ArticleThe American journal of pathology2004
alpha-internexin is present in the pathological inclusions of neuronal intermediate filament inclusion disease.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 124 citations in OpenAlex.
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- Alpha-internexin as a brain-specific neurodegeneration marker: development and validation of a novel CSF assay.Journal of neurology · 2025Article
- O-GlcNAcylation regulates neurofilament-light assembly and function and is perturbed by Charcot-Marie-Tooth disease mutations.Nature communications · 2023Article
- Posttranscriptional regulation of neurofilament proteins and tau in health and disease.Brain research bulletin · 2023Review
- Genotype by environment interactions for chronic wasting disease in farmed US white-tailed deer.G3 (Bethesda, Md.) · 2022Article
- A human tau seeded neuronal cell model recapitulates molecular responses associated with Alzheimer's disease.Scientific reports · 2022Article
- Neurofilament Proteins as Biomarkers to Monitor Neurological Diseases and the Efficacy of Therapies.Frontiers in neuroscience · 2021Review
- Neuronal intermediate filament inclusion disease may be incorrectly classified as a subtype of FTLD-FUS.Free neuropathology · 2020Article
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- Frontotemporal lobar degeneration: Pathogenesis, pathology and pathways to phenotype.Brain pathology (Zurich, Switzerland) · 2017Review
- Neurofilaments and Neurofilament Proteins in Health and Disease.Cold Spring Harbor perspectives in biology · 2017Review
- Specialized roles of neurofilament proteins in synapses: Relevance to neuropsychiatric disorders.Brain research bulletin · 2016Review
- Parkinsonism, movement disorders and genetics in frontotemporal dementia.Nature reviews. Neurology · 2016Review
- Comparative quantitative study of 'signature' pathological lesions in the hippocampus and adjacent gyri of 12 neurodegenerative disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
- Integrated analyses of zebrafish miRNA and mRNA expression profiles identify miR-29b and miR-223 as potential regulators of optic nerve regeneration.BMC genomics · 2015Article
- Neurofilament subunits are integral components of synapses and modulate neurotransmission and behavior in vivo.Molecular psychiatry · 2015Article
- A truncating SOD1 mutation, p.Gly141X, is associated with clinical and pathologic heterogeneity, including frontotemporal lobar degeneration.Acta neuropathologica · 2015Article
- PRKAR1B mutations are a rare cause of FUS negative neuronal intermediate filament inclusion disease.Brain : a journal of neurology · 2015Article
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Authors and funding
14 authors at 7 institutions in 5 countries.
Funding
Abstract
Neuronal intermediate filament (IF) inclusion disease (NIFID) is a novel neurological disease of early onset with a variable clinical phenotype including frontotemporal dementia, pyramidal, and extrapyramidal signs. Pathologically, in affected areas, there is neuronal loss, astrocytosis, and neuronal intracytoplasmic aggregates of abnormal neuronal IFs that contain neither tau nor alpha-synuclein. Thus, to characterize the neuronal IF protein profile of inclusions in NIFID, immunohistochemistry (IHC) was performed on 10 cases of NIFID, four normal aged controls (NL), and two cases of Alzheimer's disease (AD) using a panel of anti-neuronal IF proteins. Immunoelectron microscopy was performed on selected cases and frozen tissue from the frontal lobe of four cases was used for biochemical studies including sequential extractions and Western blotting. Based on these studies, we report here for the first time that alpha-internexin, a neuronal IF protein, is present within the inclusions of NIFID as are all three neurofilament subunits: heavy, medium, and light. Thus, all class IV neuronal IF proteins are present within the pathological inclusions of this disease. Biochemistry revealed that IF aggregates were soluble in sodium dodecyl sulfate (SDS) and no post-translational modification was detected when compared with Alzheimer's disease or aged control brains. Hence, we conclude that NIFID is characterized by the pathological cytoplasmic aggregation of all class IV neuronal IF proteins in brain. The discovery of alpha-internexin in the cytoplasmic inclusions implicates novel mechanisms of pathogenesis in NIFID and other neurological diseases with pathological accumulations of IFs.
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