Evidence map›Paper›PMID 18568057›Full record

ArticleNeuropsychiatric disease and treatment2005

Genetic and molecular aspects of spinocerebellar ataxias.

Viktor Honti, László Vécsei

Abstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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

2 authors.

Viktor HontiDepartment of Neurology, Albert Szent-Györgyi Medical and Pharmaceutical Center, University of Szeged, Szeged, Hungary. vecsei@nepsy.szote.u-szeged.hu
László Vécsei

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The group of spinocerebellar ataxias (SCAs) includes more than 20 subgroups based only on genetic research. The "ataxia genes" are autosomal; the "disease-alleles" are dominant, and many of them, but not all, encode a protein with an abnormally long polyglutamine domain. In DNA, this domain can be detected as an elongated CAG repeat region, which is the basis of genetic diagnostics. The polyglutamine tails often tend to aggregate and form inclusions. In some cases, protein-protein interactions are the key to understanding the disease. Protein partners of ataxia proteins include phosphatases and components of chromatin and the transcriptional machinery. To date, investigation of spinocerebellar ataxias involves population genetics, molecular methods, and studying model organisms. However, there is still no efficient therapy for patients. Here, we review the genetic and molecular data gained on spinocerebellar ataxias.

Indexed as

ataxiaautosomaldominantpolyglutaminerepeat

Identifiers

PMID18568057
PMCPMC2413192

What OpenQuestion holds

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Registered trials

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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.