ReviewInternational journal of molecular sciences2022
Neuroinflammation in Friedreich's Ataxia.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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
23 citing papers in PubMed.
- Myeloid cell replacement induces intercellular mitochondrial transfer and restores metabolism in a mouse model of mitochondrial disease.Nature communications · 2026Article
- Review
- Hypomagnetic Fields Influence the Developmental Duration, Fecundity and Temperature Stress Resistance ofBiology · 2026Article
- Role of iron in brain development, aging, and neurodegenerative diseases.Annals of medicine · 2025Review
- Microgliopathy as a primary mediator of neuronal death in models of Friedreich's Ataxia.Nature communications · 2025Article
- Base editing of trinucleotide repeats that cause Huntington's disease and Friedreich's ataxia reduces somatic repeat expansions in patient cells and in mice.Nature genetics · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk.Frontiers in molecular neuroscience · 2025Article
- Frataxin deficiency and the pathology of Friedreich's Ataxia across tissues.Tissue barriers · 2025Review
- Rock inhibitors in Alzheimer's disease.Frontiers in aging · 2025Review
- Loss of homeostatic functions in microglia from a murine model of Friedreich's ataxia.Genes & diseases · 2024Article
- Differential Gene Expression in Late-Onset Friedreich Ataxia: A Comparative Transcriptomic Analysis Between Symptomatic and Asymptomatic Sisters.International journal of molecular sciences · 2024Article
- PPARγ activation ameliorates cognitive impairment and chronic microglial activation in the aftermath of r-mTBI.Journal of neuroinflammation · 2024Article
- Frataxin deficiency shifts metabolism to promote reactive microglia via glucose catabolism.Life science alliance · 2024Article
- Iron imbalance in neurodegeneration.Molecular psychiatry · 2024Review
- Inflammation and olfactory loss are associated with at least 139 medical conditions.Frontiers in molecular neuroscience · 2024Article
- Inflammation in the CNS and PNS: From Molecular Basis to Therapy.International journal of molecular sciences · 2023Article
- Review
- Development of PPARγ Agonists for the Treatment of Neuroinflammatory and Neurodegenerative Diseases: Leriglitazone as a Promising Candidate.International journal of molecular sciences · 2023Review
- [Adult-onset sensory neuropathy and ataxia as a clinical manifestation of POLG gene mutations].Revista de neurologia · 2023Review
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.
Funding
Abstract
Friedreich's ataxia (FRDA) is a rare genetic disorder caused by mutations in the gene frataxin, encoding for a mitochondrial protein involved in iron handling and in the biogenesis of iron-sulphur clusters, and leading to progressive nervous system damage. Although the overt manifestations of FRDA in the nervous system are mainly observed in the neurons, alterations in non-neuronal cells may also contribute to the pathogenesis of the disease, as recently suggested for other neurodegenerative disorders. In FRDA, the involvement of glial cells can be ascribed to direct effects caused by frataxin loss, eliciting different aberrant mechanisms. Iron accumulation, mitochondria dysfunction, and reactive species overproduction, mechanisms identified as etiopathogenic in neurons in FRDA, can similarly affect glial cells, leading them to assume phenotypes that can concur to and exacerbate neuron loss. Recent findings obtained in FRDA patients and cellular and animal models of the disease have suggested that neuroinflammation can accompany and contribute to the neuropathology. In this review article, we discuss evidence about the involvement of neuroinflammatory-related mechanisms in models of FRDA and provide clues for the modulation of glial-related mechanisms as a possible strategy to improve disease features.
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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.