ArticleActa neuropathologica2004
alpha-Internexin aggregates are abundant in neuronal intermediate filament inclusion disease (NIFID) but rare in other neurodegenerative diseases.
Article in Acta neuropathologica, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 61 citations in OpenAlex.
- Short-lived Niemann-Pick type C mice with accelerated brain aging as a novel model for Alzheimer's disease research.Neural regeneration research · 2026Article
- Cerebrospinal fluid alpha-internexin concentrations measured in patients with Guillain-Barré syndrome: a possible prognostic biomarker for disability at 12 months.Journal of neurology · 2026Article
- Wdfy3-dependent autophagy impairment recapitulates presymptomatic neurodegenerative signatures in mice.Scientific reports · 2026Article
- Alpha-internexin as a brain-specific neurodegeneration marker: development and validation of a novel CSF assay.Journal of neurology · 2025Article
- Diffuse argyrophilic grain disease with TDP-43 proteinopathy and neuronal intermediate filament inclusion disease: FTLD with mixed tau, TDP-43 and FUS pathologies.Acta neuropathologica communications · 2023Article
- Assembly of NFL and desmin intermediate filaments: Headed in the right direction.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Expression pattern of neuronal intermediate filament α-internexin in anterior pituitary gland and related tumors.Pituitary · 2015Article
- Article
- Novel types of frontotemporal lobar degeneration: beyond tau and TDP-43.Journal of molecular neuroscience : MN · 2011Review
- FUS immunogold labeling TEM analysis of the neuronal cytoplasmic inclusions of neuronal intermediate filament inclusion disease: a frontotemporal lobar degeneration with FUS proteinopathy.Journal of molecular neuroscience : MN · 2011Article
- Gigaxonin mutation analysis in patients with NIFID.Neurobiology of aging · 2011Article
- Fronto-temporal lobar degeneration: neuropathology in 60 cases.Journal of neural transmission (Vienna, Austria : 1996) · 2011Article
- FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration.Acta neuropathologica · 2010Article
- Article
- Article
- Identification and characterization of a novel endogenous murine parkin mutation.Journal of neurochemistry · 2010Article
- Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update.Acta neuropathologica · 2010Article
- Abundant FUS-immunoreactive pathology in neuronal intermediate filament inclusion disease.Acta neuropathologica · 2009Article
- Dysfunctions of neuronal and glial intermediate filaments in disease.The Journal of clinical investigation · 2009Review
- Modest loss of peripheral axons, muscle atrophy and formation of brain inclusions in mice with targeted deletion of gigaxonin exon 1.Journal of neurochemistry · 2008Article
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13 authors at 7 institutions in 5 countries.
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Abstract
Abnormal neuronal aggregates of alpha-internexin and the three neurofilament (NF) subunits, NF-L, NF-M, and NF-H have recently been identified as the pathological hallmarks of neuronal intermediate filament (IF) inclusion disease (NIFID), a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal and extrapyramidal signs. alpha-Internexin, a class IV IF protein, a major component of inclusions in NIFID, has not previously been identified as a component of the pathological protein aggregates of any other neurodegenerative disease. Therefore, to determine the specificity of this protein, alpha-internexin immunohistochemistry was undertaken on cases of NIFID, non-tau frontotemporal dementias, motor neuron disease, alpha-synucleinopathies, tauopathies, and normal aged control brains. Our results indicate that class IV IF proteins are present within the pleomorphic inclusions of all cases of NIFID. Small subsets of abnormal neuronal inclusions in Alzheimer's disease, Lewy body diseases, and motor neuron disease also contain epitopes of alpha-internexin. Thus, alpha-internexin is a major component of the neuronal inclusions in NIFID and a relatively minor component of inclusions in other neurodegenerative diseases. The discovery of alpha-internexin in neuronal cytoplasmic inclusions implicates novel mechanisms of pathogenesis in NIFID and other neurological diseases with pathological filamentous neuronal inclusions.
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