Статті в журналах: "Glial Fibrillary Acidic Protein (GFAP)"

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Gravier-Dumonceau, Alice, Roxana Ameli, Veronique Rogemond, Anne Ruiz, Bastien Joubert, Sergio Muñiz-Castrillo, Alberto Vogrig, et al. "Glial Fibrillary Acidic Protein Autoimmunity." Neurology 98, no. 6 (November 19, 2021): e653-e668. http://dx.doi.org/10.1212/wnl.0000000000013087.

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Background and ObjectivesTo report the clinical, biological, and imaging features and clinical course of a French cohort of patients with glial fibrillary acidic protein (GFAP) autoantibodies.MethodsWe retrospectively included all patients who tested positive for GFAP antibodies in the CSF by immunohistochemistry and confirmed by cell-based assay using cells expressing human GFAPα since 2017 from 2 French referral centers.ResultsWe identified 46 patients with GFAP antibodies. Median age at onset was 43 years, and 65% were men. Infectious prodromal symptoms were found in 82%. Other autoimmune diseases were found in 22% of patients, and coexisting neural autoantibodies in 11%. Tumors were present in 24%, and T-cell dysfunction in 23%. The most frequent presentation was subacute meningoencephalitis (85%), with cerebellar dysfunction in 57% of cases. Other clinical presentations included myelitis (30%) and visual (35%) and peripheral nervous system involvement (24%). MRI showed perivascular radial enhancement in 32%, periventricular T2 hyperintensity in 41%, brainstem involvement in 31%, leptomeningeal enhancement in 26%, and reversible splenial lesions in 4 cases. A total of 33 of 40 patients had a monophasic course, associated with a good outcome at last follow-up (Rankin Score ≤2: 89%), despite a severe clinical presentation. Adult and pediatric features are similar. Thirty-two patients were treated with immunotherapy. A total of 11/22 patients showed negative conversion of GFAP antibodies.DiscussionGFAP autoimmunity is mainly associated with acute/subacute meningoencephalomyelitis with prodromal symptoms, for which tumors and T-cell dysfunction are frequent triggers. The majority of patients followed a monophasic course with a good outcome.

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Brenner, Michael. "Glial Fibrillary Acidic Protein (GFAP)." Brain Pathology 4, no. 3 (July 1994): 219–20. http://dx.doi.org/10.1111/j.1750-3639.1994.tb00836.x.

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Yadav, Nidhi, Keshav Mishra, Anil Kumar B. C., Daljit Singh, and Manju Subberwal. "Clinical utility of serum glial fibrillary acidic protein in glial neoplasm." Surgical Neurology International 13 (December 30, 2022): 601. http://dx.doi.org/10.25259/sni_889_2022.

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Background: Glial fibrillary acidic protein (GFAP) is a member of the cytoskeletal protein family and is widely expressed in astroglial and neural stem cells, also in glial tumors such as astrocytoma and Glioblastoma (GBM). Increased GFAP expression and disruption of the blood–brain barrier are the characteristic features of GBM. Higher serum GFAP levels can help differentiate GBM from GBM mimics (such as primary central nervous system lymphoma, metastasis, or demyelinating lesions). Methods: This prospective study was carried out in a tertiary care center in the department of neurosurgery on newly diagnosed glioma patients who underwent surgery from January 2018 to July 2019, excluded patients with history of the previous surgery for glioma, traumatic brain injury, and ischemic or hemorrhagic stroke. The blood sample was obtained at admission before undergoing invasive procedure. Pathological examination of the tumor biopsy sample was carried out using classical hematoxylin-eosin and immunohistochemical staining. All statistical analyses were performed using SPSS version 24.0. Results: The mean preoperative tumor volume was 40 cm3 (range 17.19–65.57 cm3; standard deviation [SD] = 9.99 cm3) which showed 98.25% mean reduction in volume postsurgery (mean tumor volume = 0.7 cm3; SD = 0.19 cm3). Preoperative serum GFAP measurements show higher levels (spearman’s rho coefficient = 0.610 with P = 0.000) with increasing grade of tumor. GFAP levels also demonstrated higher value with increasing preoperative tumor volume. Conclusion: Increasing serum GFAP levels in the preoperative period correlate with higher tumor grade, especially grade III and grade IV tumors. The serum GFAP levels showed relation to tumor volume, both before and after surgery.

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van Asperen, Jessy V., Pierre A. J. T. Robe, and Elly M. Hol. "GFAP Alternative Splicing and the Relevance for Disease – A Focus on Diffuse Gliomas." ASN Neuro 14 (January 2022): 175909142211020. http://dx.doi.org/10.1177/17590914221102065.

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Glial fibrillary acidic protein (GFAP) is an intermediate filament protein that is characteristic for astrocytes and neural stem cells, and their malignant analogues in glioma. Since the discovery of the protein 50 years ago, multiple alternative splice variants of the GFAP gene have been discovered, leading to different GFAP isoforms. In this review, we will describe GFAP isoform expression from gene to protein to network, taking the canonical isoforms GFAPα and the main alternative variant GFAPδ as the starting point. We will discuss the relevance of studying GFAP and its isoforms in disease, with a specific focus on diffuse gliomas.

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Sarthy, Vijay. "Focus on Molecules: Glial fibrillary acidic protein (GFAP)." Experimental Eye Research 84, no. 3 (March 2007): 381–82. http://dx.doi.org/10.1016/j.exer.2005.12.014.

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Chen, W. J., and R. K. Liem. "The endless story of the glial fibrillary acidic protein." Journal of Cell Science 107, no. 8 (August 1, 1994): 2299–311. http://dx.doi.org/10.1242/jcs.107.8.2299.

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All intermediate filament proteins consist of an alpha-helical rod domain flanked by non-helical N-terminal head and C-terminal tail domains. The roles of the non-helical domains of various intermediate filament proteins in the assembly and co-assembly of higher-order filamentous structures have been studied by many groups but with quite contradictory results. Type III intermediate filaments are unique in that they can form homopolymers both in vitro and in vivo. The expression and assembly characteristics of carboxy- and amino-terminal deletion mutants of glial fibrillary acidic protein (GFAP), an astrocyte-specific type III intermediate filament protein, were examined by transient transfections of either vimentin-positive or vimentin-negative variants of human adrenocarcinoma-derived SW13 cell lines. Whereas complete deletion of the C-terminal tail domain of GFAP results in the formation of polymorphic aggregates, both intranuclear and cytoplasmic in self-assembly experiments, efficient co-assembly of these tail-less GFAP mutants with vimentin can be achieved as long as the KLLEGEE sequence at the C-terminal end of the rod domain is preserved. Up to one-fifth of the C-terminal end of the tail domain can be deleted without affecting the capability of GFAP to self-assemble. The highly conserved RDG-containing motif in the tail domain may be important for self-assembly but is not sufficient. The entire head domain seems to be required for self-assembly. All N-terminal deletion mutants of GFAP share the same phenotype of diffuse cytoplasmic staining when expressed in vimentin-negative SW13 cells. Although co-assembly with vimentin can still be achieved with completely head-less GFAP, preservation of some of the head domain greatly enhanced the efficiency. Our results form the basis for further, more detailed mapping of the essential regions in filament assembly of GFAP and other type III IFs.

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Joo, Jae Young, Dallah Yoo, and Tae-Beom Ahn. "Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis." Journal of Movement Disorders 15, no. 1 (January 31, 2022): 66–70. http://dx.doi.org/10.14802/jmd.21115.

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Movement disorders associated with glial fibrillary acidic protein (GFAP) autoantibodies have rarely been reported as ataxia or tremors. A 32-year-old man with headache and fever, initially diagnosed with viral meningoencephalitis, showed gradual improvement with empirical treatment. Two weeks after the illness, he suddenly developed orofacial, tongue, and neck dyskinesia accompanied by oculomotor abnormalities, which developed into severe generalized choreoballism. Brain magnetic resonance imaging (fluid-attenuated inversion recovery) showed signal hyperintensities in the bilateral globus pallidus interna. The clinical picture suggested an acute inflammatory trigger of secondary autoimmune encephalitis. The autoimmune antibody test was positive for GFAP, with the strongest reactivity in the cerebrospinal fluid (CSF) before treatment and decreased reactivity in serial CSF examinations during immunotherapy. Dyskinesia gradually improved to the extent that it could be controlled with only oral medications. This patient presented with parainfectious GFAP meningoencephalitis with distinctive clinical features and imaging findings.

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Lake, Norma, Carole Verdone-Smith, and Seymour Brownstein. "Immunocytochemical localization of taurine and glial fibrillary acidic protein in human optic nerve." Visual Neuroscience 8, no. 3 (March 1992): 251–55. http://dx.doi.org/10.1017/s095252380000290x.

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AbstractTaurine immunoreactivity (IR) in 1 -μm sections of glutaraldehyde-fixed human optic nerve was observed using light microscopy and an antibody raised in rabbit to taurine conjugated to bovine serum albumin. Throughout the nerve, taurine-lR was prominent in glial cells, in their perinuclear regions, and in their numerous branching processes, some of which extended to the pial septa. The peripheral glial mantle (glia limitans) was densely stained, whereas axons and the pial septa showed relatively little or no taurine-IR. Immunoreactivity for glial fibrillary acidic protein (GFAP), an astrocyte-specific marker, was evaluated on adjacent sections. The pattern of GFAP-IR was highly similar to that for taurine, suggesting that a subset of taurine-immunoreactive glial cells are optic nerve astrocytes. To our knowledge, this is the first localization of taurine and GFAP in human optic nerve.

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Deng, Bo, Jingguo Wang, Hai Yu, Lei Jin, Yue Qiu, Xiaoni Liu, Pengyu Wang, Xiang Zhang, and Xiangjun Chen. "Area Postrema Syndrome in Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy." Neurology - Neuroimmunology Neuroinflammation 9, no. 6 (September 26, 2022): e200029. http://dx.doi.org/10.1212/nxi.0000000000200029.

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Background and ObjectivesTo report the frequency of area postrema syndrome (APS) in glial fibrillary acidic protein-immunoglobulin G (GFAP-IgG)–positive patients and emphasize the importance of APS among the phenotypes in autoimmune GFAP astrocytopathy.MethodsEight GFAP-IgG–positive cases with APS were retrospectively identified during 2015–2021. The APS phenotypes were described. A literature review of 8 previously reported cases was also included in analysis.ResultsA total of 8 patients (11%) (1 woman, 7 men; mean age: 52.4 ± 18.4 years) presented with APS in a cohort of 74 GFAP-IgG–positive patients, 3 of whom (4%) had disease onset with APS. All patients had hiccups, and hiccups was the unique symptom of APS in 5 patients. The median time from disease onset to APS occurrence was 2 days (range 0–20), and the mean duration of APS episodes was 23.6 ± 11.4 days. No patient had isolated APS attack. All episodes were completely resolved with a mean duration of 9.3 ± 5.4 days after immunotherapy. APS manifestations of 8 cases in previous studies showed similar features with our cases. In total, coexisting aquaporin-4-IgG was only detected in one of the 16 cases.DiscussionAPS could be an early, but not isolated clinical manifestation of autoimmune GFAP astrocytopathy. Hiccups was the predominant symptom of APS in this disorder. APS attacks of autoimmune GFAP astrocytopathy have good response to immunotherapy.

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Hatfield, James S., Robert P. Skoff, Harry Maisel, Lawrence Eng, and Darell D. Bigner. "The lens epithelium contains glial fibrillary acidic protein (GFAP)." Journal of Neuroimmunology 8 (1985): 347–57. http://dx.doi.org/10.1016/s0165-5728(85)80072-2.

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Courel, Marie-Noëlle, Nicole Girard, Bertrand Delpech, and Claude Chauzy. "Specific monoclonal antibodies to glial fibrillary acidic protein (GFAP)." Journal of Neuroimmunology 11, no. 4 (June 1986): 271–76. http://dx.doi.org/10.1016/0165-5728(86)90080-9.

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Rozanski, Michal, Carolin Waldschmidt, Alexander Kunz, Ulrike Grittner, Martin Ebinger, Matthias Wendt, Benjamin Winter, et al. "Glial Fibrillary Acidic Protein for Prehospital Diagnosis of Intracerebral Hemorrhage." Cerebrovascular Diseases 43, no. 1-2 (December 13, 2016): 76–81. http://dx.doi.org/10.1159/000453460.

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Background: Both, acute ischemic stroke (AIS) and hemorrhage stroke (intracerebral hemorrhage, ICH) require early attention but different treatment strategies. Plasma glial fibrillary acidic protein (GFAP) levels were found to be elevated in ICH patients after they arrived in the hospital. Because treatment options differed, we sought to determine whether GFAP can be used to accurately differentiate between of AIS and ICH in the prehospital setting. Methods: We assessed acute stroke patients in the Stroke Emergency Mobile (STEMO). STEMO is a stroke ambulance staffed by a specialized team including a neurologist and equipped with a computed tomography scanner plus a point-of-care laboratory. The STEMO ambulance is integrated in the emergency medical system of Berlin, Germany. Following prehospital stroke diagnosis, blood was drawn and subsequently analysed using research assays from Roche diagnostics. The clinical accuracy of plasma GFAP was tested using a cut-off value of 0.29 ng/ml. Results: Blood samples of 74 patients were analysed. Twenty-five patients had ICH (mean age 69 ± 11 years, median National Institutes of Health Stroke Scale (NIHSS) 15) and 49 IS (mean age 75 ± 10 years, median NIHSS 6). Nine ICH (0 IS patients) had GFAP-levels above 0.29 ng/ml. The sensitivity and specificity of GFAP for differentiating between ICH and AIS were 36.0 and 100%. The sensitivity for ICH volume >15 ml was 61.5%. ICH patients without GFAP elevation had significantly smaller hemorrhage volumes (median 4.5 vs. 37.6 ml, p = 0.004) and were less likely to deteriorate (19 vs. 56%, p = 0.087). Conclusions: GFAP levels >0.29 ng/ml were seen only in ICH, thus confirming the diagnosis of ICH during prehospital care. However, sensitivity is low particularly in smaller hemorrhages.

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Galou, M., E. Colucci-Guyon, D. Ensergueix, J. L. Ridet, M. Gimenez y Ribotta, A. Privat, C. Babinet, and P. Dupouey. "Disrupted glial fibrillary acidic protein network in astrocytes from vimentin knockout mice." Journal of Cell Biology 133, no. 4 (May 15, 1996): 853–63. http://dx.doi.org/10.1083/jcb.133.4.853.

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Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed predominantly in astrocytes. The study of its expression in the astrocyte lineage during development and in reactive astrocytes has revealed an intricate relationship with the expression of vimentin, another intermediate filament protein widely expressed in embryonic development. these findings suggested that vimentin could be implicated in the organization of the GFAP network. To address this question, we have examined GFAP expression and network formation in the recently generated vimentin knockout (Vim-) mice. We show that the GFAP network is disrupted in astrocytes that normally coexpress vimentin and GFAP, e.g., those of the corpus callosum or the Bergmann glia of cerebellum. Furthermore, Western blot analysis of GFAP protein content in the cerebellum suggests that posttranslational mechanisms are implicated in the disturbance of GFAP network formation. The role of vimentin in this process was further suggested by transfection of Vim-cultured astrocytes with a vimentin cDNA, which resulted in the normal assembly of the GFAP network. Finally, we examined GFAP expression after stab wound-induced astrogliosis. We demonstrate that in Vim- mice, reactive astrocytes that normally express both GFAP and vimentin do not exhibit GFAP immunoreactivity, whereas those that normally express GFAP only retain GFAP immunoreactivity. Taken together, these results show that in astrocytes, where vimentin is normally expressed with GFAP fails to assemble into a filamentous network in the absence of vimentin. In these cells, therefore, vimentin appears necessary to stabilize GFAP filaments and consequently the network formation.

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Messing, Albee, and Michael Brenner. "GFAP at 50." ASN Neuro 12 (January 2020): 175909142094968. http://dx.doi.org/10.1177/1759091420949680.

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Fifty years have passed since the discovery of glial fibrillary acidic protein (GFAP) by Lawrence Eng and colleagues. Now recognized as a member of the intermediate filament family of proteins, it has become a subject for study in fields as diverse as structural biology, cell biology, gene expression, basic neuroscience, clinical genetics and gene therapy. This review covers each of these areas, presenting an overview of current understanding and controversies regarding GFAP with the goal of stimulating continued study of this fascinating protein.

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Ganne, Akshatha, Meenakshisundaram Balasubramaniam, W. Sue T. Griffin, Robert J. Shmookler Reis, and Srinivas Ayyadevara. "Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease." Pharmaceutics 14, no. 7 (June 26, 2022): 1354. http://dx.doi.org/10.3390/pharmaceutics14071354.

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Glial fibrillary acidic protein (GFAP) is an intermediate filament structural protein involved in cytoskeleton assembly and integrity, expressed in high abundance in activated glial cells. GFAP is neuroprotective, as knockout mice are hypersensitive to traumatic brain injury. GFAP in cerebrospinal fluid is a biomarker of Alzheimer’s disease (AD), dementia with Lewy bodies, and frontotemporal dementia (FTD). Here, we present novel evidence that GFAP is markedly overexpressed and differentially phosphorylated in AD hippocampus, especially in AD with the apolipoprotein E [ε4, ε4] genotype, relative to age-matched controls (AMCs). Kinases that phosphorylate GFAP are upregulated in AD relative to AMC. A knockdown of these kinases in SH-SY5Y-APPSw human neuroblastoma cells reduced amyloid accrual and lowered protein aggregation and associated behavioral traits in C. elegans models of polyglutamine aggregation (as observed in Huntington’s disease) and of Alzheimer’s-like amyloid formation. In silico screening of the ChemBridge structural library identified a small molecule, MSR1, with stable and specific binding to GFAP. Both MSR1 exposure and GF AP-specific RNAi knockdown reduce aggregation with remarkably high concordance of aggregate proteins depleted. These data imply that GFAP and its phosphorylation play key roles in neuropathic aggregate accrual and provide valuable new biomarkers, as well as novel therapeutic targets to alleviate, delay, or prevent AD.

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Yamakawa, Mai, Keenan O. Hogan, John Leever, and Yasir N. Jassam. "Autopsy Case of Meningoencephalomyelitis Associated With Glial Fibrillary Acidic Protein Antibody." Neurology - Neuroimmunology Neuroinflammation 8, no. 6 (October 12, 2021): e1081. http://dx.doi.org/10.1212/nxi.0000000000001081.

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Background and ObjectivesTo describe the autopsy findings and neuropathologic evaluation of autoimmune meningoencephalomyelitis associated with glial fibrillary acidic protein (GFAP) antibody.MethodsWe reviewed the clinical course, imaging, laboratory, and autopsy findings of a patient with autoimmune meningoencephalomyelitis associated with GFAP antibody who had a refractory course to multiple immunosuppressive therapies.ResultsThe patient was a 70-year-old man who was diagnosed as GFAP antibody-associated autoimmune meningoencephalomyelitis. MRI of the head showed linear perivascular enhancement in the midbrain and the basal ganglia. Despite treatment with high-dose corticosteroids, plasma exchange, IV immunoglobulins, and cyclophosphamide, he died with devastating neurologic complications. Autopsy revealed a coexistent neuroendocrine tumor in the small intestine and diffuse inflammation in the brain parenchyma, perivascular spaces, and leptomeninges, with predominant T-cells, macrophages, and activated microglia. B-cells and plasma cells were absent. There was no astrocyte involvement with change in GFAP immunostaining.DiscussionThis case illustrates autoimmune meningoencephalomyelitis associated with GFAP antibody in the CSF and coexistent neuroendocrine tumor. The autopsy findings were nonspecific and did not demonstrate astrocyte involvement. Further accumulation of cases is warranted to delineate the utility and pathogenic significance of the GFAP autoantibody.

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Pekny, Milos, Clas B. Johansson, Camilla Eliasson, Josefina Stakeberg, Åsa Wallén, Thomas Perlmann, Urban Lendahl, Christer Betsholtz, Claes-Henric Berthold, and Jonas Frisén. "Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin." Journal of Cell Biology 145, no. 3 (May 3, 1999): 503–14. http://dx.doi.org/10.1083/jcb.145.3.503.

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In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.

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Högel, Heidi, Eero Rissanen, Christian Barro, Markus Matilainen, Marjo Nylund, Jens Kuhle, and Laura Airas. "Serum glial fibrillary acidic protein correlates with multiple sclerosis disease severity." Multiple Sclerosis Journal 26, no. 2 (December 20, 2018): 210–19. http://dx.doi.org/10.1177/1352458518819380.

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Background: Cerebrospinal fluid (CSF) levels of two soluble biomarkers, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL), have been shown to associate with multiple sclerosis (MS) disease progression. Now, both biomarkers can be detected reliably in serum, and importantly, their serum levels correlate well with their CSF levels. Objective: To evaluate the usability of serum GFAP measurement as a biomarker of progressive disease and disease severity in MS. Methods: Clinical course, Expanded Disability Status Scale (EDSS), disease duration, patient age and magnetic resonance imaging (MRI) parameters were reviewed in 79 MS patients in this cross-sectional hospital-based study. Serum samples were collected for measurement of GFAP and NfL concentrations using single molecule array (Simoa) assay. A cohort of healthy controls was evaluated for comparison. Results: Higher serum concentrations of both GFAP and NfL were associated with higher EDSS, older age, longer disease duration, progressive disease course and MRI pathology. Conclusion: Earlier studies have demonstrated that GFAP, unlike NfL, is not increased in association with acute focal inflammation-related nervous system damage. Our work suggests that GFAP serum level associates with disease progression in MS and could potentially serve as an easily measurable biomarker of central nervous system (CNS) pathology related to disease progression in MS.

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O'Callaghan, James P. "The Use of Glial Fibrillary Acidic Protein in First-Tier Assessments of Neurotoxicity." Journal of the American College of Toxicology 10, no. 6 (November 1991): 719–26. http://dx.doi.org/10.3109/10915819109078664.

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Diverse neurotoxic insults result in proliferation and hypertrophy of astrocytes, a subtype of central nervous system glia. The hallmark of this response, often termed “reactive gliosis,” is the enhanced expression of the major intermediate filament protein of astrocytes, glial fibrillary acidic protein (GFAP). These morphological observations suggest that GFAP may be a useful biochemical indicator of neurotoxicity. To investigate this possibility we have administered prototype neurotoxicants to experimental animals and then assessed the effects of these agents on the tissue content of GFAP, as determined by radioimmunoassay. We found that assays of GFAP reveal dose-, time-, and region-dependent patterns of neurotoxicity at toxicant dosages below those that cause light microscopic evidence of cell loss or damage. No false positives have been seen following exposure to a variety of pharmacological agents. By using regional assessments of GFAP in a first-tier evaluation, it should be possible to localize areas of damage. A second-tier evaluation, using assays of proteins or transmitters associated with cells in the affected region, may reveal the cellular targets of neurotoxicity. This two-tiered approach should serve as a foundation for guiding studies aimed at determining mechanisms of neurotoxicity.

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Liu, G., and J. Geng. "Glial fibrillary acidic protein as a prognostic marker of acute ischemic stroke." Human & Experimental Toxicology 37, no. 10 (January 8, 2018): 1048–53. http://dx.doi.org/10.1177/0960327117751236.

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Background: We investigated the association between serum levels of glial fibrillary acidic protein (GFAP) and stroke functional outcomes in a cohort of 286 patients with acute ischemic stroke (AIS). Methods: We prospectively studied 286 patients with AIS who were admitted within 24 h after the onset of symptoms. Serum levels of GFAP and National Institutes of Health Stroke Scale (NIHSS) were measured at admission. The primary end point was stroke functional outcome among 1-year after stroke onset. We used logistic regression models to assess the relationship between GFAP levels and stroke outcomes. Results: The GFAP level was obtained with a median value of 0.18 (interquartile ranges (IQRs): 0.09–0.28) ng/ml. In multivariable models adjusted for age, gender, and other risk factors, GFAP levels were associated with an increased risk of a NIHSS>6 (odds ratio (OR) = 1.55; 95% confidence interval (CI): 1.16–1.89; p = 0.012). The poor outcome distribution across the GFAP quartiles ranged between 12.7% (first quartile) and 70.4% (fourth quartile). After adjusting for other established risk factors, in multivariate models comparing the Q3 and Q 4 quartiles against the Q1 of the GFAP, the levels of GFAP were associated with poor outcome, and the adjusted risk of poor outcome increased by 211% (3.11[1.80–5.05], p < 0.001) and 522% (6.22[2.98–11.83], p < 0.001), respectively. Interestingly, GFAP improved the ability of NIHSS score to diagnose poor outcomes (area under the curve [AUC] of the combined model 0.82; 95% CI: 0.77–0.88; p = 0.02). Conclusion: GFAP levels are a novel and complementary biomarker to predict functional outcome 1 year after AIS

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Budka, H. "Non-glial specificities of immunocytochemistry for the glial fibrillary acidic protein (GFAP)." Acta Neuropathologica 72, no. 1 (1986): 43–54. http://dx.doi.org/10.1007/bf00687946.

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Gill, Jessica, Lawrence Latour, Ramon Diaz-Arrastia, Vida Motamedi, Christine Turtzo, Pashtun Shahim, Stefania Mondello, et al. "Glial fibrillary acidic protein elevations relate to neuroimaging abnormalities after mild TBI." Neurology 91, no. 15 (September 12, 2018): e1385-e1389. http://dx.doi.org/10.1212/wnl.0000000000006321.

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ObjectivesTo determine whether a panel of blood-based biomarkers can discriminate between patients with suspected mild traumatic brain injury (mTBI) with and without neuroimaging findings (CT and MRI).MethodsStudy participants presented to the emergency department with suspected mTBI (n = 277) with a CT and MRI scan and healthy controls (n = 49). Plasma concentrations of tau, glial fibrillary acidic protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1, and neurofilament light chain (NFL) were measured using the single-molecule array technology.ResultsConcentrations of GFAP, tau, and NFL were higher in patients with mTBI, compared with those of controls (p's < 0.01). GFAP yielded an area under the curve (AUC) of 0.93 (95% confidence interval [CI] 0.90–0.96), confirming its discriminatory power for distinguishing mTBI from controls. Levels of GFAP, tau, and NFL were higher in patients with trauma-related intracranial findings on CT compared with those with normal CT, with the only significant predictor being GFAP (AUC 0.77, 95% CI 0.70–0.84). Among patients with mTBI, tau, NFL, and GFAP differentiated subjects with and without MRI abnormalities with an AUC of 0.83, with GFAP being the strongest predictor. Combining tau, NFL, and GFAP showed a good discriminatory power (AUC 0.80, 95% CI 0.69–0.90) for detecting MRI abnormalities, even in patients with mTBI with a normal CT.ConclusionOur study confirms GFAP as a promising marker of brain injury in patients with acute mTBI. A combination of various biomarkers linked to different pathophysiologic mechanisms increases diagnostic subgroup accuracy. This multimarker strategy may guide medical decision making, facilitate the use of MRI scanning, and prove valuable in the stratification of patients with brain injuries in future clinical trials.Classification of evidenceClass I evidence that blood concentrations of GFAP, tau, and NFL discriminate patients with mTBI with and without neuroimaging findings.

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Matthews, Elizabeth, Ide Smets, Ryan Kammeyer, Maarten Titulaer, and Amanda Piquet. "Glial Fibrillary Acidic Protein (GFAP) Antibody-Associated Astrocytopathy in Systemic Sarcoidosis." Neurology 99, no. 23 Supplement 2 (December 5, 2022): S57.1—S57. http://dx.doi.org/10.1212/01.wnl.0000903452.01952.40.

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ObjectiveTo report two cases of glial fibrillary acidic protein (GFAP) antibody-associated meningoencephalitis in patients with biopsy-proven systemic sarcoidosis.BackgroundGFAP astrocytopathy is an autoimmune neurologic disease first defined in 2016. To our knowledge, no association with systemic sarcoidosis has been previously reported.Design/MethodsCase SeriesResultsPatient 1 is a 47-year-old woman with pre-existing pulmonary sarcoidosis treated with steroids and methotrexate with remission 6 years prior. She subsequently developed new-onset epilepsy, progressive ataxia and vertical diplopia. GFAP antibodies were positive in the cerebrospinal fluid (CSF) by cell-based assay (CBA). Body PET scan showed diffuse FDG avidity in her lungs, spleen, and lymph nodes, suggesting simultaneous reactivation of her systemic sarcoidosis. She was treated with steroids followed by infliximab with resolution of her symptoms. Patient 2 is a 58-year-old man with known pulmonary sarcoidosis, who was off immunosuppression at the time of his presentation but had received steroids 17 years prior. He presented with progressive apathy, memory disturbance, dysarthria, and gait instability. MRI revealed widespread T2 hyperintensities. GFAP antibodies were positive in CSF on CBA and confirmed by tissue-based immunofluorescence assay. He received steroids with initial response but relapsed after steroid discontinuation. He improved after restarting steroids and was subsequently transitioned to infliximab with sustained neurologic recovery.ConclusionsSarcoidosis is a poorly understood multi-system disorder that is presumably an immune-mediated response to yet unidentified antigen(s). It is known to co-exist with other autoimmune diseases, with autoimmune thyroiditis being most common. GFAP astrocytopathy is also poorly understood. GFAP is found intracellularly and similar to other antibody-mediated diseases against intracellular epitopes, the antibodies are believed to be a biomarker of underlying autoimmunity but not directly pathogenic. We report these cases to highlight a potential association between production of intrathecal GFAP antibodies and systemic sarcoidosis, which may provide insights into the pathogenesis of these two diseases.

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Regoli, Marì, Daniela Orazioli, Renato Gerli, and Eugenio Bertelli. "Glial Fibrillary Acidic Protein (GFAP)-like Immunoreactivity in Rat Endocrine Pancreas." Journal of Histochemistry & Cytochemistry 48, no. 2 (February 2000): 259–65. http://dx.doi.org/10.1177/002215540004800211.

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The study of intermediate filament expression in the pancreatic epithelium has been previously focused almost exclusively on cytokeratins. Transient vimentin immunoreactivity has also been detected in duct cells of rat fetal pancreas. Here we report that, in rat pancreas, intense GFAP-like immunoreactivity is detectable in a subpopulation of endocrine cells located in the periphery of the islet of Langerhans. In addition, staining appeared to be preferentially localized to the apical pole of the cells. Two different polyclonal antibodies were employed in this study, with analogous results. Staining of consecutive sections with anti-GFAP, anti-glucagon, and anti-somatostatin antibodies demonstrates that GFAP-like immunoreactivity is present in glucagon-secreting cells. The relevance of this finding is discussed.

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Hainfellner, Johannes A., Till Voigtländer, Thomas Ströbel, Peter R. Mazal, Alessia S. Maddalena, Adriano Aguzzi, and Herbert Budka. "Fibroblasts Can Express Glial Fibrillary Acidic protein (GFAP) In Vivo." Journal of Neuropathology & Experimental Neurology 60, no. 5 (May 2001): 449–61. http://dx.doi.org/10.1093/jnen/60.5.449.

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Mokuno, K., J. Kamholz, T. Behrman, C. Black, M. Sessa, D. Feinstein, V. Lee, and D. Pleasure. "Neuronal modulation of schwann cell glial fibrillary acidic protein (GFAP)." Journal of Neuroscience Research 23, no. 4 (August 1989): 396–405. http://dx.doi.org/10.1002/jnr.490230405.

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Rutka, James T., Masaji Murakami, Peter B. Dirks, Sherri Lynn Hubbard, Laurence E. Becker, Kozo Fukuyama, Shin Jung, Atsushi Tsugu, and Kazuhito Matsuzawa. "Role of glial filaments in cells and tumors of glial origin: a review." Journal of Neurosurgery 87, no. 3 (September 1997): 420–30. http://dx.doi.org/10.3171/jns.1997.87.3.0420.

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✓ In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). Glial fibrillary acidic protein is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.

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Rozovsky, Irina, Min Wei, David J. Stone, Hadi Zanjani, Christopher P. Anderson, Todd E. Morgan, and Caleb E. Finch. "Estradiol (E2) Enhances Neurite Outgrowth by Repressing Glial Fibrillary Acidic Protein Expression and Reorganizing Laminin." Endocrinology 143, no. 2 (February 1, 2002): 636–46. http://dx.doi.org/10.1210/endo.143.2.8615.

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Abstract Neuronal remodeling in response to deafferenting lesions in the brain can be enhanced by estradiol (E2). Astrocytes are among the targets of E2 in complex interactions with neurons and may support or inhibit neuronal remodeling. In ovariectomized female rats given entorhinal cortex lesions, E2 replacement inhibited the increase of glial fibrillary acidic protein (GFAP) protein. To model the role of E2 in these complex processes, we used the “wounding-in-a-dish” of astrocyte-neuron cocultures. Low physiological E2 (1 pm) blocks the wound-induced increase of GFAP expression (transcription and protein) and enhances neurite outgrowth. The transcriptional responses to E2 during wounding are mediated by sequences in the 5′-upstream region of the rat GFAP promoter. Concurrently, E2 reorganized astrocytic laminin into extracellular fibrillar arrays, which others have shown support neurite outgrowth. The inhibition of GFAP expression by E2 in this model is consistent with in vivo findings that E2 enhanced recovery from deafferenting cortical lesions by increased neurite outgrowth in association with decreased GFAP expression. More generally, we hypothesize that physiological variations in E2 levels modulate neuronal plasticity through direct effects on GFAP transcription that, in turn, modify GFAP-containing intermediate filaments and reorganize astrocytic laminin.

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Qin, Bing, Ruizhen Wu, Yaqing Shu, Yuge Wang, Boguang Yu, Xiaobo Sun, and Wei Qiu. "Protein A Immunoadsorption Relieves Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy after Unsuccessful Methylprednisolone Treatment." Neuroimmunomodulation 28, no. 3 (2021): 187–92. http://dx.doi.org/10.1159/000514547.

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Background: Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) is a recently defined autoimmune inflammatory disease of the central nervous system in which GFAP IgG is present in the cerebrospinal fluid (CSF). Its primary clinical manifestation is meningoencephalitis, and it usually responds well to corticosteroids. Herein, we report a case of a patient with GFAP-A with initial symptoms of psychological and cognitive impairment, which did not respond to high-dose methylprednisolone therapy but was successfully treated with protein A immunoadsorption (PAIA) therapy. Methods: GFAP IgG was detected by indirect immunofluorescence assay. The patient’s data were analyzed retrospectively. Results: A 48-year-old man presented with anxiety, depression, cognitive decline, tremor, gait disturbance, and fecal and urine incontinence. Autoimmune GFAP-A was diagnosed based on the following: (1) T2-weighted and fluid-attenuated inversion recovery MRI findings of hypersensitive lesions in the subcortical and deep white matter of the brain, with multiple longitudinally extensive lesions in the cervical and chest regions of the spinal cord, and (2) high levels of GFAP IgG in the CSF. Clinical symptoms and abnormalities detected on neuroimaging worsened after administration of high-dose intravenous methylprednisolone (IVMP) and intravenous immunoglobulin (IVIG) but improved significantly after PAIA therapy. Conclusion: Psychological impairment can be the first sign of autoimmune GFAP-A. PAIA might be an effective treatment for patients with GFAP-A who respond poorly to conventional IVMP and IVIG therapy.

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Heller, Carolin, Martha S. Foiani, Katrina Moore, Rhian Convery, Martina Bocchetta, Mollie Neason, David M. Cash, et al. "Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 3 (January 14, 2020): 263–70. http://dx.doi.org/10.1136/jnnp-2019-321954.

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BackgroundThere are few validated fluid biomarkers in frontotemporal dementia (FTD). Glial fibrillary acidic protein (GFAP) is a measure of astrogliosis, a known pathological process of FTD, but has yet to be explored as potential biomarker.MethodsPlasma GFAP and neurofilament light chain (NfL) concentration were measured in 469 individuals enrolled in the Genetic FTD Initiative: 114 C9orf72 expansion carriers (74 presymptomatic, 40 symptomatic), 119 GRN mutation carriers (88 presymptomatic, 31 symptomatic), 53 MAPT mutation carriers (34 presymptomatic, 19 symptomatic) and 183 non-carrier controls. Biomarker measures were compared between groups using linear regression models adjusted for age and sex with family membership included as random effect. Participants underwent standardised clinical assessments including the Mini-Mental State Examination (MMSE), Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale and MRI. Spearman’s correlation coefficient was used to investigate the relationship of plasma GFAP to clinical and imaging measures.ResultsPlasma GFAP concentration was significantly increased in symptomatic GRN mutation carriers (adjusted mean difference from controls 192.3 pg/mL, 95% CI 126.5 to 445.6), but not in those with C9orf72 expansions (9.0, –61.3 to 54.6), MAPT mutations (12.7, –33.3 to 90.4) or the presymptomatic groups. GFAP concentration was significantly positively correlated with age in both controls and the majority of the disease groups, as well as with NfL concentration. In the presymptomatic period, higher GFAP concentrations were correlated with a lower cognitive score (MMSE) and lower brain volume, while in the symptomatic period, higher concentrations were associated with faster rates of atrophy in the temporal lobe.ConclusionsRaised GFAP concentrations appear to be unique to GRN-related FTD, with levels potentially increasing just prior to symptom onset, suggesting that GFAP may be an important marker of proximity to onset, and helpful for forthcoming therapeutic prevention trials.

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Sugimoto, Naotoshi, Shinji Miwa, Hiroyuki Nakamura, Hiroyuki Tsuchiya, and Akihiro Yachie. "Protein kinase A and Epac activation by cAMP regulates the expression of glial fibrillary acidic protein in glial cells." Archives of Biological Sciences 68, no. 4 (2016): 795–801. http://dx.doi.org/10.2298/abs160112067s.

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Cyclic adenosine monophosphate (cAMP) controls differentiation in several types of cells during brain development. However, the molecular mechanism of cAMP-controlled differentiation is not fully understood. We investigated the role of protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac) on cAMP-induced glial fibrillary acidic protein (GFAP), an astrocyte marker, in cultured glial cells. B92 glial cells were treated with cAMP-elevating drugs, an activator of adenylate cyclase, phosphodiesterase inhibitor and a ? adrenal receptor agonist. These cAMP-elevating agents induced dramatic morphological changes and expression of GFAP. A cAMP analog, 8-Br-cAMP, which activates Epac as well as PKA, induced GFAP expression and morphological changes, while another cAMP analog, 8-CPT-cAMP, which activates Epac with greater efficacy when compared to PKA, induced GFAP expression but very weak morphological changes. Most importantly, the treatment with a PKA inhibitor partially reduced cAMP-induced GFAP expression. Taken together, these results indicate that cAMP-elevating drugs lead to the induction of GFAP via PKA and/or Epac activation in B92 glial cells.

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Tuba, Andrea, Lázló Kállai, and Mihály Kálmán. "A Rapid Replacement of Vimentin-Containing Radial Glia by Glial Fibrillary Acidic Protein-Containing Astrocytes in Transplanted Telencephalon." Journal of Neural Transplantation and Plasticity 6, no. 1 (1997): 21–29. http://dx.doi.org/10.1155/np.1997.21.

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The present study follows the early events in the development of astroglia in rat embryonic (El5) tissue grafted into the cortex of adult rats. Astroglial elements (radial glia and astrocytes) were studied by glial fibrillary acidic protein (GFAP) and vimentin immunohistochemistry on post-transplantation (PT) days 7, 11, 14, 17, and 21. At PT7, GFAP-immunopositive elements were only scarce fibers in the transplants. At PTll, a dense network of long, GFAP-immunopositive fibers enmeshed the entire transplant, and astrocytes were already recognized. The fibers also showed vimentin immunoreactivity. By PT14, astrocytes became the predominant GFAP-labeled elements, although a few long fibers persisted. When compared with in situ development, the grafts showed earlier GFAP-immunoreactivity and earlier appearance of astrocytes, as well as a more rapid transition from the immature to the mature form of the glial system.

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Toda, Y., N. Matsuki, M. Shibuya, I. Fujioka, S. Tamahara, and K. Ono. "Glial fibrillary acidic protein (GFAP) and anti-GFAP autoantibody in canine necrotising meningoencephalitis." Veterinary Record 161, no. 8 (August 25, 2007): 261–64. http://dx.doi.org/10.1136/vr.161.8.261.

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Jagadha, V., W. C. Halliday, and L. E. Becker. "Glial Fibrillary Acidic Protein (GFAP) in Oligodendrogliomas: A Reflection of Transient GFAP Expression by Immature Oligodendroglia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, no. 4 (November 1986): 307–11. http://dx.doi.org/10.1017/s0317167100036623.

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ABSTRACT:Fourteen pure oligodendrogliomas were studied by light- and electronmicroscopy and immunohistochemistry to examine glial fibrillary acidic protein (GFAP) positivity in the tumors. To compare the immunohistochemical staining patterns of neoplastic oligodendroglia and immature oligodendroglia, myelination glia in the white matter of eight normal brains from children under 6 months of age were studied. The tumors possessed light microscopic and ultrastructural features characteristic of oligodendrogliomas. Microtubules were found in the cytoplasm of nine tumors on electronmicroscopy. In one, intermediate filaments and microtubules were observed in occasional tumor cells with polygonal crystalline structures in the cytoplasm. Using the peroxidase-antiperoxidase technique, all specimens were stained for GFAP, vimentin, S-100 and neuron-specific enolase (NSE). In nine tumors, variable numbers of cells with an oligodendroglial morphology reacted positively for GFAP. All tumors were positive for S-100 and negative for vimentin and NSE. The myelination glia in the eight normal brains stained positively for GFAP but not for vimentin. Vimentin is expressed by developing, reactive and neoplastic astrocytes. Thus, GFAP positivity combined with vimentin negativity in both neoplastic and immature oligodendroglia suggests that GFAP positivity in oligodendrogliomas may reflect the transient expression of this intermediate filament by immature oligodendroglia.

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Deshmukh, Vishwajit Ravindra, Pranav Prasoon, and Subrata Basu Ray. "Expression of gap junctions bearing connexin-43 subunits and glial fibrillary acidic protein in the rat dorsal root ganglia following hind paw incision." International Journal of Research in Medical Sciences 5, no. 1 (December 19, 2016): 306. http://dx.doi.org/10.18203/2320-6012.ijrms20164568.

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Background: Dorsal root ganglion (DRG) neurons mediate the transmission of sensation from the periphery. DRG neurons are pseudounipolar in nature and enveloped by the satellite glial cells (SC). Satellite glial cells have been reported to influence neuronal excitability via gap junctions. Postoperative pain causes induction of various neurotransmitters such as connexin-43 and glial fibrillary acidic protein (GFAP), in the satellite cells surrounding neuronal cell bodiesObjective: To study the expression of connexin-43 and Glial fibrillary acidic protein after hind paw incision.Methods: Male adult Sprague-Dawley rats (n=12) were used. Rats were randomly divided into two groups. Group I (n=6) and Group II (n=6) for immunohistochemical study with glial fibrillary acidic protein (GFAP) and connexin-43 (Cx-43) respectively. In this study, rats were subjected to noxious stimuli on the right hind paw under general anesthesia. Dorsal root ganglia of both sides (L4 spinal nerves) were isolated after transcardiac fixation with 4% paraformaldehyde. The ganglia from the non-incised side were taken as the control group.Results: Unipolar neurons in the DRG were surrounded by satellite cells. The satellite cells were positive for GFAP, which showed increased expression on the surgical side after noxious stimuli. Cx-43 immunostaining also showed an increased expression in the periphery of neuronal cell bodies of surgical side representing the location of gap junctions and hyperexcitability of neurons.Conclusions: Small to medium sized neurons carry pain sensation from the periphery to the central nervous system. Increased gap junctions were noted in small neurons and satellite cells after surgery. Gap junctions might contribute to increased excitability of small neurons in postoperative pain.

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Bortoli, Erica, Juliana K. Frizzo, and Carlos Alberto Gonçalves. "Modulação do estado de polimerização in vitro dos filamentos intermediários em astrócitos pela fosforilação e proteína S100B." Ciência e Natura 25, no. 25 (December 9, 2003): 41. http://dx.doi.org/10.5902/2179460x27235.

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Intermediate filaments represent a major cytoskeleton constituent in eukaryotic cells. GFAP ("glial fibrillary acidic protein") is the monomer of these filaments in astrocytes and its polymerization is apparently modulated by phosphorylation and by interaction with S100B, a calcium-binding protein. In this study we investigate in vitro polymerization of GFAP, using an assay based on imidazol/high magnesium-induced sedimentation. In fact, soluble GFAP (nonpolymerized) increased about 25% in presence of S100B or PKA (protein kinase A). These data suggest that both mechanisms could be acting in the cycle of polymerization/depolymerization of GFAP at different times and/or conditions, therefore affecting glial plasticity.

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Traub, Jan, Katja Grondey, Tobias Gassenmaier, Dominik Schmitt, Georg Fette, Stefan Frantz, Valérie Boivin-Jahns, et al. "Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction." International Journal of Molecular Sciences 23, no. 18 (September 7, 2022): 10304. http://dx.doi.org/10.3390/ijms231810304.

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Acute ischemic cardiac injury predisposes one to cognitive impairment, dementia, and depression. Pathophysiologically, recent positron emission tomography data suggest astroglial activation after experimental myocardial infarction (MI). We analyzed peripheral surrogate markers of glial (and neuronal) damage serially within 12 months after the first ST-elevation MI (STEMI). Serum levels of glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were quantified using ultra-sensitive molecular immunoassays. Sufficient biomaterial was available from 45 STEMI patients (aged 28 to 78 years, median 56 years, 11% female). The median (quartiles) of GFAP was 63.8 (47.0, 89.9) pg/mL and of NfL 10.6 (7.2, 14.8) pg/mL at study entry 0–4 days after STEMI. GFAP after STEMI increased in the first 3 months, with a median change of +7.8 (0.4, 19.4) pg/mL (p = 0.007). It remained elevated without further relevant increases after 6 months (+11.7 (0.6, 23.5) pg/mL; p = 0.015), and 12 months (+10.3 (1.5, 22.7) pg/mL; p = 0.010) compared to the baseline. Larger relative infarction size was associated with a higher increase in GFAP (ρ = 0.41; p = 0.009). In contrast, NfL remained unaltered in the course of one year. Our findings support the idea of central nervous system involvement after MI, with GFAP as a potential peripheral biomarker of chronic glial damage as one pathophysiologic pathway.

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Amalia, Lisda. "Glial Fibrillary Acidic Protein (GFAP): Neuroinflammation Biomarker in Acute Ischemic Stroke." Journal of Inflammation Research Volume 14 (December 2021): 7501–6. http://dx.doi.org/10.2147/jir.s342097.

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Bozoky, Béla, Dankwart Stiller, and Jenö Ormos. "Immunohistochemical demonstration of glial fibrillary acidic protein (GFAP) in nasal gliomas." Acta Histochemica 81, no. 1 (January 1987): 117—IN3. http://dx.doi.org/10.1016/s0065-1281(87)80093-4.

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Hajós, Ferenc. "Changes in Glial Fibrillary Acidic Protein (GFAP) Immonureactivity Reflect Neuronal States." Neurochemical Research 33, no. 8 (May 16, 2008): 1643–50. http://dx.doi.org/10.1007/s11064-008-9745-2.

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Fukuyama, Ryuichi, Shinji Fushiki, and Setsuya Fujita. "Purification of glial fibrillary acidic protein (GFAP) from normal bovine brain." Journal of Neuroscience Methods 40, no. 2-3 (December 1991): 133–37. http://dx.doi.org/10.1016/0165-0270(91)90062-5.

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Arellano, Janetta, and Michael Sy. "Treatment-Refractory Autoimmune Glial Fibrillary Acidic Protein Meningoencephalomyelitis in a Young Adult Female." Neurology 99, no. 23 Supplement 2 (December 5, 2022): S55.1—S55. http://dx.doi.org/10.1212/01.wnl.0000903444.16135.69.

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ObjectiveTo describe a case of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy refractory to immunotherapy without evidence of malignancy or coexisting autoimmunity.BackgroundAutoimmune GFAP astrocytopathy is an autoimmune disease of the central nervous system associated with the presence of GFAP-IgG in the CSF. Patients may present with acute or subacute onset of headache, encephalopathy, seizures, abnormal vision, weakness or numbness, postural tremor and cerebellar ataxia. GFAP astrocytopathy is usually corticocorticosteroid-responsive in the acute setting but may rarely require maintenance immunotherapy to prevent relapse. Treatment refractory cases should trigger work up for coexisting autoimmunity or malignancy.Design/MethodsA 35-year-old female patient presented with subacute meningoencephalomyelitis with prodromal symptoms.ResultsHer cerebrospinal fluid revealed lymphocytic pleocytosis and elevated protein. Brain magnetic resonance imaging (MRI) with and without contrast showed perivascular radial enhancement and periventricular T2 FLAIR hyperintensity. Spinal MRI with and without contrast demonstrated longitudinal T2 FLAIR hyperintensity from T1-T2 to T7-T8. Despite high dose steroid treatment, her disease progressed with an enlarging periventricular lesion and worsening visual acuity. Biopsy of the enhancing periventricular lesion showed perivascular inflammation. After five cycles of plasma exchange along with a five-day course of intravenous methylprednisolone 1 gram daily, her symptoms stabilized. The CSF autoimmune encephalopathy panel (Mayo Clinic Laboratories) came back positive for GFAP-IgG antibody on tissue immunofluorescence assay, and was confirmed positive by GFAP cell-based assay. No neoplastic disease was identified using high resolution PET/CT scans. Based on the aggressiveness of her disease, she received one cycle of cyclophosphamide, and was discharged home on an oral corticosteroid taper. Even one year after addition of both mycophenolate mofetil and rituximab, MRI imaging continued to reveal new enhancing lesions.ConclusionsAutoimmune GFAP astrocytopathy may sometimes require long-term immunosuppression even without presence of malignancy or other coexisting autoimmune disease.

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Natarajan, Satheesh, and Jayaraj Joseph. "A novel time-resolved fluorescent lateral flow immunoassay for quantitative detection of the trauma brain injury biomarker-glial fibrillary acidic protein." Sensors & Diagnostics 1, no. 1 (2022): 193–97. http://dx.doi.org/10.1039/d1sd00021g.

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A highly sensitive time-resolved fluorescence lateral flow immunoassay (TRF-LFIA) was developed to quantify glial fibrillary acidic protein (GFAP), a trauma brain injury (TBI) biomarker in blood, for the purpose of providing a diagnosis of mild brain injury.

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Eng, Lawrence F. "Glial fibrillary acidic protein (GFAP): the major protein of glial intermediate filaments in differentiated astrocytes." Journal of Neuroimmunology 8 (1985): 203–14. http://dx.doi.org/10.1016/s0165-5728(85)80063-1.

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Loncarevic-Vasiljkovic, Natasa, Vesna Pesic, N. Tanic, Desanka Milanovic, Aleksandra Mladenovic-Djordjevic, Milka Perovic, Selma Kanazir, and Sabera Ruzdijic. "Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury." Archives of Biological Sciences 65, no. 1 (2013): 255–64. http://dx.doi.org/10.2298/abs1301255l.

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The recovery period following cortical injury (CI) is characterized by a dynamic and highly complex interplay between beneficial and detrimental events. The aim of this study was to examine the expressions of Glial Fibrillary Acidic Protein (GFAP), Apolipoprotein E (ApoE) and Amyloid Precursor Protein (APP), all of which are involved in brain plasticity and neurodegeneration. Our results reveal that CI strongly influenced GFAP, ApoE and APP mRNA expression, as well as GFAP and ApoE protein expression. Considering the pivotal role of these proteins in the brain, the obtained results point to their potential contribution in neurodegeneration and consequent Alzheimer?s disease development.

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Goyne, Christopher E., David Piccioni, Jason Handwerker, and Amutha Rajagopal. "Radiographic evolution of myelitis in a case of glial fibrillary acidic protein (GFAP) astrocytopathy." BMJ Case Reports 16, no. 3 (March 2023): e248921. http://dx.doi.org/10.1136/bcr-2022-248921.

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Autoimmune glial fibrillar acidic protein (GFAP) astrocytopathy is a rare autoimmune neuroinflammatory disorder that affects the central nervous system. We present a case of GFAP astrocytopathy in a middle-aged male who presented with constitutional symptoms, encephalopathy and lower extremity weakness and numbness. Initially MRI of the spine was normal, but he subsequently developed longitudinally extensive myelitis and meningoencephalitis. Workup for infectious aetiologies was negative and the patient’s clinical course worsened despite broad antimicrobial coverage. Ultimately, he was found to have anti-GFAP antibodies in his cerebral spinal fluid consistent with GFAP astrocytopathy. He was treated with steroids and plasmapheresis with clinical and radiographic improvement. This case demonstrates the temporal evolution of myelitis on MRI in a case of steroid-refractory GFAP astrocytopathy.

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Murphy, Katrina G., James D. Hatton, and Hoi Sang U. "Role of glial fibrillary acidic protein expression in the biology of human glioblastoma U-373MG cells." Journal of Neurosurgery 89, no. 6 (December 1998): 997–1006. http://dx.doi.org/10.3171/jns.1998.89.6.0997.

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Object. The relationship between glial fibrillary acidic protein (GFAP) expression and glial tumor cell behavior has not been well defined. The goal of this study was to examine this relationship further. Methods. To investigate the relationship between GFAP expression and glial tumor cell behavior, the authors isolated clones from the human glioblastoma cell line, U-373MG, according to their level of GFAP expression. Immunochemical analysis demonstrated that one clone had consistently low GFAP expression (approximately 93% of cells were GFAP negative), whereas a second clone had consistently high GFAP expression (approximately 80% of the cells were GFAP positive). The structure, population doubling time, saturation density, anchorage-independent growth, migratory rate, and invasive potential of these two clones were determined in relation to their level of GFAP expression. Morphologically, both clones were composed of ameboid as well as stellate components. Although the population doubling times of the two clones were equally rapid, the clone with low GFAP expression demonstrated a slightly higher saturation density compared with the clone with high GFAP expression. In an anchorage-independent environment (soft agar), a greater difference in growth characteristics was noted between the two clones: the high-expression clone formed more colonies and these colonies were compact, well defined, and spherical, whereas the low-expression clone formed predominantly smaller, two-dimensional colonies with vague boundaries and isolated cells or groups of cells at the periphery. In contrast to these minor differences between the clones, the low-expression clone showed a markedly increased migratory rate and invasive potential compared with the high-expression clone. Therefore, the clone with reduced GFAP expression appeared more aggressive, demonstrating decreased contact inhibition, increased migratory rate, and increased invasive potential. Conclusions. These results suggest a direct correlation between GFAP expression and some measures of aggressive tumor growth and transformation properties.

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Koh, Kyungmi, Karim Lee, Jin-Hyun Ahn, and Sunyoung Kim. "Human cytomegalovirus infection downregulates the expression of glial fibrillary acidic protein in human glioblastoma U373MG cells: identification of viral genes and protein domains involved." Journal of General Virology 90, no. 4 (April 1, 2009): 954–62. http://dx.doi.org/10.1099/vir.0.006486-0.

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Human cytomegalovirus (HCMV) has tropism for glial cells, among many other cell types. It was reported previously that the stable expression of HCMV immediate-early protein 1 (IE1) could dramatically reduce the RNA level of glial fibrillary acidic protein (GFAP), an astroglial cell-specific intermediate filament protein, which is progressively lost with an increase in glioma malignancy. To understand this phenomenon in the context of virus infection, a human glioblastoma cell line, U373MG, was infected with HCMV (strain AD169 or Towne). The RNA level of GFAP was reduced by more than 10-fold at an m.o.i. of 3 at 48 h post-infection, whilst virus treated with neutralizing antibody C23 or with UV light had a much-reduced effect. Treatment of infected cells with ganciclovir did not prevent HCMV-mediated downregulation of GFAP. Although the expression of GFAP RNA is downregulated in IE1-expressing cells, a mutant HCMV strain lacking IE1 still suppressed GFAP, indicating that other IE proteins may be involved. IE2 is also proposed to be involved in GFAP downregulation, as an adenoviral vector expressing IE2 could also reduce the RNA level of GFAP. Data from the mutational analysis indicated that HCMV infection might affect the expression of this structural protein significantly, primarily through the C-terminal acidic region of the IE1 protein.

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Hariyanto, Arief S., Endang Retnowati, and Agus Turchan. "SERUM GLIAL FIBRILLARY ACIDIC PROTEIN LEVELS PROFILE IN PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURY." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 24, no. 1 (March 29, 2018): 24. http://dx.doi.org/10.24293/ijcpml.v24i1.1151.

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Glial Fibrillary Acidic Protein (GFAP) sangat khas untuk otak (highly brain specific protein), sebagai petunjuk kerusakan sel,merupakan protein yang berhubungan dengan peningkatan tekanan intrakranial dan sebagai petanda perjalanan penyakit di pasiencedera otak. Penelitian ini menganalisis profil kadar GFAP serum pasien cedera otak berat sebagai petanda perjalanan penyakit dankeluarannya. Desain penelitian deskriptif observasional. Kadar GFAP serum dari sampel darah vena, diperiksa dengan metode ELISApada hari pertama datang ke Instalasi Gawat Darurat dan hari ke-2,3,4 perawatan. Jumlah sampel 25 orang, laki-laki 20 orang (80%),perempuan 5 orang (20%). Umur terbanyak ≤ 25 tahun, 8 orang (32%), rerata umur 35,92 ± 13,80 tahun. Jejas berdasarkan hasilCT Scan kepala terbanyak Diffuse Axonal Injury (DAI) 7 (28%), tindakan operasi sebanyak 18 (72 %), non-operasi 7 (28%), penyebabcedera, kecelakaan lalu lintas 23 (92%), jatuh 2 (8%). Rerata kadar GFAP serum hari ke-1,2,3,4 berturut-turut 2,72±1,44 ng/mL,1,85±0,85 ng/mL, 1,67±1,26 ng/mL, 0,79±0,35 ng/mL. Keluaran pasien, hidup 19 (76%), meninggal 6 (24%). GFAP sangat khaspada otak berguna sebagai petanda di pasien cedera otak berat, yaitu peningkatan kadarnya dapat digunakan sebagai faktor perjalananpenyakit untuk kematian dan keluarannya. Peningkatan kadar GFAP serum dapat digunakan sebagai faktor perjalanan penyakit.Penelitian lanjutan diperlukan dengan sampel yang lebih besar

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Guma, Fatima C. R., Tanira G. Mello, Claudia S. Mermelstein, Vitor A. Fortuna, Susana T. Wofchuk, Carmem Gottfried, Regina M. Guaragna, Manoel L. Costa, and Radovan Borojevic. "Intermediate filaments modulation in an in vitro model of the hepatic stellate cell activation or conversion into the lipocyte phenotype." Biochemistry and Cell Biology 79, no. 4 (August 1, 2001): 409–17. http://dx.doi.org/10.1139/o01-027.

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Hepatic stellate cells are intralobular connective tissue cells expressing the myofibroblast or the lipocyte phenotypes. They participate in homeostasis of the liver extracellular matrix, repair, regeneration, and fibrosis under the former phenotype, and control the retinol metabolism, storage, and release under the latter one. They are heterogeneous in terms of their tissue distribution, function, and expression of cytoskeletal proteins. We have studied the expressions of intermediate filaments in the cloned GRX cell line representative of murine hepatic stellate cells, by immunolabeling, reverse transcription polymerase chain reaction (RT-PCR), immunoprecipitation and Western blots. GRX cells expressed vimentin, desmin, glial fibrillary acidic protein (GFAP), and smooth muscle α actin (SM-αA). Vimentin, desmin, and SM-αA were expressed in all cultures. GFAP showed a heterogeneous intensity of expression and did not form a filamentous cytoskeletal network, showing a distinct punctuate cytoplasmic distribution. When activated by inflammatory mediators, GRX cells increased expression of desmin and GFAP. Retinol-mediated induction of the lipocyte phenotype elicited a strong decrease of intermediate filament protein expression and the collapse of the filamentous structure of the cytoskeleton. Quiescent hepatic stellate precursors can respond to physiologic or pathologic stimuli, expressing activated myofibroblast or lipocyte phenotypes with distinct patterns of cytoskeleton structure, metabolic function, and interaction with the tissue environment.Key words: intermediate filaments, desmin, glial fibrillary acidic protein, GFAP, hepatic stellate cells, liver.

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