ReviewMediators of inflammation2015
The role of the immune system in triplet repeat expansion diseases.
Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Multiomics approach identifies SERPINB1 as candidate biomarker for spinocerebellar ataxia type 2.Scientific reports · 2025Article
- Unraveling the intricate link between cell death and neuroinflammation usingFrontiers in cell and developmental biology · 2024Review
- Polyglutamine-expanded ATXN7 alters a specific epigenetic signature underlying photoreceptor identity gene expression in SCA7 mouse retinopathy.Journal of biomedical science · 2022Article
- Conditioned medium from BV2 microglial cells having polyleucine specifically alters startle response in mice.Scientific reports · 2022Article
- Neurodegenerative diseases associated with non-coding CGG tandem repeat expansions.Nature reviews. Neurology · 2022Review
- Exogenous polyserine and polyleucine are toxic to recipient cells.Scientific reports · 2022Article
- Myotonic dystrophy type 1 as a major risk factor for severe COVID-19?Acta neurologica Belgica · 2021Observational
- Autophagy in Spinocerebellar ataxia type 2, a dysregulated pathway, and a target for therapy.Cell death & disease · 2021Article
- Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Polyglutamine-containing microglia leads to disturbed differentiation and neurite retraction of neuron-like cells.Heliyon · 2020Article
- Universal RNAi Triggers for the Specific Inhibition of Mutant Huntingtin, Atrophin-1, Ataxin-3, and Ataxin-7 Expression.Molecular therapy. Nucleic acids · 2020Article
- Expression of Human Endogenous Retrovirus-K in Spinal and Bulbar Muscular Atrophy.Frontiers in neurology · 2019Article
- Yorkie Regulates Neurodegeneration Through Canonical Pathway and Innate Immune Response.Molecular neurobiology · 2018Article
- Ophthalmic features of spinocerebellar ataxia type 7.Eye (London, England) · 2018Article
- What Can We Learn About Human Disease from the Nematode C. elegans?Methods in molecular biology (Clifton, N.J.) · 2018Review
- Stress-induced changes in miRNA biogenesis and functioning.Cellular and molecular life sciences : CMLS · 2018Review
- Disease-modifying effects of ganglioside GM1 in Huntington's disease models.EMBO molecular medicine · 2017Article
- Promoter Variation and Expression Levels of Inflammatory Genes IL1A, IL1B, IL6 and TNF in Blood of Spinocerebellar Ataxia Type 3 (SCA3) Patients.Neuromolecular medicine · 2017Article
- Bone mineral density in patients with multiple sclerosis, hereditary ataxia or hereditary spastic paraplegia after at least 10 years of disease - a case control study.BMC neurology · 2016Article
- A low absolute number of expanded transcripts is involved in myotonic dystrophy type 1 manifestation in muscle.Human molecular genetics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trinucleotide repeat expansion disorders (TREDs) are a group of dominantly inherited neurological diseases caused by the expansion of unstable repeats in specific regions of the associated genes. Expansion of CAG repeat tracts in translated regions of the respective genes results in polyglutamine- (polyQ-) rich proteins that form intracellular aggregates that affect numerous cellular activities. Recent evidence suggests the involvement of an RNA toxicity component in polyQ expansion disorders, thus increasing the complexity of the pathogenic processes. Neurodegeneration, accompanied by reactive gliosis and astrocytosis is the common feature of most TREDs, which may suggest involvement of inflammation in pathogenesis. Indeed, a number of immune response markers have been observed in the blood and CNS of patients and mouse models, and the activation of these markers was even observed in the premanifest stage of the disease. Although inflammation is not an initiating factor of TREDs, growing evidence indicates that inflammatory responses involving astrocytes, microglia, and the peripheral immune system may contribute to disease progression. Herein, we review the involvement of the immune system in the pathogenesis of triplet repeat expansion diseases, with particular emphasis on polyglutamine disorders. We also present various therapeutic approaches targeting the dysregulated inflammation pathways in these diseases.
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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.