ArticleNeurobiology of aging2011
Gigaxonin mutation analysis in patients with NIFID.
Article in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Specialized roles of neurofilament proteins in synapses: Relevance to neuropsychiatric disorders.Brain research bulletin · 2016Review
- 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
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Authors and funding
4 authors at 3 institutions in 2 countries.
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Abstract
Neuronal intermediate filament inclusion disease (NIFID) is a frontotemporal lobar degeneration (FTLD) characterized by frontotemporal dementia (FTD), pyramidal and extrapyramidal signs. The disease is histologically characterized by the presence of abnormal neuronal cytoplasmic inclusions (NCIs) which contain α-internexin and other neuronal intermediate filament (IF) proteins. Gigaxonin (GAN) is a cytoskeletal regulating protein and the genetic cause of giant axonal neuropathy. Since the immunoreactive profile of NCIs in NIFID is similar to that observed in brain sections from Gan(Δex1/Δex1) mice, we speculated that GAN could be a candidate gene causing NIFID. Therefore, we performed a mutation analysis of GAN in NIFID patients. Although the NCIs of NIFID and Gan(Δex1/Δex1) mice were immunohistochemically similar, no GAN variant was identified in DNA obtained from well-characterized cases of NIFID.
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