Novel candidate blood-based transcriptional biomarkers of Machado-Joseph disease.
Identifieur interne : 000141 ( Main/Exploration ); précédent : 000140; suivant : 000142Novel candidate blood-based transcriptional biomarkers of Machado-Joseph disease.
Auteurs : Mafalda Raposo [Portugal] ; Conceição Bettencourt [Royaume-Uni] ; Patrícia Maciel [Portugal] ; Fuying Gao [États-Unis] ; Amanda Ramos [Portugal] ; Nadiya Kazachkova [Portugal] ; João Vasconcelos [Portugal] ; Teresa Kay [Portugal] ; Ana João Rodrigues [Portugal] ; Bruno Bettencourt [Portugal] ; Jácome Bruges-Armas [Portugal] ; Daniel Geschwind [États-Unis] ; Giovanni Coppola [États-Unis] ; Manuela Lima [Portugal]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
Abstract
Machado-Joseph disease (or spinocerebellar ataxia type 3) is a late-onset polyglutamine neurodegenerative disorder caused by a mutation in the ATXN3 gene, which encodes for the ubiquitously expressed protein ataxin-3. Previous studies on cell and animal models have suggested that mutated ataxin-3 is involved in transcriptional dysregulation. Starting with a whole-transcriptome profiling of peripheral blood samples from patients and controls, we aimed to confirm abnormal expression profiles in Machado-Joseph disease and to identify promising up-regulated genes as potential candidate biomarkers of disease status.
DOI: 10.1002/mds.26238
PubMed: 25914309
Affiliations:
- Portugal, Royaume-Uni, États-Unis
- Angleterre, Grand Londres, Région Nord (Portugal)
- Braga, Londres
- Université du Minho
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Machado-Joseph disease (or spinocerebellar ataxia type 3) is a late-onset polyglutamine neurodegenerative disorder caused by a mutation in the ATXN3 gene, which encodes for the ubiquitously expressed protein ataxin-3. Previous studies on cell and animal models have suggested that mutated ataxin-3 is involved in transcriptional dysregulation. Starting with a whole-transcriptome profiling of peripheral blood samples from patients and controls, we aimed to confirm abnormal expression profiles in Machado-Joseph disease and to identify promising up-regulated genes as potential candidate biomarkers of disease status.</div>
</front>
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