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The Caudate Nucleus Undergoes Dramatic and Unique Transcriptional Changes in Human Prodromal Huntington's Disease Brain

ABSTRACT: The Caudate Nucleus Undergoes Dramatic and Unique Transcriptional Changes in Human Prodromal Huntington's Disease Brain

PROVIDER: PRJNA531456 | ENA |

REPOSITORIES: ENA

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The Caudate Nucleus Undergoes Dramatic and Unique Transcriptional Changes in Human Prodromal Huntington's Disease Brain

Project description:The mechanisms underlying degeneration of the specific neurons in the striatum of Huntingon's Disease (HD) brain are currently unknown. The striatum is massively degenerated in late stage HD, making examination of post-mortem brain tissue from symptomatic individuals problematic. In this study, caudate nucleus (CAU) tissue from two asymptomatic HD+ individuals was subjected for comparison with similar datasets with symptomatic HD individuals and healthy controls.

2019-04-09 | GSE129473 | GEO

The caudate nucleus undergoes dramatic and unique transcriptional changes in human prodromal Huntington's disease brain.

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Profiling of mRNA transcriptomic changes using RNA-seq in postmortem caudate nucleus of subjects with alcohol use disorder

Project description:Purpose: The goal of this study to examine mRNA transcriptomic changes in reward-related brain regions of subjects with alcohol use disorder. Methods: Total RNAs were extracted from postmortem caudate nucleus of 12 AUD and 12 control subjects. rRNA depletion RNA sequencing was performed and the sequence reads were processed using the bulk RNA-seq processing pipeline Pipeliner workflow (Federico et al. Front Genet 2019; 10, 614). AUD-associated mRNA transcriptomic changes were analyzed by the Limma-Voom method. Results: Differentially expressed mRNAs (absolute FC>2.0 & P<0.05) were identified in postmortem caudate nucleus of subjects with alcohol use disorder (AUD). Chronic alcohol consumption may alter mRNA transcriptome profiles in reward-related brain regions, resulting in alcohol-induced neuroadaptations.

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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.

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