ArticleFrontiers in immunology2021
Case Report: Semantic Variant of Primary Progressive Aphasia Associated With Anti-Glial Fibrillary Acid Protein Autoantibodies.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 8 citations in OpenAlex.
- A Case of Optic Neuritis with Glial Fibrillary Acidic Protein Antibody and Secondary Ophthalmoplegia.Neuro-ophthalmology (Aeolus Press) · 2026Article
- Anti-NMDA receptor encephalitis with coexisting autoimmune GFAP astrocytopathy presenting with psychiatric symptoms leading to a suicide attempt: a case report.International journal of emergency medicine · 2025Article
- Cognitive Function and Proteomic Changes in Patients with Autoantibody-Positive Neurodegenerative Dementia.Neurology and therapy · 2025Article
- Brain-targeting autoantibodies in patients with dementia.Frontiers in neurology · 2024Article
- Immunoreactivity to astrocytes in different forms of dementia: High prevalence of autoantibodies to GFAP.Brain, behavior, & immunity - health · 2023Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
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Abstract
Background: Frontotemporal lobar degeneration is a heterogeneous disorder entailing a semantic variant of primary progressive aphasia (svPPA). A subtype of frontotemporal dementia associated with glutamate receptor subunit 3 (GluA3) antibody of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) was recently identified. Here, we describe the novelty of a svPPA associated with anti-glial fibrillary acid protein (GFAP) antibodies. Methods: To diagnose this 68-year-old woman we conducted a clinical examination, neuropsychological testing, CSF analysis, MRI and 18F-fluorodeoxyglucose (18F-FDG) Positron Emission Tomography (PET)/computed tomography (CT) imaging. Results: The clinical phenotype corresponds to a svPPA based on impaired confrontation naming and single-word comprehension. In addition, we observed spared speech production, impaired object knowledge, and surface dyslexia - further supporting the diagnosis of svPPA. Additional characteristic imaging features such as anterior temporal hypometabolism in 18F-FDG PET/CT confirmed patient's svPPA diagnosis. CSF analysis revealed signs of axonal degeneration, as both tau and phosphorylated tau proteins exceeded normal levels. Her serum showed anti-GFAP autoantibodies. Conclusion: We diagnosed a svPPA in this patient and report an association between serum anti-GFAP antibodies and svPPA never reported in the literature so far, thereby expanding the clinical spectrum of svPPA and anti-GFAP-antibody related disease. Further research is needed to elucidate the underlying immunopathology of this disease entity to ultimately improve treatment.
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