Evidence map›Paper›PMID 20856912›Full record

ArticleNeuropsychiatric disease and treatment2010

Current and emerging treatment options in the management of Friedreich ataxia.

Michelangelo Mancuso, Daniele Orsucci, Anna Choub, Gabriele Siciliano

Open access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. The impact of histone post-translational modifications in neurodegenerative diseases.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Cardiac involvement in hereditary ataxias.Journal of child neurology · 2012
    Review
  10. Anaesthesia for a patient with Friedreich's ataxia.Indian journal of anaesthesia · 2011
    Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Michelangelo MancusoDepartment of Neuroscience, Neurological Clinic, University of Pisa, Pisa, Italy.
Daniele Orsucci
Anna Choub
Gabriele Siciliano
University of Pisa · IT

Funding

Telethon GUP09004
6 · The paper itself

Abstract

Friedreich ataxia (FRDA) is the most common autosomal recessive ataxia. Oxidative damage within the mitochondria seems to have a key role in the disease phenotype. Therefore, FRDA treatment options have been mostly directed at antioxidant protection against mitochondrial damage. Available evidence seems to suggest that patients with FRDA should be treated with idebenone, because it is well tolerated and may reduce cardiac hypertrophy and, at higher doses, also improve neurological function, but large controlled clinical trials are still needed. Alternatively, gene-based strategies for the treatment of FRDA may involve the development of small-molecules increasing frataxin gene transcription. Animal and human studies are strongly needed to assess whether any of the potential new treatment strategies, such as iron-chelating therapies or treatment with erythropoietin or histone deacetylase inhibitors and other gene-based strategies, may translate into an effective therapy for this devastating disorder. In this review, we try to provide an answer to some questions related to current and emerging treatment options in the management of FRDA.

Indexed as

frataxinidebenoneoxidative stress

Identifiers

PMID20856912
PMCPMC2938298
OpenAlexW2154969830

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.