Evidence map›Paper›PMID 18418689›Full record

ReviewCerebellum (London, England)2008

SCA3: neurological features, pathogenesis and animal models.

Olaf Riess, Udo Rüb, Annalisa Pastore, Peter Bauer, Ludger Schöls

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cerebellum (London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
–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

113 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  19. Genetic Ablation of Inositol 1,4,5-Trisphosphate Receptor Type 2 (IPInternational journal of molecular sciences · 2023
    Article
  20. Review

53 more citing papers are in PubMed but not listed here.

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

5 authors.

Olaf RiessDepartment of Medical Genetics, University of Tuebingen, Calwerstrasse 7, D-72076 Tuebingen, Germany. olaf.riess@med.uni-tuebingen.de
Udo Rüb
Annalisa Pastore
Peter Bauer
Ludger Schöls

Funding

Medical Research Council MC_U117584256
6 · The paper itself

Abstract

The most frequent subtype of autosomal dominant inherited spinocerebellar ataxias is caused by CAG repeat expansions of more than 55 units in the ataxin-3 gene. The clinical variability of the phenotype depends on the length of the expanded repeat and the age at onset (and thus indirectly with the repeat size). Anticipation of the phenotype is most frequently associated with repeat expansions in paternal transmission. In this review we describe four clinical subphenotypes and correlate them to the respective repeat expansions. We also provide a detailed description of the neuropathological features. Finally, we discuss the current knowledge on the function of normal and dysfunction of altered ataxin-3 and how this translates to the predicted structure of the protein.

Indexed as

Chromosomes, Human, Pair 14AnimalsBotulinum ToxinsBrainDisease Models, AnimalHumansMachado-Joseph DiseaseMagnetic Resonance ImagingNerve Tissue ProteinsPolymorphism, GeneticTrinucleotide Repeat ExpansionTrinucleotide RepeatsBotulinum ToxinsNerve Tissue Proteins

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.