ArticleActa neuropathologica2009
Abundant FUS-immunoreactive pathology in neuronal intermediate filament inclusion disease.
Article in Acta neuropathologica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.
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Who cites it
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 251 citations in OpenAlex.
- Cerebrospinal fluid and blood exosomes as biomarkers for amyotrophic lateral sclerosis; a systematic review.Diagnostic pathology · 2024Pooled it
- Caudate atrophy on MRI is a characteristic feature of FTLD-FUS.European journal of neurology · 2010Trial
- Mesenchymal stem cell-derived extracellular vesicle treatment of induced pluripotent stem cell-derived motor neurons with different amyotrophic lateral sclerosis genetic backgrounds.Neural regeneration research · 2026Article
- TAF15 amyloids propagate via defined motifs in a prion-like fashion.Nature communications · 2026Article
- Granules Gone Rogue: Nuclear and Cytoplasmic Ribonucleoprotein Structures in Amyotrophic Lateral Sclerosis-Fused in Sarcoma (ALS-FUS) Pathology.Molecular neurobiology · 2026Review
- Distinct TAF15 amyloid filament folds define multiple subtypes of FTLD-TAF15.bioRxiv : the preprint server for biology · 2026Article
- Biomolecular condensates: molecular structure, biological functions, diseases, and therapeutic targets.Molecular biomedicine · 2025Review
- Direct and Indirect Protein Interactions Link FUS Aggregation to Histone Post-Translational Modification Dysregulation and Growth Suppression in an ALS/FTD Yeast Model.Journal of fungi (Basel, Switzerland) · 2025Article
- Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases.Advances in neurobiology · 2025Review
- Selective cellular and regional vulnerability in frontotemporal lobar degeneration: a scoping review.Free neuropathology · 2025Review
- Molecular Mechanisms of Phase Separation and Amyloidosis of ALS/FTD-linked FUS and TDP-43.Aging and disease · 2024Review
- Mutations in FUS lead to synaptic dysregulation in ALS-iPSC derived neurons.Stem cell reports · 2024Article
- Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS.Frontiers in molecular biosciences · 2024Review
- Article
- Frontotemporal-TDP and LATE Neurocognitive Disorders: A Pathophysiological and Genetic Approach.Brain sciences · 2023Review
- Expression of IL-13Rα2 and FUS in glioma: clinicopathological and prognostic correlation.BMC neurology · 2023Article
- Functional Role of RBP in Osteosarcoma: Regulatory Mechanism and Clinical Therapy.Analytical cellular pathology (Amsterdam) · 2023Review
- MicroRNA biomarkers in frontotemporal dementia and to distinguish from Alzheimer's disease and amyotrophic lateral sclerosis.Neural regeneration research · 2022Review
- Biomarkers and molecular mechanisms of Amyotrophic Lateral Sclerosis.AIMS neuroscience · 2022Review
- HnRNP K mislocalisation is a novel protein pathology of frontotemporal lobar degeneration and ageing and leads to cryptic splicing.Acta neuropathologica · 2021Article
69 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 5 institutions in 4 countries.
Funding
Abstract
Neuronal intermediate filament inclusion disease (NIFID) is an uncommon neurodegenerative condition that typically presents as early-onset, sporadic frontotemporal dementia (FTD), associated with a pyramidal and/or extrapyramidal movement disorder. The neuropathology is characterized by frontotemporal lobar degeneration with neuronal inclusions that are immunoreactive for all class IV intermediate filaments (IF), light, medium and heavy neurofilament subunits and alpha-internexin. However, not all the inclusions in NIFID are IF-positive and the primary molecular defect remains uncertain. Mutations in the gene encoding the fused in sarcoma (FUS) protein have recently been identified as a cause of familial amyotrophic lateral sclerosis (ALS). Because of the recognized clinical, genetic and pathological overlap between FTD and ALS, we investigated the possible role of FUS in NIFID. We found abnormal intracellular accumulation of FUS to be a consistent feature of our NIFID cases (n = 5). More neuronal inclusions were labeled using FUS immunohistochemistry than for IF. Several types of inclusions were consistently FUS-positive but IF-negative, including neuronal intranuclear inclusions and glial cytoplasmic inclusions. Double-label immunofluorescence confirmed that many cells had only FUS-positive inclusions and that all cells with IF-positive inclusions also contained pathological FUS. No mutation in the FUS gene was identified in a single case with DNA available. These findings suggest that FUS may play an important role in the pathogenesis of NIFID.
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