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Artykuły w czasopismach na temat „GFAP/Gfap”

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Data publikacji: 2 czerwca 2025

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1

Perng, Ming-Der, Shu-Fang Wen, Terry Gibbon та ін. "Glial Fibrillary Acidic Protein Filaments Can Tolerate the Incorporation of Assembly-compromised GFAP-δ, but with Consequences for Filament Organization and αB-Crystallin Association". Molecular Biology of the Cell 19, № 10 (2008): 4521–33. http://dx.doi.org/10.1091/mbc.e08-03-0284.

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The glial fibrillary acidic protein (GFAP) gene is alternatively spliced to give GFAP-α, the most abundant isoform, and seven other differentially expressed transcripts including GFAP-δ. GFAP-δ has an altered C-terminal domain that renders it incapable of self-assembly in vitro. When titrated with GFAP-α, assembly was restored providing GFAP-δ levels were kept low (∼10%). In a range of immortalized and transformed astrocyte derived cell lines and human spinal cord, we show that GFAP-δ is naturally part of the endogenous intermediate filaments, although levels were low (∼10%). This suggests tha

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Bernardos, Rebecca L., and Pamela A. Raymond. "GFAP transgenic zebrafish." Gene Expression Patterns 6, no. 8 (2006): 1007–13. http://dx.doi.org/10.1016/j.modgep.2006.04.006.

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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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Eng, Lawrence F., and Roopa S. Ghirnikar. "GFAP and Astrogliosis." Brain Pathology 4, no. 3 (1994): 229–37. http://dx.doi.org/10.1111/j.1750-3639.1994.tb00838.x.

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Brenner, Michael, and Albee Messing. "GFAP Transgenic Mice." Methods 10, no. 3 (1996): 351–64. http://dx.doi.org/10.1006/meth.1996.0113.

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Shafit-Zagardo, B., C. Peterson, and J. E. Goldman. "INCREASES IN GFAP AND GFAP mRNA IN BRINDLED MOUSE CNS." Journal of Neuropathology and Experimental Neurology 46, no. 3 (1987): 361. http://dx.doi.org/10.1097/00005072-198705000-00095.

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Galou, M., E. Colucci-Guyon, D. Ensergueix, et al. "Disrupted glial fibrillary acidic protein network in astrocytes from vimentin knockout mice." Journal of Cell Biology 133, no. 4 (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-) mi

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Zoltewicz, J. Susie, Dancia Scharf, Boxuan Yang, Aarti Chawla, Kimberly J. Newsom, and Lijuan Fang. "Characterization of Antibodies that Detect Human GFAP after Traumatic Brain Injury." Biomarker Insights 7 (January 2012): BMI.S9873. http://dx.doi.org/10.4137/bmi.s9873.

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After traumatic brain injury (TBI), glial fibrillary acidic protein (GFAP) and other brain-derived proteins and their breakdown products are released into biofluids such as CSF and blood. Recently, a sandwich ELISA was constructed that measured GFAP concentrations in CSF or serum from human mild-moderate TBI patients. The goals of the present study were to characterize the same two antibodies used in this ELISA, and to determine which GFAP bands are detected by this antibody combination. Here, both antibodies recognized GFAP specifically in human brain and post-TBI CSF in a cluster of bands ra

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Chekanova, Ekaterina O., Аlla А. Shabalina, Taras O. Simaniv, et al. "Relapsing Autoimmune GFAP Astrocytopathy: Case Report." Annals of Clinical and Experimental Neurology 17, no. 4 (2024): 89–96. http://dx.doi.org/10.54101/acen.2023.4.11.

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Introduction. Glial fibrillary acidic protein (GFAP) is the main component of intermediate astrocyte filaments. In 2016, anti-GFAP antibodies (Ab) were identified as the specific biomarker for the first established CNS inflammatory disorder subsequently called autoimmune astrocytopathy associated with anti-GFAP Ab (A-GFAP-A). Since GFAP is localized intracellularly, GFAP Ab do not appear to be directly pathogenic though serve as a biomarker of immune inflammation. Although presence of GFAP-Ab in the serum (but not in the CSF) could be observed in various CNS immune-mediated diseases, detection

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10

Yuan, Wei, Liaoxun Lu, Muding Rao, et al. "GFAP hyperpalmitoylation exacerbates astrogliosis and neurodegenerative pathology in PPT1-deficient mice." Proceedings of the National Academy of Sciences 118, no. 13 (2021): e2022261118. http://dx.doi.org/10.1073/pnas.2022261118.

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The homeostasis of protein palmitoylation and depalmitoylation is essential for proper physiological functions in various tissues, in particular the central nervous system (CNS). The dysfunction of PPT1 (PPT1-KI, infantile neuronal ceroid lipofuscinosis [INCL] mouse model), which catalyze the depalmitoylation process, results in serious neurodegeneration accompanied by severe astrogliosis in the brain. Endeavoring to determine critical factors that might account for the pathogenesis in CNS by palm-proteomics, glial fibrillary acidic protein (GFAP) was spotted, indicating that GFAP is probably

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11

Kimura, Akio, Akira Takekoshi, and Takayoshi Shimohata. "Characteristics of Movement Disorders in Patients with Autoimmune GFAP Astrocytopathy." Brain Sciences 12, no. 4 (2022): 462. http://dx.doi.org/10.3390/brainsci12040462.

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Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) is a type of autoimmune corticosteroid-responsive meningoencephalitis that occurs with or without myelitis. Movement disorders have been reported in GFAP-A patients but have not been characterized. In this study, we examined the characteristics of movement disorders in GFAP-A patients. We retrospectively reviewed clinical data from 87 consecutive patients with GFAP-A attending Gifu University Hospital in Japan. We compared the demographics, clinical features, cerebrospinal fluid characteristics, and neuroimaging findings

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12

Pekny, Milos, Clas B. Johansson, Camilla Eliasson, et al. "Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin." Journal of Cell Biology 145, no. 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

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Lin, Ni-Hsuan, Yu-Shan Huang, Puneet Opal, Robert D. Goldman, Albee Messing, and Ming-Der Perng. "The role of gigaxonin in the degradation of the glial-specific intermediate filament protein GFAP." Molecular Biology of the Cell 27, no. 25 (2016): 3980–90. http://dx.doi.org/10.1091/mbc.e16-06-0362.

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Alexander disease (AxD) is a primary genetic disorder of astrocytes caused by dominant mutations in the gene encoding the intermediate filament (IF) protein GFAP. This disease is characterized by excessive accumulation of GFAP, known as Rosenthal fibers, within astrocytes. Abnormal GFAP aggregation also occurs in giant axon neuropathy (GAN), which is caused by recessive mutations in the gene encoding gigaxonin. Given that one of the functions of gigaxonin is to facilitate proteasomal degradation of several IF proteins, we sought to determine whether gigaxonin is involved in the degradation of

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Hagemann, Tracy L., Sierra Coyne, Alder Levin, Liqun Wang, Mel B. Feany, and Albee Messing. "STAT3 Drives GFAP Accumulation and Astrocyte Pathology in a Mouse Model of Alexander Disease." Cells 12, no. 7 (2023): 978. http://dx.doi.org/10.3390/cells12070978.

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Alexander disease (AxD) is caused by mutations in the gene for glial fibrillary acidic protein (GFAP), an intermediate filament expressed by astrocytes in the central nervous system. AxD-associated mutations cause GFAP aggregation and astrogliosis, and GFAP is elevated with the astrocyte stress response, exacerbating mutant protein toxicity. Studies in mouse models suggest disease severity is tied to Gfap expression levels, and signal transducer and activator of transcription (STAT)-3 regulates Gfap during astrocyte development and in response to injury and is activated in astrocytes in rodent

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15

Konnova, Elena A., Alexandru-Florian Deftu, Paul Chu Sin Chung, et al. "Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury." International Journal of Molecular Sciences 24, no. 21 (2023): 15559. http://dx.doi.org/10.3390/ijms242115559.

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Satellite glial cells (SGCs), enveloping primary sensory neurons’ somas in the dorsal root ganglion (DRG), contribute to neuropathic pain upon nerve injury. Glial fibrillary acidic protein (GFAP) serves as an SGC activation marker, though its DRG satellite cell specificity is debated. We employed the hGFAP-CFP transgenic mouse line, designed for astrocyte studies, to explore its expression within the peripheral nervous system (PNS) after spared nerve injury (SNI). We used diverse immunostaining techniques, Western blot analysis, and electrophysiology to evaluate GFAP+ cell changes. Post-SNI, G

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16

Maria, B. L., D. Wong, and V. I. Kalnins. "Dibutyryl Cyclic AMP Induces Vimentin and GFAP Expression in Cultured Medulloblastoma Cells." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 1 (1990): 15–20. http://dx.doi.org/10.1017/s0317167100029954.

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ABSTRACT:Evidence for the astrocytic lineage in medulloblastomas rests largely on the detection of the glial fibrillary acidic protein (GFAP) from which intermediate filaments (IF) specific for astrocytes are assembled. Astrocyte progenitor cells from the mouse neopallium however express another IF protein, vimentin, before they acquire GFAP in vivo and in vitro. The purpose of the current study was to determine if cells obtained from a focally GFAP-positive posterior fossa medulloblastoma previously shown to acquire GFAP in response to dibutyryl cyclic AMP (dBcAMP), also express vimentin befo

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Fernández-Albarral, Jose A., Rosa de Hoz, José A. Matamoros, et al. "Retinal Changes in Astrocytes and Müller Glia in a Mouse Model of Laser-Induced Glaucoma: A Time-Course Study." Biomedicines 10, no. 5 (2022): 939. http://dx.doi.org/10.3390/biomedicines10050939.

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Macroglia (astrocytes and Müller glia) may play an important role in the pathogenesis of glaucoma. In a glaucoma mouse model, we studied the effects of unilateral laser-induced ocular hypertension (OHT) on macroglia in OHT and contralateral eyes at different time points after laser treatment (1, 3, 5, 8 and 15 days) using anti-GFAP and anti-MHC-II, analyzing the morphological changes, GFAP-labelled retinal area (GFAP-PA), and GFAP and MHC-II immunoreactivity intensities ((GFAP-IRI and MHC-II-IRI)). In OHT and contralateral eyes, with respect to naïve eyes, at all the time points, we found the

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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 (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

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Chen, W. J., and R. K. Liem. "Reexpression of glial fibrillary acidic protein rescues the ability of astrocytoma cells to form processes in response to neurons." Journal of Cell Biology 127, no. 3 (1994): 813–23. http://dx.doi.org/10.1083/jcb.127.3.813.

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Astroglial cells play an important role in orchestrating the migration and positioning of neurons during central nervous system development. Primary astroglia, as well as astrocytoma cells will extend long stable processes when co-cultured with granule neurons. In order to determine the function of the glial fibrillary acidic protein (GFAP), the major intermediate filament protein in astroglia and astrocytoma cells, we suppressed the expression of GFAP by stable transfection of an anti-sense GFAP construct in human astrocytoma U251MG cells. The resulting AS2-U251 cells can no longer extend sta

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Benussi, Alberto, Nicholas J. Ashton, Thomas K. Karikari, et al. "Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration." Journal of Alzheimer's Disease 77, no. 3 (2020): 1129–41. http://dx.doi.org/10.3233/jad-200608.

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Background: It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD). Objective: To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD. Methods: In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer’s disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the corre

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Brenner, Michael, and Albee Messing. "Regulation of GFAP Expression." ASN Neuro 13 (January 2021): 175909142098120. http://dx.doi.org/10.1177/1759091420981206.

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Expression of the GFAP gene has attracted considerable attention because its onset is a marker for astrocyte development, its upregulation is a marker for reactive gliosis, and its predominance in astrocytes provides a tool for their genetic manipulation. The literature on GFAP regulation is voluminous, as almost any perturbation of development or homeostasis in the CNS will lead to changes in its expression. In this review, we limit our discussion to mechanisms proposed to regulate GFAP synthesis through a direct interaction with its gene or mRNA. Strengths and weaknesses of the supportive ex

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de Boer, Sterre Catharina Maria, Chiara Fenoglio, Andrea Arighi, et al. "Serum neurofilament light is superior to glial fibrillary acidic protein to distinguish sporadic frontotemporal dementia from late-onset primary psychiatric disorders: a retrospective DIPPA-FTD study." BMJ Neurology Open 7, no. 1 (2025): e001007. https://doi.org/10.1136/bmjno-2024-001007.

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BackgroundSporadic behavioural variant frontotemporal dementia (bvFTD) is often misdiagnosed as late-onset primary psychiatric disorder (PPD). Previous research in small sample sizes has shown that neurofilament light (NfL) and glial fibrillary acidic protein (GFAP) are promising biomarkers to distinguish FTD from PPD. We aimed to investigate the discriminative value of NfL and GFAP in a multicentre cohort of sporadic bvFTD and late-onset PPD.MethodsIn total, n=275 sporadic bvFTD and n=82 PPD were included from our DIPPA-FTD study. Baseline serum NfL and GFAP levels were measured using Simoa.

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Cho, Woosung, and Albee Messing. "Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice." Experimental Cell Research 315, no. 7 (2009): 1260–72. http://dx.doi.org/10.1016/j.yexcr.2008.12.012.

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Green, Lydia, Ian Berry, Anne-Marie Childs, et al. "Whole Exon Deletion in the GFAP Gene Is a Novel Molecular Mechanism Causing Alexander Disease." Neuropediatrics 49, no. 02 (2017): 118–22. http://dx.doi.org/10.1055/s-0037-1608921.

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AbstractAlexander disease (AD) is a leukodystrophy caused by heterozygous mutations in the gene encoding the glial fibrillary acidic protein (GFAP). Currently, de novo heterozygous missense mutations in the GFAP gene are identified in over 95% of patients with AD. However, patients with biopsy-proven AD have been reported in whom no GFAP mutation has been identified. We report identical twin boys presenting in infancy with seizures and developmental delay in whom MR appearances were suggestive of AD with the exception of an unusual, bilateral, arc of calcification at the frontal white–gray jun

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Chandra, David, Prananda Surya Airlangga, Hamzah, Kohar Hari Santoso, and Christrijogo Sumartono. "Relationship between serum Glial Fibrillary Acidic Protein (GFAP) levels and severity of traumatic brain injury as measured by Glasgow Coma Scale (GCS) and Rotterdam Computed Tomography (CT) score." Bali Medical Journal 13, no. 3 (2024): 1111–15. https://doi.org/10.15562/bmj.v13i3.5336.

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Background: Traumatic brain injury is a serious physical injury that can cause brain function impairment. Evaluating the severity of traumatic brain injury is crucial for patient management. Glial Fibrillary Acidic Protein (GFAP) has been identified as a potential biomarker for brain injury. This study aims to evaluate the relationship between serum GFAP levels and the severity of traumatic brain injury measured using the Glasgow Coma Scale (GCS) and Rotterdam Computed Tomography (CT) score. Methods: This study was conducted using a cross-sectional design to analyse the relationship between GF

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Wickel, Jonathan, Ha-Yeun Chung, Klaus Kirchhof, et al. "Encephalitis with radial perivascular emphasis." Neurology - Neuroimmunology Neuroinflammation 7, no. 2 (2020): e670. http://dx.doi.org/10.1212/nxi.0000000000000670.

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ObjectiveAutoimmune steroid-responsive meningoencephalomyelitis with linear perivascular gadolinium enhancement in brain MRI is regarded as glial fibrillary acidic protein (GFAP) astrocytopathy characterized by anti-GFAP antibodies (ABs). We questioned whether anti-GFAP ABs are necessarily associated with this syndrome.MethodsTwo patients with a strikingly similar disease course suggestive of autoimmune GFAP astrocytopathy are reported. Clinical examination, MRI, laboratory, and CSF analysis were performed. Neuropathologic examination of brain tissue was obtained from one patient. Serum and CS

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Tugasworo, Dodik, Locoporta Agung, Retnaningsih Retnaningsih, Amin Husni, Aris Catur Bintoro, and Arinta Puspita Wati. "The Correlation of Glial Fibrillary Acid Protein Level to Cognitive Function Outcome in Acute Lacunar Ischemic Stroke Patient." Open Access Macedonian Journal of Medical Sciences 11, B (2023): 330–34. http://dx.doi.org/10.3889/oamjms.2023.11393.

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ABSTRACT : Introduction : Glial fibrillary acidic protein (GFAP) is a filamentous protein found in central nervous system astrocytes. Increased serum GFAP levels are caused by the process of astrogliosis after ischemic stroke and are associated with multisynaptic disorders so that they are at risk of causing cognitive disorders. Objective: To analyze the correlation between GFAP levels and cognitive function output in acute lacunar ischemic stroke patients. Research Methods : Analytical observational with prospective cohort approach. The subjects of this study were Acute lacu

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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

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Schiffer, Davide, Maria Teresa Giordana, Isabella Germano, and Alessandro Mauro. "Anaplasia and Heterogeneity of Gfap Expression in Gliomas." Tumori Journal 72, no. 2 (1986): 163–70. http://dx.doi.org/10.1177/030089168607200208.

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GFAP (glial fibrillary acidic protein) distribution was investigated in selected areas of glioblastomas and astrocytomas. The proliferating cell population of glioblastomas was GFAP negative and contained many mitoses which were also negative. The old, deeply located areas were composed of cells with visible cytoplasm, intensely GFAP-positive; mitoses in these areas were both GFAP-positive and negative. GFAP-positive reactive astrocytes, once trapped in the tumor, were no longer distinguishable from positive tumor cells. They sometimes contained mitoses. In astrocytoma, anaplasia was due to th

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Yang, Zhihui, Rawad Daniel Arja, Tian Zhu, et al. "Characterization of Calpain and Caspase-6-Generated Glial Fibrillary Acidic Protein Breakdown Products Following Traumatic Brain Injury and Astroglial Cell Injury." International Journal of Molecular Sciences 23, no. 16 (2022): 8960. http://dx.doi.org/10.3390/ijms23168960.

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Glial fibrillary acidic protein (GFAP) is the major intermediate filament III protein of astroglia cells which is upregulated in traumatic brain injury (TBI). Here we reported that GFAP is truncated at both the C- and N-terminals by cytosolic protease calpain to GFAP breakdown products (GBDP) of 46-40K then 38K following pro-necrotic (A23187) and pro-apoptotic (staurosporine) challenges to primary cultured astroglia or neuron-glia mixed cells. In addition, with another pro-apoptotic challenge (EDTA) where caspases are activated but not calpain, GFAP was fragmented internally, generating a C-te

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Singh, Arpana, A. S. Ramesh, Prashant Shankarrao Adole, and Pooja Verma. "Serum Glial Fibrillary Acidic Protein and S100B Profiles in Severity and Outcome Assessment of Moderate and Severe Head Injury Patients in India." Current Medical Issues 22, no. 4 (2024): 187–94. http://dx.doi.org/10.4103/cmi.cmi_49_24.

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Abstract Background: Traumatic brain injury (TBI) is a significant global health issue, with India witnessing approximately 150,000 deaths and 50,000 TBI-related fatalities annually. Severity is classified as mild, moderate, or severe using the Glasgow Coma Scale (GCS). Imaging and blood biomarkers such as serum glial fibrillary acidic protein (GFAP) and S100B aid in diagnosis and outcome prediction, yet imaging facilities are scarce in India. This highlights the necessity for dependable biomarkers. GFAP indicates astroglial injury, while S100B suggests neuronal injury, both in TBI patients’ b

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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 (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 out

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Luger, Sebastian, Jens Witsch, Andreas Dietz, et al. "Glial Fibrillary Acidic Protein Serum Levels Distinguish between Intracerebral Hemorrhage and Cerebral Ischemia in the Early Phase of Stroke." Clinical Chemistry 63, no. 1 (2017): 377–85. http://dx.doi.org/10.1373/clinchem.2016.263335.

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Abstract BACKGROUND Recent studies have suggested that glial fibrillary acidic protein (GFAP) serum concentrations distinguish between intracerebral hemorrhage (ICH) and ischemic stroke (IS) shortly after symptom onset. In this prospective multicenter trial we validated GFAP in an independent patient cohort and assessed the quantitative relationship between GFAP release, bleeding size, and localization. METHODS We included patients with a persistent neurological deficit (NIH Stroke Scale ≥4) suggestive of stroke within 6 h of symptom onset. Blood samples were drawn at hospital admission. GFAP

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Bentivenga, Giuseppe Mario, Simone Baiardi, Andrea Mastrangelo, et al. "Diagnostic and Prognostic Value of Plasma GFAP in Sporadic Creutzfeldt–Jakob Disease in the Clinical Setting of Rapidly Progressive Dementia." International Journal of Molecular Sciences 25, no. 10 (2024): 5106. http://dx.doi.org/10.3390/ijms25105106.

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The diagnostic and prognostic value of plasma glial fibrillary acidic protein (pl-GFAP) in sporadic Creutzfeldt–Jakob disease (sCJD) has never been assessed in the clinical setting of rapidly progressive dementia (RPD). Using commercially available immunoassays, we assayed the plasma levels of GFAP, tau (pl-tau), and neurofilament light chain (pl-NfL) and the CSF total tau (t-tau), 14-3-3, NfL, phospho-tau181 (p-tau), and amyloid-beta isoforms 42 (Aβ42) and 40 (Aβ40) in sCJD (n = 132) and non-prion RPD (np-RPD) (n = 94) patients, and healthy controls (HC) (n = 54). We also measured the CSF GFA

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Sekimata, M., K. Tsujimura, J. Tanaka, Y. Takeuchi, N. Inagaki, and M. Inagaki. "Detection of protein kinase activity specifically activated at metaphase-anaphase transition." Journal of Cell Biology 132, no. 4 (1996): 635–41. http://dx.doi.org/10.1083/jcb.132.4.635.

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We have previously reported that Ser13 and Ser34 on glial fibrillary acidic protein (GFAP) in the cleavage furrow of glioma cells are phosphorylated during late mitotic phase (Matsuoka, Y., K. Nishizawa, T. Yano, M. Shibata, S. Ando, T. Takahashi, and M. Inagaki. 1992, EMBO (Eur. Mol. Biol. Organ.) J. 11:2895-2902). This observation implies a possibility that there is a protein kinase specifically activated at metaphase-anaphase transition. To further analyze the cell cycle-dependent GFAP phosphorylation, we prepared monoclonal antibodies KT13 and KT34 which recognize the phosphorylation of GF

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Ozcelikay, Goksu, Fariba Mollarasouli, Mehmet Altay Unal, Kıvılcım Gucuyener, and Sibel A. Ozkan. "Ultrasensitive Determination of Glial-Fibrillary-Acidic-Protein (GFAP) in Human Serum-Matrix with a Label-Free Impedimetric Immunosensor." Biosensors 12, no. 12 (2022): 1165. http://dx.doi.org/10.3390/bios12121165.

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In this work, immobilizing anti-GFAP antibodies via covalent attachment onto L-cysteine/gold nanoparticles that were modified with screen-printed carbon electrodes (Anti-GFAP/L-cys/AuNps/SPCE) resulted in the development of a sensitive label-free impedance immunosensor for the detection of Glial Fibrillary Acidic Protein (GFAP). The immunosensor’s stepwise construction was studied using cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). L-cysteine was chosen as the linker between GFAP antibodies and Au NPs/SPCE because it enables the guided and stable immobilization of G

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Rutka, James T., Masaji Murakami, Peter B. Dirks, et al. "Role of glial filaments in cells and tumors of glial origin: a review." Neurosurgical Focus 3, no. 1 (1997): E2. http://dx.doi.org/10.3171/foc.1997.3.1.2.

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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 extrace

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Stefanus, Robert, Sophie Yolanda, and Radiana D. Antarianto. "Comparison of GFAP and HSP27 concentrations in acute moderate-intensity aerobic exercise of different duration." Medical Journal of Indonesia 25, no. 2 (2016): 112–7. http://dx.doi.org/10.13181/mji.v25i2.1267.

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Background: Glial fibrillary acidic protein (GFAP) and heat shock protein -27 (HSP27) plasma can be used as the parameters of exercise-induced astrocyte reactivity. The American College of Sports Medicine (ACSM) recommends an exercise of 30 minutes or 10 minutes duration (each performing bout accumulated toward 30 minutes). The aim of this study was to compare GFAP and HSP27 plasma concentrations in young adults undergoing acute moderate-intensity aerobic exercise of different durations (10 minutes vs 30 minutes).Methods: An experimental study with pre-post design was conducted on 22 participa

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Gill, Jessica, Lawrence Latour, Ramon Diaz-Arrastia, et al. "Glial fibrillary acidic protein elevations relate to neuroimaging abnormalities after mild TBI." Neurology 91, no. 15 (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 we

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Bai, Runhua, Li An, Wei Du, et al. "Autoimmune glial fibrillary acidic protein astrocytopathy misdiagnosed as intracranial infectious diseases: case reports and literature review." Frontiers in Immunology 16 (January 22, 2025). https://doi.org/10.3389/fimmu.2025.1519700.

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BackgroundAutoimmune glial fibrillary acidic protein astrocytopathy (A-GFAP-A) is an autoimmune central nervous system(CNS) disease characterized by GFAP IgG as a biomarker. Several cases of individuals with A-GFAP-A initially misdiagnosed as infectious diseases of the central nervous system have been reported in research. We report three cases of A-GFAP-A misdiagnosed as viral meningitis or tuberculous meningitis (TBM). We summarize recent cases of A-GFAP-A misdiagnosed as central nervous system infections through a literature review.Materials and methodsThree cases of A-GFAP-A were initially

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Fu, Cong-Cong, Lu Huang, Lu-Fen Xu, et al. "Serological biomarkers in autoimmune GFAP astrocytopathy." Frontiers in Immunology 13 (August 2, 2022). http://dx.doi.org/10.3389/fimmu.2022.957361.

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Autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A) is a newly defined meningoencephalomyelitis. The pathogenesis of GFAP-A is not well understood. The present study measured the expression levels of 200 serological cytokines in GFAP-A patients, NMOSD patients and healthy controls (HCs). The correlations between serum cytokine levels and clinical information in GFAP-A patients were analyzed. A total of 147 serological proteins were differentially expressed in GFAP-A patients compared to HCs, and 33 of these proteins were not observed in NMOSD patients. Serum levels of EG-VEGF ne

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Battaglia, Rachel A., Adriana S. Beltran, Samed Delic, et al. "Site-specific phosphorylation and caspase cleavage of GFAP are new markers of Alexander disease severity." eLife 8 (November 4, 2019). http://dx.doi.org/10.7554/elife.47789.

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Alexander disease (AxD) is a fatal neurodegenerative disorder caused by mutations in glial fibrillary acidic protein (GFAP), which supports the structural integrity of astrocytes. Over 70 GFAP missense mutations cause AxD, but the mechanism linking different mutations to disease-relevant phenotypes remains unknown. We used AxD patient brain tissue and induced pluripotent stem cell (iPSC)-derived astrocytes to investigate the hypothesis that AxD-causing mutations perturb key post-translational modifications (PTMs) on GFAP. Our findings reveal selective phosphorylation of GFAP-Ser13 in patients

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Bock, Nathalie, Hannah Alter, Emre Koc, Veit Roessner, Aribert Rothenberger, and Till Manzke. "Chronic Fluoxetine Administration during Different Postnatal Development Stages Leads to Stage Dependent Changes of Glial Fibrillary Acidic Protein Expression in Rat Brain." April 14, 2012. https://doi.org/10.5281/zenodo.7808.

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Aims: Depressive symptoms in children and adolescents are commonly treated with serotonin re-uptake inhibitors like fluoxetine. Astrocytes expressing different serotonin receptors (5-HTRs) and the serotonin transporter (5-HTT) are affected by fluoxetine administration. The study was conducted to revise whether fluoxetine treatment during postnatal brain development results in long-term changes of astroglia. Methodology: Thus, immunohistochemistry and real-time PCR analyses were performed at different postnatal periods in rats to investigate short- and long-term changes following by a 14-day ad

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Kálmán, Mihály, and Olivér M. Sebők. "Entopallium lost GFAP immunoreactivity during avian evolution -- is GFAP a ’condition sine qua non’?" Brain, Behavior and Evolution, December 9, 2023. http://dx.doi.org/10.1159/000535281.

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TThe present study demonstrates that in the same brain area the astroglia can express GFAP (the main cytoskeletal protein of astroglia) in some species but not in the others of the same vertebrate class. It contrasts the former opinions that the distribution of GFAP found in a species is characteristic of the entire class. The present study investigated birds in different phylogenetic positions: duck (Cairina moschata domestica), chicken (Gallus gallus domesticus), and quails (Coturnix japonica and Excalfactoria chinensis) of Galloanserae; pigeon (Columba livia domestica) of a group of Neoaves

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Zwirner, Johann, Julia Lier, Heike Franke, et al. "GFAP positivity in neurons following traumatic brain injuries." International Journal of Legal Medicine, June 11, 2021. http://dx.doi.org/10.1007/s00414-021-02568-1.

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AbstractGlial fibrillary acidic protein (GFAP) is a well-established astrocytic biomarker for the diagnosis, monitoring and outcome prediction of traumatic brain injury (TBI). Few studies stated an accumulation of neuronal GFAP that was observed in various brain pathologies, including traumatic brain injuries. As the neuronal immunopositivity for GFAP in Alzheimer patients was shown to cross-react with non-GFAP epitopes, the neuronal immunopositivity for GFAP in TBI patients should be challenged. In this study, cerebral and cerebellar tissues of 52 TBI fatalities and 17 controls were screened

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Jia, Nan, Jiawei Wang, Yuhong He, Zhong Li, and Chuntao Lai. "Isolated optic neuritis with positive glial fibrillary acidic protein antibody." BMC Ophthalmology 23, no. 1 (2023). http://dx.doi.org/10.1186/s12886-023-02927-z.

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Abstract Background and objectives Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) has been reported as a spectrum of autoimmune, inflammatory central nervous system disorders. Linear perivascular radial gadolinium enhancement patterns on brain magnetic resonance imaging (MRI) are a hallmark of these disorders. GFAP-A is associated with cerebrospinal fluid (CSF) GFAP antibody (GFAP-Ab), while the association with serum GFAP-Ab is less clear. This study aimed to observe the clinical characteristic and MRI changes of GFAP-Ab-positive optic neuritis (ON). Methods We perf

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Yang, Hyun‐Sik, Pia Kivisäkk, Andrea M. Román Viera та ін. "The relationship between amyloid‐β, plasma/brain GFAP, and neocortical tau: a Mendelian randomization study". Alzheimer's & Dementia 20, S2 (2024). https://doi.org/10.1002/alz.091415.

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AbstractBackgroundPlasma glial fibrillary acidic protein (GFAP) is associated with amyloid‐β (Aβ) and tau, but their causal relationships remain unclear. We used Mendelian randomization (MR; using genetic causal anchors to avoid reverse causation) to clarify the causal relationship between plasma/brain GFAP, Aβ, and tau.MethodsStudy participants are from two independent datasets: the Harvard Aging Brain Study (HABS) and the Religious Orders Study/the Rush Memory and Aging Project (ROSMAP) (Table 1). From HABS, we used baseline plasma GFAP (MSD platform) and Aβ (PiB PET cortical composite with

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Letra-Vilela, Ricardo, Ricardo Quiteres, Fernanda Murtinheira, Alvaro Crevenna, Zach Hensel, and Federico Herrera. "New tools for the visualization of glial fibrillary acidic protein in living cells." Experimental Results 1 (2020). http://dx.doi.org/10.1017/exp.2020.1.

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AbstractThe glial fibrillary acidic protein (GFAP) is an intermediate filament widely used to identify and label astroglial cells, a very abundant and relevant glial cell type in the central nervous system. A major hurdle in studying its behavior and function arises from the fact that GFAP does not tolerate well the addition of protein tags to its termini. Here, we tagged human GFAP (hGFAP) with an enhanced green fluorescent protein (EGFP) for the first time, and substituted a previously reported EGFP tag on mouse GFAP (mGFAP) by a more versatile Halo Tag. Both versions of tagged GFAP were abl

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Fazeli, Badrieh, André Huss, Nerea Gómez de San José, Markus Otto, Hayrettin Tumani, and Steffen Halbgebauer. "Development of an ultrasensitive microfluidic assay for the analysis of Glial fibrillary acidic protein (GFAP) in blood." Frontiers in Molecular Biosciences 10 (April 24, 2023). http://dx.doi.org/10.3389/fmolb.2023.1175230.

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Introduction: A rapid and reliable detection of glial fibrillary acidic protein (GFAP) in biological samples could assist in the diagnostic evaluation of neurodegenerative disorders. Sensitive assays applicable in the routine setting are needed to validate the existing GFAP tests. This study aimed to develop a highly sensitive and clinically applicable microfluidic immunoassay for the measurement of GFAP in blood.Methods: A microfluidic GFAP assay was developed and validated regarding its performance. Subsequently, serum and cerebrospinal fluid (CSF) of Alzheimer’s disease (AD), Multiple Scler

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Zhang, Shifeng, Huilu Li, Peihao Lin, et al. "A Comparative Study of 141 Glial Fibrillary Acidic Protein Immunoglobulin G Positive Cases." European Journal of Neurology 32, no. 3 (2025). https://doi.org/10.1111/ene.70102.

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ABSTRACTBackgroundGlial fibrillary acidic protein‐immunoglobulin G (GFAP‐IgG) positivity is associated with autoimmune GFAP astrocytopathy (GFAP‐A), but also with other autoimmune encephalitides and viral infections. We attempted to elucidate the characteristics of GFAP‐A in relation to other GFAP‐IgG‐positive encephalitides and constructed a differential diagnosis model.Methods141 GFAP‐IgG‐positive cases were identified, including 52 astrocytopathy (GFAP‐A group), 48 autoimmune encephalitis (AE‐G), and 41 viral encephalitis (VE‐G). Multivariate logistic regression was employed to create a dia

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