ReviewCerebellum & ataxias2017
Friedreich Ataxia: current status and future prospects.
Review in Cerebellum & ataxias, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.
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
81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 150 citations in OpenAlex.
- Balance and coordination training for patients with genetic degenerative ataxia: a systematic review.Journal of neurology · 2021Pooled it
- CRISPR-cas gene-editing as plausible treatment of neuromuscular and nucleotide-repeat-expansion diseases: A systematic review.PloS one · 2019Pooled it
- Effect of a Home-Base Core Stability Exercises in Hereditary Ataxia. A Randomized Controlled Trial. A Pilot Randomized Controlled Trial.Movement disorders clinical practice · 2024Trial
- Longitudinal analysis shows GAA1 length and baseline clinical status as robust predictors of progression in Friedreich ataxia.Journal of neurology · 2026Article
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- Novel genetic variants identification and immune profiling in ataxia telangiectasia patients.Journal of translational medicine · 2026Article
- Changes in Gait After Training for Individuals With Cerebellar Ataxia.Archives of rehabilitation research and clinical translation · 2025Article
- Multi-Center National Study of Genotype-Phenotype Correlation and Clinical Characteristics in Children and Young Adults with Friedreich's Ataxia from Serbia.Biomedicines · 2025Article
- Evaluation of Mitochondrial Complex 1 Density with [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Advancing neurogenetics in Africa: past achievements, current developments and shaping the future.Nature reviews. Neurology · 2025Review
- Plasma miRNAs Correlate with Structural Brain and Cardiac Damage in Friedreich's Ataxia.Cerebellum (London, England) · 2024Article
- Loss of homeostatic functions in microglia from a murine model of Friedreich's ataxia.Genes & diseases · 2024Article
- Health-Related Quality of Life in Patients with Inherited Ataxia in Ireland.Cerebellum (London, England) · 2024Article
- Mapping Novel Frataxin Mitochondrial Networks Through Protein- Protein Interactions.Research square · 2024Article
- Expression and processing of mature human frataxin after gene therapy in mice.Scientific reports · 2024Article
- METTL17 is an Fe-S cluster checkpoint for mitochondrial translation.Molecular cell · 2024Article
- Clinical stage and plasma neurofilament concentration in adults with Friedreich ataxia.Heliyon · 2024Article
- Expression and processing of mature human frataxin after gene therapy in mice.Research square · 2023Article
- Article
- Multifaceted nanoparticles: emerging mechanisms and therapies in neurodegenerative diseases.Brain : a journal of neurology · 2023Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Friedreich ataxia (FA) represents the most frequent type of inherited ataxia. Most patients carry homozygous GAA expansions in the first intron of the frataxin gene on chromosome 9. Due to epigenetic alterations, frataxin expression is significantly reduced. Frataxin is a mitochondrial protein. Its deficiency leads to mitochondrial iron overload, defective energy supply and generation of reactive oxygen species. This review gives an overview over clinical and genetic aspects of FA and discusses current concepts of frataxin biogenesis and function as well as new therapeutic strategies.
Identifiers
What 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.