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Metagenomic analysis Huntington's disease patients

ABSTRACT: Presence of bacterial infection in brains of patients with Huntington's disease

PROVIDER: PRJEB32814 | ENA |

REPOSITORIES: ENA

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3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.

2017-09-21 | GSE96099 | GEO

Reprogrammed neurons from adult dermal fibroblasts of patients with Huntington's disease

Project description:Reprogrammed neurons from adult dermal fibroblasts of patients with Huntington's disease

2017-12-11 | GSE84013 | GEO

Presence of bacterial infection in brains of patients with Huntington's disease (HD)

Project description:Bacterial isolation in infected brains in patients with Huntington's disease. Here we used next generation sequencing of 16S ribosomal RNA gene PCR amplicons (NGS 16S amplicon analysis)

| EGAS00001003678 | EGA

Bacteria in patients with Parkinson's disease (PD)

Project description:Presence of bacterial infection in brains of patients with Parkinson's disease (PD)

| PRJEB32365 | ENA

Proteomic analysis of mitochondria from Huntington's Disease patient iPSC-derived neurons

Project description:Huntington's disease is caused by an expanded CAG repeat in the huntingtin gene, yeilding a Huntingtin protein with an expanded polyglutamine tract. Patient-derived induced pluripotent stem cells (iPSCs) can help understand disease; however, defining pathological biomarkers in challanging. Here we used LC-MS/MS to determine differences in mitochondrial proteome between iPSC-derived neurons from healthy donors and Huntington's disease patients.

2023-02-10 | PXD037526 | Pride

Human blood expression for Huntington's disease versus control

Project description:Affymetrix U133A expression levels for 12 symptomatic and 5 presymptomatic Huntington's disease patients versus 14 healthy controls. Keywords: other

2005-09-13 | E-GEOD-1751 | biostudies-arrayexpress

Human blood expression for Huntington's disease versus control

Project description:Affymetrix U133A expression levels for 12 symptomatic and 5 presymptomatic Huntington's disease patients versus 14 healthy controls. Keywords: other

2005-09-13 | GSE1751 | GEO

Transcriptome sequencing reveals aberrant alternative splicing in Huntington's disease

Project description:Huntingtonâs disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG expansion in the gene encoding Huntingtin (HTT). Transcriptome dysregulation is a major feature of HD pathogenesis, as revealed by a large body of work on gene expression profiling of tissues from human HD patients and mouse models. These studies were primarily focused on transcriptional changes affecting steady-state overall gene expression levels using microarray based approaches. A major missing component however has been the study of transcriptome changes at the post-transcriptional level, such as alternative splicing. Alternative splicing is a critical mechanism for expanding regulatory and functional diversity from a limited number of genes, and is particularly complex in the mammalian brain. Here we carried out a deep RNA-seq analysis of 7 human HD brains and 7 controls to systematically discover aberrant alternative splicing events and characterize potential associated splicing factors in HD. We identified 593 differential alternative splicing events between HD and control brains. Using an expanded panel of 54 brain tissues from patients and controls, we also identified 9 splicing factors exhibiting significantly altered expression levels in HD patient brains. Moreover, follow-up molecular analyses of one splicing factor PTBP1 revealed its impact on disease-associated splicing patterns in HD. Collectively, our data provide genomic evidence for widespread splicing dysregulation in HD brains, and suggest the role of aberrant alternative splicing in the pathogenesis of HD RNA-seq analysis of the BA4 motor cortex of 7 control and 7 Huntington's disease patients. 1.5 ug of total RNA was used for RNA-seq library preparation using the TruSeqâ¢ Stranded mRNA LT Sample Prep Kit (Illumina). 100x2 bp paired-end RNA-seq reads were generated on a HiSeq 2000 sequencer.

2016-06-14 | E-GEOD-79666 | biostudies-arrayexpress

Genetic Modifiers of Huntington's Disease

Project description:Genetic Modifiers of Huntington's Disease

| PRJNA75833 | ENA

Human blood expression for Huntington's disease versus control, Codelink

Project description:Codelink Human Uniset I, II, and 20K expression levels for 12 symptomatic and 5 presymptomatic Huntington's disease patients versus 14 healthy controls. Keywords: other

2005-07-22 | GSE1767 | GEO

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