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- Title
Elevated Global DNA Methylation Is Not Exclusive to Amyotrophic Lateral Sclerosis and Is Also Observed in Spinocerebellar Ataxia Types 1 and 2.
- Authors
Hamzeiy, Hamid; Savaş, Doruk; Tunca, Ceren; Şen, Nesli Ece; Gündoğdu Eken, Aslı; Şahbaz, Irmak; Calini, Daniela; Tiloca, Cinzia; Ticozzi, Nicola; Ratti, Antonia; Silani, Vincenzo; Başak, A. Nazlı
- Abstract
Adult-onset neurological disorders are caused and influenced by a multitude of different factors, including epigenetic modifications. Here, using an ELISA kit selected upon careful testing, we investigated global 5-methylcytosine (5-mC) levels in sporadic and familial amyotrophic lateral sclerosis (sALS and fALS), spinocerebellar ataxia types 1 and 2 (SCA1 and SCA2), Huntington’s disease, Friedreich’s ataxia, and myotonic dystrophy type 1. We report a significant elevation in global 5-mC levels of about 2–7% on average for sALS (<italic>p</italic> < 0.01 [F(1, 243) = 9.159, <italic>p</italic> = 0.0027]) and various forms of fALS along with SCA1 (<italic>p</italic> < 0.01 [F(1, 83) = 11.285], <italic>p</italic> = 0.0012) and SCA2 (<italic>p</italic> < 0.001 [F(1, 122) = 29.996, <italic>p</italic> = 0.0001]) when compared to age- and sex-matched healthy controls. <italic>C9orf72</italic> expansion carrier ALS patients exhibit the highest global 5-mC levels along with <italic>C9orf72</italic> promoter hypermethylation. We failed to measure global 5-hydroxymethylcytosine (5-hmC) levels in blood, probably due to the very low levels of 5-hmC and the limitations of the commercially available ELISA kits. Our results point towards a role for epigenetics modification in ALS, SCA1, and SCA2, and help conclude a dispute on the global 5-mC levels in sALS blood.
- Subjects
AMYOTROPHIC lateral sclerosis; DNA methylation; SPINOCEREBELLAR ataxia; TRINUCLEOTIDE repeats; ENZYME-linked immunosorbent assay; METHYLCYTOSINE; HUNTINGTON disease; FRIEDREICH'S ataxia
- Publication
Neurodegenerative Diseases, 2018, Vol 18, Issue 1, p38
- ISSN
1660-2854
- Publication type
Article
- DOI
10.1159/000486201