Project description:An Infinium microarray platform (HorvathMammalMethylChip40) was used to generate DNA methylation data from n=168 blood samples of a transgenic sheep model of Huntington's disease. 84 transgenic sheep and age matched control sheep.
Project description:Human DNA methylation Beadchip v1.2 was used to profile n=475 samples from various brain regions of subjects with Huntington's disease and control samples. The main goal of the study was to relate Huntington's disease status to measures of epigenetic age acceleration based on DNA methylation data. To measure DNA methylation age, we used the epigenetic clock software described in Horvath S (n=2013) DNA methylation age of human tissues and cell types. Genome Biology.2013, 14:R115. DOI: 10.1186/10.1186/gb-2013-14-10-r115 PMID: 24138928.
Project description:An Infinium microarray platform (HorvathMammalMethylChip40) was used to generate DNA methylation data from mouse tissues of a heterozygous Huntingtin expansion knock-in (Q175) and wildtype (WT) controls. Mouse tissues: blood, liver, brain cortex, brain cerebellum, and striatum.
Project description:Primary neuron model of Huntington's Disease. 2 treatment groups: A) Infected 4 weeks prior with TRE-Htt-N853-18Q-expressing recombinant lentivirus, B) Infected 4 weeks prior with TRE-Htt-N853-82Q-expressing recombinant lentivirus Keywords: gene expression study
Project description:Analysis of proteomic consequences of Tyrobp deletion in a Huntington's disease mouse model. Examination of protein expression alterations in the striatum of mutant huntingtin-Q175 with and without TYROBP (protein tyrosine kinase-binding protein).
Project description:Epigenetic mechanisms, especially DNA methylation, are suggested to play a role in the age-of-onset in Huntington's disease (HD) based on studies on patient brains, and cellular and animal models. Methylation is tissue-specific and it is not clear how HD specific methylation in the brain correlates with the blood compartment, which represents a much more clinically accessible sample. Therefore, we explored the presence of HD specific DNA methylation patterns in whole blood on a cohort of HDM and healthy controls from Slovenia. We compared CpG site-specific DNA methylation in whole blood of 11 symptomatic and 9 pre-symptomatic HDM (HDM), and 15 healthy controls, by using bisulfite converted DNA on the Infinium® Human Methylation27 BeadChip microarray (Illumina) covering 27,578 CpG sites and 14,495 genes. Of the examined 14,495 genes, 437 were differentially methylated (p < 0.01) in pre-symptomatic HDM compared to controls, with three genes (CLDN16, DDC, NXT2) retaining statistical significance after the correction for multiple testing (false discovery rate, FDR < 0.05). Comparisons between symptomatic HDM and controls, and the comparison of symptomatic and pre-symptomatic HDM further identified 260 and 198 differentially methylated genes (p < 0.01), respectively, whereas the comparison of all HDM (symptomatic and pre-symptomatic) and healthy controls identified 326 differentially methylated genes (p < 0.01), however, none of these changes retained significance (FDR < 0.05) after the correction for multiple testing. The results of our study suggest that methylation signatures in the blood compartment are not robust enough to prove as valuable biomarkers for predicting HD progression, but recognizable changes in methylation deserve further research.
Project description:Human DNA methylation Beadchip v1.2 was used to profile buffy coat samples. The main goal of the study was to relate DNA methylation data to Huntington disease status (control, pre-manifest disease, manifest motor disease).