Dement Geriatr CognDisord. 2008;26(4):343-350.18849605
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
13. Kawata K, Liu CY, Merkel SF, Ramierez SH, Tierney RT, Langford D. Blood biomarkers for brain injury: What are we measuring? Neurosci Biobehav Rev. 2016 Sep;68:460-473.27181909
14. Mondello S, Muller U, Jeromin A, Streeter J, Hayes RL, Wang KKW. Blood-based diagnostics of traumatic brain injuries. Expert Rev Mol Diagn. 2011 Jan;11(1):65-78.21171922
15. Plog BA, Dashnaw ML, Hitomi E, et al. Biomarkers of traumatic injury are transported from brain to blood via the glymphatic system. J Neurosci. 2015 Jan 14;35(2):518-526.25589747
16. Petzold A. Glial fibrillary acidic protein is a body fluid biomarker for glial pathology in human disease. Brain Res. 2015 Mar 10;1600:17-31.25543069
17. Abdelhak A, Hottenrott T, Morenas-Rodríguez E, et al. Glial Activation Markers in CSF and Serum From Patients With Primary Progressive Multiple Sclerosis: Potential of Serum GFAP as Disease Severity Marker? Front Neurol. 2019 Mar 26;10:280.30972011
18. Ishiki A, Kamada M, Kawamura Y, et al. Glial fibrillar acidic protein in the cerebrospinal fluid of Alzheimer's disease, dementia with Lewy bodies, and frontotemporal lobar degeneration. J Neurochem. 2016 Jan;136(2):258-261.26485083
19. Martínez MA, Olsson B, Bau L, et al. Glial and neuronal markers in cerebrospinal fluid predict progression in multiple sclerosis. Mult Scler. 2015 Apr;21(5):550-561.25732842
20. Gonzales MM, Wiedner C, Wang CP, et al. A population-based meta-analysis of circulating GFAP for cognition and dementia risk. Ann Clin TranslNeurol. 2022 Oct;9(10):1574-1585.36056631
21. Chouliaras L, Thomas A, Malpetti M, Donaghy P, Kane J, Mak E, et al. Differential levels of plasma biomarkers of neurodegeneration in Lewy body dementia, Alzheimer’s disease, frontotemporal dementia and progressive supranuclear palsy. J Neurol Neurosurg Psychiatry. 2022 Jun;93(6):651-658.35078917
22. Katisko K, Cajanus A, Huber N, et al. GFAP as a biomarker in frontotemporal dementia and primary psychiatric disorders: diagnostic and prognostic performance. J Neurol Neurosurg Psychiatry. 2021 Dec;92(12):1305-1312.34187866
23. Zhu N, Santos-Santos M, Illán-Gala I, et al. Plasma glial fibrillary acidic protein and neurofilament light chain for the diagnostic and prognostic evaluation of frontotemporal dementia. Transl Neurodegener. 2021 Dec 10;10(1):50.34893073
24. Heller C, Foiani MS, Moore Ket al. Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia. J Neurol Neurosurg Psychiatry. 2020 Mar;91(3):263-270.31937580
25. Messing A, Brenner M, Feany MB, Nedergaard M, Goldman JE. Alexander disease. J Neurosci. 2012 Apr 11;32(15):5017-5023.22496548
26. Jany PL, Agosta GE, Benko WS, et al. CSF and Blood Levels of GFAP in Alexander Disease. eNeuro. 2015 Oct 1;2(5):ENEURO.0080-15.2015.26478912
27. Jung CS, Foerch C, Schänzer A, et al. Serum GFAP is a diagnostic marker for glioblastoma multiforme. Brain. 2007 Dec;130(Pt 12):3336-3341.17998256
28. Gállego Pérez-Larraya J, Paris S, et al. Diagnostic and prognostic value of preoperative combined GFAP, IGFBP-2, and YKL-40 plasma levels in patients with glioblastoma. Cancer. 2014 Dec 15;120(24):3972-3980.25139333
29. Lyubimova NV, Timofeev YS, Mitrofanov AA, Bekyashev AK, Goncharova ZA, Kushlinskii NE. Glial Fibrillary Acidic Protein in the Diagnosis and Prognosis of Malignant Glial Tumors. Bull Exp Biol Med. 2020 Feb;168(4):503-506.32147765
30. Kiviniemi A, Gardberg M, Frantzén J, et al. Serum levels of GFAP and EGFR in primary and recurrent high-grade gliomas: correlation to tumor volume, molecular markers, and progression-free survival. J Neurooncol. 2015 Sep;124(2):237-245.26033547
31. Ilhan-Mutlu A, Wagner L, Widhalm G, et al. Exploratory investigation of eight circulating plasma markers in brain tumor patients. Neurosurg Rev. 2013 Jan;36(1):45-55; discussion 55-56.22763625
32. Ilhan-Mutlu A, Berghoff AS, Furtner J, et al. High plasma-GFAP levels in metastatic myxopapillary ependymoma. J Neurooncol. 2013 Jul;113(3):359-363.23624779
33. Brommeland T, Rosengren L, Fridlund S, Hennig R, Isaksen V. Serum levels of glial fibrillary acidic protein correlate to tumour volume of high-grade gliomas. Acta Neurol Scand. 2007 Dec;116(6):380-384.17986096
34. Tichy J, Spechtmeyer S, Mittelbronn M, et al. Prospective evaluation of serum glial fibrillary acidic protein (GFAP) as a diagnostic marker for glioblastoma. J Neurooncol. 2016 Jan;126(2):361-369.26518540
35. Papa L, Lewis LM, Falk JL, et al. Elevated levels of serum glial fibrillary acidic protein breakdown products in mild and moderate traumatic brain injury are associated with intracranial lesions and neurosurgical intervention. Ann Emerg Med. 2012 Jun;59(6):471-483.22071014
36. Papa L, Silvestri S, Brophy GM, et al. GFAP out-performs S100β in detecting traumatic intracranial lesions on computed tomography in trauma patients with mild traumatic brain injury and those with extracranial lesions. J Neurotrauma. 2014 Nov 15;31(22):1815-1822.24903744
37. Papa L, Brophy GM, Welch RD, et al. Time Course and Diagnostic Accuracy of Glial and Neuronal Blood Biomarkers GFAP and UCH-L1 in a Large Cohort of Trauma Patients With and Without Mild Traumatic Brain Injury. JAMA Neurol. 2016 May 1;73(5):551-560.27018834
38. Diaz-Arrastia R, Wang KK, Papa L, et al. Acute biomarkers of traumatic brain injury: relationship between plasma levels of ubiquitin C-terminal hydrolase-L1 and glial fibrillary acidic protein. J Neurotrauma. 2014 Jan 1;31(1):19-25.23865516
39. Posti JP, Takala RS, Runtti H, et al. The Levels of Glial Fibrillary Acidic Protein and Ubiquitin C-Terminal Hydrolase-L1 During the First Week After a Traumatic Brain Injury: Correlations With Clinical and Imaging Findings. Neurosurgery. 2016 Sep;79(3):456-464.26963330
40. Bogoslovsky T, Wilson D, Chen Y, et al. Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury. J Neurotrauma. 2017 Jan 1;34(1):66-73.27312416
41. Bazarian JJ, Biberthaler P, Welch RD, et al. Serum GFAP and UCH-L1 for prediction of absence of intracranial injuries on head CT (ALERT-TBI): a multicentre observational study. Lancet Neurol. 2018 Sep;17(9):782-789.30054151
42. Frankel M, Fan L, Yeatts SD, et al. Association of Very Early Serum Levels of S100B, Glial Fibrillary Acidic Protein, Ubiquitin C-Terminal Hydrolase-L1, and Spectrin Breakdown Product with Outcome in ProTECT III. J Neurotrauma. 2019 Oct 15;36(20):2863-2871.30794101
43. Mahan MY, Thorpe M, Ahmadi A, et al. Glial Fibrillary Acidic Protein (GFAP) Outperforms S100 Calcium-Binding Protein B (S100B) and Ubiquitin C-Terminal Hydrolase L1 (UCH-L1) as Predictor for Positive Computed Tomography of the Head in Trauma Subjects. World Neurosurg. 2019 Aug;128:e434-e444.31051301
44. Yue JK, Yuh EL, Korley FK, et al. Association between plasma GFAP concentrations and MRI abnormalities in patients with CT-negative traumatic brain injury in the TRACK-TBI cohort: a prospective multicentre study. Lancet Neurol. 2019 Oct;18(10):953-961.31451409
45. Anderson TN, Hwang J, Munar M, et al. Blood-based biomarkers for prediction of intracranial hemorrhage and outcome in patients with moderate or severe traumatic brain injury. J Trauma Acute Care Surg. 2020 Jul;89(1):80-86.32251265
46. Czeiter E, Amrein K, Gravesteijn BY, et al. Blood biomarkers on admission in acute traumatic brain injury: Relations to severity, CT findings and care path in the CENTER-TBI study. EBioMedicine. 2020 Jun;56:102785.32464528
47. Huebschmann NA, Luoto TM, Karr JE, et al. Comparing Glial Fibrillary Acidic Protein (GFAP) in Serum and Plasma Following Mild Traumatic Brain Injury in Older Adults. Front Neurol. 2020 Sep 18;11:1054.33071938
48. Shahim P, Politis A, van der Merwe A, et al. Time course and diagnostic utility of NfL, tau, GFAP, and UCH-L1 in subacute and chronic TBI. Neurology. 2020 Aug 11;95(6):e623-e636.32641529
49. Metting Z, Wilczak N, Rodiger LA, Schaaf JM, van der Naalt J. GFAP and S100B in the acute phase of mild traumatic brain injury. Neurology. 2012 May 1;78(18):1428-1433.22517109
50. Di Battista AP, Buonora JE, Rhind SG, et al. Blood Biomarkers in Moderate-To-Severe Traumatic Brain Injury: Potential Utility of a Multi-Marker Approach in Characterizing Outcome. Front Neurol. 2015 May 26;6:110.26074866
51. Vos PE, Jacobs B, Andriessen TM, et al. GFAP and S100B are biomarkers of traumatic brain injury: an observational cohort study. Neurology. 2010 Nov 16;75(20):1786-1793.21079180
52. Takala RS, Posti JP, Runtti H, et al. Glial Fibrillary Acidic Protein and Ubiquitin C-Terminal Hydrolase-L1 as Outcome Predictors in Traumatic Brain Injury. World Neurosurg. 2016 Mar;87:8-20.26547005
53. Papa L, Zonfrillo MR, Ramirez J, et al. Performance of Glial Fibrillary Acidic Protein in Detecting Traumatic Intracranial Lesions on Computed Tomography in Children and Youth With Mild Head Trauma. Acad Emerg Med. 2015 Nov;22(11):1274-1282.26469937
54. Welch RD, Ellis M, Lewis LM, et al. Modeling the Kinetics of Serum Glial Fibrillary Acidic Protein, Ubiquitin Carboxyl-Terminal Hydrolase-L1, and S100B Concentrations in Patients with Traumatic Brain Injury. J Neurotrauma. 2017 Jun 1;34(11):1957-1971.28031000
55. Thelin EP, Zeiler FA, Ercole A, et al. Serial Sampling of Serum Protein Biomarkers for Monitoring Human Traumatic Brain Injury Dynamics: A Systematic Review. Front Neurol. 2017 Jul 3;8:300.28717351
56. Luoto TM, Raj R, Posti JP, Gardner AJ, Panenka WJ, Iverson GL. A Systematic Review of the Usefulness of Glial Fibrillary Acidic Protein for Predicting Acute Intracranial Lesions following Head Trauma. Front Neurol. 2017 Dec;8:652.29255443
57. Pelinka LE, Kroepfl A, Schmidhammer R, et al. Glial fibrillary acidic protein in serum after traumatic brain injury and multiple trauma. J Trauma. 2004 Nov;57(5):1006-1012.15580024
58. van Geel WJ, de Reus HP, Nijzing H, Verbeek MM, Vos PE, Lamers KJB. Measurement of glial fibrillary acidic protein in blood: an analytical method. Clin Chim Acta. 2002 Dec;326(1-2):151-154.12417106
59. Yang Z, Wang KK. Glial fibrillary acidic protein: from intermediate filament assembly and gliosis to neurobiomarker. Trends Neurosci. 2015 Jun;38(6):364-374.25975510
60. Foerch C, Curdt I, Yan B, et al. Serum glial fibrillary acidic protein as a biomarker for intracerebral haemorrhage in patients with acute stroke. J Neurol Neurosurg Psychiatry. 2006 Feb;77(2):181-184.16174653
61. Luger S, Witsch J, Dietz A, et al. Glial Fibrillary Acidic Protein Serum Levels Distinguish between Intracerebral Hemorrhage and Cerebral Ischemia in the Early Phase of Stroke. Clin Chem. 2017 Jan;63(1):377-385.27881450
62. Dvorak F, Haberer I, Sitzer M, Foerch C. Characterisation of the diagnostic window of serum glial fibrillary acidic protein for the differentiation of intracerebral haemorrhage and ischaemic stroke. Cerebrovasc Dis. 2009;27(1):37-41.19018136
63. Foerch C, Pfeilschifter W, Zeiner P, Brunkhorst R. Glial fibrillary acidic protein in patients with symptoms of acute stroke: diagnostic marker of cerebral hemorrhage. Nervenarzt. 2014 Aug;85(8):982-989.25057113
64. Undén J, Strandberg K, Malm J, et al. Explorative investigation of biomarkers of brain damage and coagulation system activation in clinical stroke differentiation. J Neurol. 2009 Jan;256(1):72-77.19221847
65. Puspitasari V, Gunawan PY, Wiradarma HD, Hartoyo V. Glial Fibrillary Acidic Protein Serum Level as a Predictor of Clinical Outcome in Ischemic Stroke. Open Access Maced J Med Sci. 2019 May 14;7(9):1471-1474.31198457
66. Liu G, Geng J. Glial fibrillary acidic protein as a prognostic marker of acute ischemic stroke. Hum Exp Toxicol. 2018 Oct;37(10):1048-1053.29308673
67. Vos PE, van Gils M, Beems T, Zimmerman C, Verbeek MM. Increased GFAP and S100beta but not NSE serum levels after subarachnoid haemorrhage are associated with clinical severity. Eur J Neurol. 2006 Jun;13(6):632-638.16796588
68. Kedziora J, Burzynska M, Gozdzik W, Kübler A Kobylinska K, Adamik B. Biomarkers of Neurological Outcome After Aneurysmal Subarachnoid Hemorrhage as Early Predictors at Discharge from an Intensive Care Unit. Neurocrit Care. 2021 Jun;34(3):856-866.32978732
69. Abdelhak A, Huss A, Kassubek J, Tumani H, Otto M. Serum GFAP as a biomarker for disease severity in multiple sclerosis. Sci Rep. 2018 Oct 4;8(1):14798.30287870
70. Högel H, Rissanen E, Barro C, et al. Serum glial fibrillary acidic protein correlates with multiple sclerosis disease severity. Mult Scler. 2020 Feb;26(2):210-219.30570436
71. Ayrignac X, Le Bars E, Duflos C, et al. Serum GFAP in multiple sclerosis: correlation with disease type and MRI markers of disease severity. Sci Rep. 2020 Jul 2;10(1):10923.32616916
72. Meier S, Willemse EAJ, Schaedelin S, et al. Serum Glial Fibrillary Acidic Protein Compared With Neurofilament Light Chain as a Biomarker for Disease Progression in Multiple Sclerosis. JAMA Neurol. 2023 Mar 1;80(3):287-297.36745446
73. Watanabe M, Nakamura Y, Michalak Z, et al. Serum GFAP and neurofilament light as biomarkers of disease activity and disability in NMOSD. Neurology. 2019 Sep 24;93(13):e1299-e1311.31471502
74. Storoni M, Verbeek MM, Illes Z, et al. Serum GFAP levels in optic neuropathies. J Neurol Sci. 2012 Jun 15;317(1-2):117-122.22410258
75. Aktas O, Smith MA, Rees WA, et al. Serum Glial Fibrillary Acidic Protein: A Neuromyelitis Optica Spectrum Disorder Biomarker. Ann Neurol. 2021 May;89(5):895-910.33724534
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
77. Oeckl P, Steinacker P, Feneberg E, Otto M. Cerebrospinal fluid proteomics and protein biomarkers in frontotemporal lobar degeneration: Current status and future perspectives. Biochim Biophys Acta. 2015 Jul;1854(7):757-768.2552688
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
81. Oeckl P, Halbgebauer S, Anderl-Straub S, et al. Glial Fibrillary Acidic Protein in Serum is Increased in Alzheimer's Disease and Correlates with Cognitive Impairment. J Alzheimers Dis. 2019;67(2):481-488.30594925
82. Oeckl P, Anderl-Straub S, Von Arnim CAF, et al. Serum GFAP differentiates Alzheimer's disease from frontotemporal dementia and predicts MCI-to-dementia conversion. J Neurol Neurosurg Psychiatry. 2022 Apr 27:jnnp-2021-328547.35477892
83. Pascoal T, Bellaver B, Povala G, et al. Astrocyte reactivity influences the association of amyloid-β and tau biomarkers in preclinical Alzheimer's disease. Res Sq [Preprint]. 2023 Feb 1:rs.3.rs-2507179.36778243
84. Bellaver B, Povala G, Ferreira PCL, et al. Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer's disease. Nat Med. 2023 Jul;29(7):1775-1781.37248300
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
86. Kwon HS, Koh SH. Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes. Transl Neurodegener. 2020 Nov 26;9(1):42.33239064
87. Porchet R, Probst A, Bouras C, Dráberová E, Dráber P, Riederer BM. Analysis of glial acidic fibrillary protein in the human entorhinal cortex during aging and in Alzheimer's disease. Proteomics. 2003 Aug;3(8):1476-1485.12923773
88. Herskowitz JH, Seyfried NT, Duong DM, et al. Phosphoproteomic analysis reveals site-specific changes in GFAP and NDRG2 phosphorylation in frontotemporal lobar degeneration. J Proteome Res. 2010 Dec 3;9(12):6368-6379.20886841
89. Elahi FM, Casaletto KB, La Joie R, et al. Plasma biomarkers of astrocytic and neuronal dysfunction in early- and late-onset Alzheimer's disease. Alzheimers Dement. 2020 Apr;16(4):681-695.31879236
90. Asken BM, Elahi FM, La Joie R, et al. Plasma Glial Fibrillary Acidic Protein Levels Differ Along the Spectra of Amyloid Burden and Clinical Disease Stage. J Alzheimers Dis. 2020;78(1):265-276.32986672
91. Verberk IMW, Thijssen E, Koelewijn J, et al. Combination of plasma amyloid beta(1-42/1-40) and glial fibrillary acidic protein strongly associates with cerebral amyloid pathology. Alzheimers Res Ther. 2020 Sep 28;12(1):118.32988409
92. Benedet AL, Milà-Alomà M, Vrillon A, et al. Differences Between Plasma and Cerebrospinal Fluid Glial Fibrillary Acidic Protein Levels Across the Alzheimer Disease Continuum. JAMA Neurol. 2021 Dec 1;78(12):1471-1483.34661615
93. Chatterjee P, Pedrini S, Stoops E, et al. Plasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer's disease. Transl Psychiatry. 2021 Jan 11;11(1):27.33431793
94. Cicognola C, Janelidze S, Hertze J, et al. Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment. Alzheimers Res Ther. 2021 Mar 27;13(1):68.33773595
95. Abu-Rumeileh S, Steinacker P, Polischi B, et al. CSF biomarkers of neuroinflammation in distinct forms and subtypes of neurodegenerative dementia. Alzheimers Res Ther. 2019 Dec 31;12(1):2.31892365
96. Bellaver B, Ferrari-Souza JP, Uglione da Ros L, et al. Astrocyte Biomarkers in Alzheimer Disease: A Systematic Review and Meta-analysis. Neurology. 2021 Jun 14;96(24):e2944-e2955.33952650
97. Rajan KB, Aggarwal NT, McAninch EA, et al. Remote Blood Biomarkers of Longitudinal Cognitive Outcomes in a Population Study. Ann Neurol. 2020 Dec;88(6):1065-1076.32799383
98. Bettcher BM, Olson KE, Carlson NE, et al. Astrogliosis and episodic memory in late life: higher GFAP is related to worse memory and white matter microstructure in healthy aging and Alzheimer's disease. Neurobiol Aging. 2021 Jul;103:68-77.33845398
99. Chatterjee P, Pedrini S, Doecke JD, et al. Plasma Aβ42/40 ratio, p-tau181, GFAP, and NfL across the Alzheimer's disease continuum: A cross-sectional and longitudinal study in the AIBL cohort. Alzheimers Dement. 2023 Apr;19(4):1117-1134.36574591
100. Pereira JB, Janelidze S, Smith R, et al. Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease. Brain. 2021 Dec 16;144(11):3505-3516.34259835
101. Ebenau JL, Pelkmans W, Verberk IMW, et al. Association of CSF, Plasma, and Imaging Markers of Neurodegeneration With Clinical Progression in People With Subjective Cognitive Decline. Neurology. 2022 Mar 29;98(13):e1315-e1326.35110378
102. Chatterjee P, Pedrini S, Ashton NJ, et al. Diagnostic and prognostic plasma biomarkers for preclinical Alzheimer's disease. Alzheimers Dement. 2022 Jun;18(6):1141-1154.34494715
LOINC® Map
© 2021 Laboratory Corporation of America® Holdings and Lexi-Comp Inc. All Rights Reserved.
CPT Statement/Profile Statement
The LOINC® codes are copyright © 1994-2021, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee. Permission is granted in perpetuity, without payment of license fees or royalties, to use, copy, or distribute the LOINC® codes for any commercial or non-commercial purpose, subject to the terms under the license agreement found at https://loinc.org/license/. Additional information regarding LOINC® codes can be found at LOINC.org, including the LOINC Manual, which can be downloaded at LOINC.org/downloads/files/LOINCManual.pdf