| Literature DB >> 29274668 |
Serena Lattante1, Maria Grazia Pomponi1, Amelia Conte2, Giuseppe Marangi1, Giulia Bisogni2, Agata Katia Patanella2, Emiliana Meleo2, Christian Lunetta3, Nilo Riva4, Lorena Mosca5, Paola Carrera6, Marco Bee7, Marcella Zollino1, Mario Sabatelli8.
Abstract
To clarify the possible involvement of intermediate ATXN1 alleles as risk factors for amyotrophic lateral sclerosis (ALS), we tested ATXN1 in a cohort of 1146 Italian ALS patients, previously screened for variants in other ALS genes, and in 529 controls. We detected ATXN1 alleles with ≥33 polyglutamine repeats in 105 of 1146 patients (9.16%) and 29 of 529 controls (5.48%) (p = 0.003). The frequency of ATXN1 alleles with ≥33 polyglutamine repeats was particularly high in the group of ALS patients carrying the C9orf72 expansion (12/59, 20.3%). We confirmed this result in an independent cohort of C9orf72 Italian patients (10/80 cases, 12.5%), thus finding a cumulative frequency of ATXN1 expansion of 15.82% in C9orf72 carriers (p = 2.40E-05). Our results strongly support the hypothesis that ATXN1 could act as a disease risk gene in ALS, mostly in C9orf72 expansion carriers. Further studies are needed to confirm our results and to define the mechanism by which ATXN1 might contribute to neuronal degeneration leading to ALS.Entities:
Keywords: ATXN1; Amyotrophic lateral sclerosis; C9orf72; Frontotemporal dementia; Spinocerebellar ataxia
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Year: 2017 PMID: 29274668 DOI: 10.1016/j.neurobiolaging.2017.11.011
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673