ArticleeNeuro2015
CSF and Blood Levels of GFAP in Alexander Disease
Article in eNeuro, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Neuroradiological patterns and prognostic implications in type I Alexander disease.Molecular genetics and metabolism · 2026Article
- Characterization of Clinical Phenotype to Glial Fibrillary Acidic Protein Concentrations in Alexander Disease.Annals of clinical and translational neurology · 2026Article
- GFAP degradation in TBI: linking novel modified products to astrocyte pathology and patient outcome.Acta neuropathologica communications · 2026Article
- Review
- Growth Differentiation Factor 15 Elevation in the Central Nervous System Is Associated With Failure to Thrive in Alexander Disease.Annals of clinical and translational neurology · 2026Article
- Description of the Hamburg Alexander Leukodystrophy Cohort-Insights into Practical Classification and the Care Situation.Journal of clinical medicine · 2025Article
- Bridging neuro-biomarkers and MR imaging: The synergistic role of glial fibrillary acidic protein in early CNS disease diagnosis.IBRO neuroscience reports · 2025Review
- The GFAP proteoform puzzle: How to advance GFAP as a fluid biomarker in neurological diseases.Journal of neurochemistry · 2025Review
- Glial fibrillary acidic protein in cerebrospinal fluid in humans is sensitive to various pre-analytical conditions: possible explanation and solution.Frontiers in neurology · 2025Article
- Neuroglial Pathophysiology of Leukodystrophies.Advances in neurobiology · 2025Review
- Plasma concentrations of glial fibrillary acidic protein, neurofilament light, and tau in Alexander disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Leukodystrophy Imaging: Insights for Diagnostic Dilemmas.Medical sciences (Basel, Switzerland) · 2024Review
- Update on leukodystrophies and developing trials.Journal of neurology · 2024Review
- GFAP and NfL increase during neurotoxicity from high baseline levels in pediatric CD19-CAR T-cell patients.Blood advances · 2023Article
- GFAP variant p. Tyr366Cys demonstrated widespread brain cavitation in neonatal Alexander disease.Radiology case reports · 2022Article
- An in vitro bioengineered model of the human arterial neurovascular unit to study neurodegenerative diseases.Molecular neurodegeneration · 2020Article
- Molecular Biomarkers in Multiple Sclerosis and Its Related Disorders: A Critical Review.International journal of molecular sciences · 2020Review
- Type II Alexander disease caused by splicing errors and aberrant overexpression of an uncharacterized GFAP isoform.Human mutation · 2020Article
- Role of Oxidative Stress, MAPKinase and Apoptosis Pathways in the Protective Effects of Thymoquinone Against Acrylamide-Induced Central Nervous System Toxicity in Rat.Neurochemical research · 2020Article
- Refining the concept of GFAP toxicity in Alexander disease.Journal of neurodevelopmental disorders · 2019Review
Corrections and comments
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Authors and funding
19 authors at 15 institutions in 6 countries.
Funding
Abstract
Alexander disease is a rare, progressive, and generally fatal neurological disorder that results from dominant mutations affecting the coding region of GFAP, the gene encoding glial fibrillary acidic protein, the major intermediate filament protein of astrocytes in the CNS. A key step in pathogenesis appears to be the accumulation of GFAP within astrocytes to excessive levels. Studies using mouse models indicate that the severity of the phenotype correlates with the level of expression, and suppression of GFAP expression and/or accumulation is one strategy that is being pursued as a potential treatment. With the goal of identifying biomarkers that indirectly reflect the levels of GFAP in brain parenchyma, we have assayed GFAP levels in two body fluids in humans that are readily accessible as biopsy sites: CSF and blood. We find that GFAP levels are consistently elevated in the CSF of patients with Alexander disease, but only occasionally and modestly elevated in blood. These results provide the foundation for future studies that will explore whether GFAP levels can serve as a convenient means to monitor the progression of disease and the response to treatment.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.