Evidence map›Paper›PMID 40983776›Full record

ReviewNature reviews. Neurology2025

Progress and challenges in sporadic late-onset cerebellar ataxias.

Thomas Wirth, Jennifer Faber, Christel Depienne, Emmanuel Roze, Jérôme Honnorat, Wassilios G Meissner, Paola Giunti, Christine Tranchant, Thomas Klockgether, Mathieu Anheim

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. 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

10 authors.

Thomas WirthDepartment of Neurology, University Hospital of Strasbourg, Strasbourg, France.ORCID 0000-0002-4427-5765
Jennifer FaberCenter of Neurology, University Hospital Bonn, Bonn, Germany.ORCID 0000-0003-3265-0262
Christel DepienneInstitute of Human Genetics, Essen University Hospital, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0002-7212-9554
Emmanuel RozeDépartement de Neurologie, Hôpital de la Pitié Salpêtrière, Assistance Publique-Hôpitaux de Paris, Institut du Cerveau, Sorbonne Universités INSERM-U1127, CNRS-UMR7225, Paris, France.
Jérôme HonnoratFrench Reference Center on Paraneoplastic Neurological Syndromes and Autoimmune Encephalitis, Hospices Civils de Lyon, Lyon, France.ORCID 0000-0002-4721-5952
Wassilios G MeissnerCentre Hospitalo-Universitaire de Bordeaux, Service de Neurologie - Maladies Neurodégénératives, Centre de Référence Maladies Rares Atrophie Multisystématisée, Bordeaux, France.ORCID 0000-0003-2172-7527
Paola GiuntiAtaxia Centre, Department of Clinical and Movement Neurosciences, University College London (UCL) Queen Square Institute of Neurology, London, UK.
Christine TranchantDepartment of Neurology, University Hospital of Strasbourg, Strasbourg, France.
Thomas KlockgetherCenter of Neurology, University Hospital Bonn, Bonn, Germany.ORCID 0000-0001-6174-5442
Mathieu AnheimDepartment of Neurology, University Hospital of Strasbourg, Strasbourg, France. mathieu.anheim@chru-strasbourg.fr.ORCID 0000-0001-8121-0605

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sporadic late-onset cerebellar ataxia (SLOCA) is a syndrome defined by subacute or chronic and progressive ataxia occurring after the age of 40 years in individuals without a family history of ataxia. The 2022 publication of revised consensus diagnostic criteria for multiple system atrophy and the emergence of promising biomarkers provides a thorough diagnostic framework that now enables the diagnosis of numerous acquired causes of SLOCA, including autoimmune disorders and neurodegenerative diseases. The ongoing development and increased availability of DNA sequencing technology have uncovered several molecular causes of SLOCA besides spastic paraplegia type 7 and very late-onset Friedreich ataxia. These additional causes include sporadic genetic disorders, such as spinocerebellar atrophy type 27B, caused by GAA expansion in the FGF14 gene, and cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS), caused by biallelic expansions in the RFC1 gene. This Review presents an updated clinical approach to the diagnosis and management of SLOCA that focuses on the most important developments in this field. Future challenges are also discussed, including the identification of additional missing genetic causes of SLOCA, especially via the use of long-read genome sequencing, improvements in SLOCA prognostication and the implementation of clinical trials of neuroprotective interventions.

Indexed as

Cerebellar AtaxiaAge of OnsetHumans

Identifiers

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.