ATXN2 intermediate repeat expansions influence the clinical phenotype in frontotemporal dementia
- 1 January 2019
- journal article
- research article
- Published by Elsevier in Neurobiology of Aging
- Vol. 73, 231.e7-231.e9
Abstract
No abstract availableKeywords
This publication has 9 references indexed in Scilit:
- Interrupted CAG expansions in ATXN2 gene expand the genetic spectrum of frontotemporal dementiasActa Neuropathologica Communications, 2018
- Intermediate-length polyglutamine in ATXN2 is a possible risk factor among Eastern Chinese patients with amyotrophic lateral sclerosisNeurobiology of Aging, 2015
- Contribution of ATXN2 intermediary polyQ expansions in a spectrum of neurodegenerative disordersNeurology, 2014
- Ataxin-2 repeat-length variation and neurodegenerationHuman Molecular Genetics, 2011
- PolyQ Repeat Expansions in ATXN2 Associated with ALS Are CAA Interrupted RepeatsPLOS ONE, 2011
- Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALSNature, 2010
- Importance of Low-Range CAG Expansion and CAA Interruption in SCA2 ParkinsonismArchives of Neurology, 2007
- Analysis of trinucleotide repeats in different SCA loci in spinocerebellar ataxia patients and in normal population of TaiwanActa Neurologica Scandinavica, 2004
- Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2Nature Genetics, 1996