ArticleAmerican journal of neurodegenerative disease2014
Optineurin immunoreactivity in neuronal and glial intranuclear inclusions in adult-onset neuronal intranuclear inclusion disease.
Article in American journal of neurodegenerative disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Recurrent Bilateral Macular Edema Linked to NOTCH2NLC GGC Repeat Expansion: A Case Report.The American journal of case reports · 2026Article
- Optineurin overexpression ameliorates neurodegeneration through regulating neuroinflammation and mitochondrial quality in a murine model of amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025Article
- Not your usual neurodegenerative disease: a case report of neuronal intranuclear inclusion disease with unconventional imaging patterns.Frontiers in neuroscience · 2023Article
- Adult-onset neuronal nuclear inclusion disease presenting with mental and behavioral disorders: A case report and literature review.Aging medicine (Milton (N.S.W)) · 2022Article
- TRIM14 inhibits OPTN-mediated autophagic degradation of KDM4D to epigenetically regulate inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Clinical and mechanism advances of neuronal intranuclear inclusion disease.Frontiers in aging neuroscience · 2022Review
- Emerging views of OPTN (optineurin) function in the autophagic process associated with disease.Autophagy · 2022Review
- Article
- Adult-onset neuronal intranuclear inclusion disease, with both stroke-like onset and encephalitic attacks: a case report.BMC neurology · 2021Article
- Recent progress in neuronal intranuclear inclusion disease: a review of the literature.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Review
- Expansion of Human-Specific GGC Repeat in Neuronal Intranuclear Inclusion Disease-Related Disorders.American journal of human genetics · 2019Article
- Molecular Pathological Classification of Neurodegenerative Diseases: Turning towards Precision Medicine.International journal of molecular sciences · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Optineurin (OPTN) is a multifunctional protein involved in cellular morphogenesis, vesicle trafficking, maintenance of the Golgi complex, and transcription activation through its interactions with the Rab8, myosin 6 (MYO6), huntingtin. Recently, OPTN immunoreactivity has been reported in intranuclear inclusions in patients with neuronal intranuclear inclusions disease (NIID). Other studies have shown that the RNA-binding protein, fused in sarcoma (FUS), is a component of intranuclear inclusions in NIID. We aimed to investigate the relationship between OPTN, its binding protein MYO6 and FUS in this study. In control subjects, OPTN (C-terminal) (OPTN-C) and MYO6 immunoreactivity was mainly demonstrated in the cytoplasm of neurons. In NIID patients, both neuronal intranuclear inclusions (NII) and glial intranuclear inclusions (GII) were immunopositive for MYO6 as well as OPTN-C. However, the intensity of OPTN-C immunostaining of the neuronal cytoplasm with and without NII was less than that of the control subjects. Double immunofluorescence staining for OPTN-C, ubiquitin (Ub), p62 and FUS revealed co-localization of these proteins within NII. Moreover, Ub positive inclusions were co-localized with MYO6. The percentage of co-localization of Ub with OPTN-C, FUS or MYO6 in NII was 100%, 52% and 92%, respectively. Ultrastructurally, the inclusions consisted of thin and thick filaments. Both filaments were immunopositive for Ub and OPTN-C. These findings suggest that OPTN plays a central role in the disease pathogenesis, and that OPTN may be a major component of NII.
Indexed as
Identifiers
25232514PMC4162590W287536323What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.