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Increased expression of myelin-associated genes in frontal cortex of SNCA overexpressing rats and Parkinson’s disease patients

ABSTRACT: Increased expression of myelin-associated genes in frontal cortex of SNCA overexpressing rats and Parkinson’s disease patients

PROVIDER: PRJNA633095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11795763_1.fastq.gz	Fastqsanger.gz
	SRR11795763_2.fastq.gz	Fastqsanger.gz
	SRR11795764_1.fastq.gz	Fastqsanger.gz
	SRR11795764_2.fastq.gz	Fastqsanger.gz
	SRR11795765_1.fastq.gz	Fastqsanger.gz

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Increased expression of myelin-associated genes in frontal cortex of SNCA overexpressing rats and Parkinson’s disease patients

Project description:Parkinson’s disease is an age-dependent neurodegenerative disorder. Besides characteristic motor symptoms, patients suffer from cognitive impairments linked to pathology in cortical areas. Due to obvious challenges in tracing molecular perturbations underlying alterations in human brain over time, we took advantage of a well-characterized rat model. Using RNA sequencing, we profiled the frontocortical transcriptome of post-mortem patient samples and aligned expression changes with perturbation patterns obtained in the model at 5 and 12 months of age reflecting a presymptomatic and symptomatic time point. Integrating cell type-specific reference data, we identified a shared expression signature between both species that pointed to oligodendrocyte-specific, myelin-associated genes. Drawing on longitudinal information from the model, their nearly identical upregulation in both species allowed tracing them to two distinctive perturbance modes they originate from. While one mode exhibited age-independent alterations that affected genes like PLP1, the other mode, impacting on genes like MAG, was characterized by interferences of disease gene and adequate adaptations of gene activity along ageing. Our results highlight that even for a small set of functionally linked genes distinct interference mechanisms may underly disease progression that cannot be distinguished by examining the terminal point alone but instead require longitudinal interrogation of the system.

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Proteomic investigation of whole cortex and synaptosomes from rats with a familial Parkinson’s G51D mutation in the Snca gene.

Project description:The glycine-51 (G51) codon in exon 3 of the rat Snca gene, encoding alpha-synuclein, was mutated to aspartic acid using CRISPR/Cas9 to generate the SncaG51D rat model of Parkinson’s (Morley et al. 2023). The G51D mutation causes an aggressive form of Parkinson’s and dementia with Lewy bodies in humans. The brains from four 6-month old rats of wild-type, heterozygous, and homozygous genotypes (Snca+/+, SncaG51D/+ and SncaG51D/G51D) were harvested and all 12 brains were bisected down the midline. Frontal cortex was isolated from one half, and synaptosomes were prepared from the other half. Following quality control the samples were processed for TMT-mass spectrometry by the Fingerprints Facility, University of Dundee. MaxQuant Version 1.6.0.16 was used for the assignment of peptides to protein using the uniport-rat-jan2018.fasta file. Pairwise comparisons were made between the different mutant samples and Snca+/+ for both the cortical and synaptosome samples. Morley V, Dolt KS, Alcaide-Corral CJ, Walton T, Lucatelli C, Mashimo T, Tavares AAS & Kunath T (2023) In vivo18F-DOPA PET imaging identifies a dopaminergic deficit in a rat model with a G51D α-synuclein mutation. Front. Neurosci. 17, 1095761.

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Increased expression of myelin-associated genes in frontal cortex of <i>SNCA</i> overexpressing rats and Parkinson's disease patients.

Project description:Parkinson's disease (PD) is an age-dependent neurodegenerative disorder. Besides characteristic motor symptoms, patients suffer from cognitive impairments linked to pathology in cortical areas. Due to obvious challenges in tracing the underlying molecular perturbations in human brain over time, we took advantage of a well-characterized PD rat model. Using RNA sequencing, we profiled the frontocortical transcriptome of post-mortem patient samples and aligned expression changes with perturbation patterns obtained in the model at 5 and 12 months of age reflecting a presymptomatic and symptomatic time point. Integrating cell type-specific reference data, we identified a shared expression signature between both species that pointed to oligodendrocyte-specific, myelin-associated genes. Drawing on longitudinal information from the model, their nearly identical upregulation in both species could be traced to two distinctive perturbance modes. While one mode exhibited age-independent alterations that affected genes including proteolipid protein 1 (PLP1), the other mode, impacting on genes like myelin-associated glycoprotein (MAG), was characterized by interferences of disease gene and adequate expression adaptations along aging. Our results highlight that even for a group of functionally linked genes distinct interference mechanisms may underlie disease progression that cannot be distinguished by examining the terminal point alone but instead require longitudinal interrogation of the system.

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Project description:The predominantly function of THAP1 has been defined as a transcription factor, but how it regulates gene expression in human neurons is not well understood. Here, we found that THAP1 is able to regulate the expression of alpha-synuclein (SNCA), a key protein in Parkinson’s disease (PD).

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Transcription regulation of SNCA by dystonia type 6 gene product THAP1 [RNA-Seq]

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Transcription regulation of SNCA by dystonia type 6 gene product THAP1 [4C-Seq]

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Transcription regulation of SNCA by dystonia type 6 gene product THAP1 [ChIP-seq]

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Enriched environmental conditions modify the gut microbiome composition and fecal markers of inflammation in Parkinson’s disease

Project description:We used a transgenic mouse model overexpressing the complete human SNCA genes modeling familial and sporadic forms of Parkinson’s disease to study whether environmental conditions such as standard versus enriched environment changes the gut microbiome and influences disease progression.

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Analysis of striatal transcriptome in transgenic mice overexpressing human wild-type alpha-synuclein

Project description:Alpha synuclein (SNCA) has been linked to neurodegenerative diseases (synucleinopathies) that include Parkinson’s disease (PD). Although the primary neurodegeneration in PD involves nigrostriatal dopaminergic neurons, more extensive yet regionally selective neurodegeneration is observed in other synucleinopathies. Furthermore, SNCA is ubiquitously expressed in neurons and numerous neuronal systems are dysfunctional in PD. Therefore it is of interest to understand how overexpression of SNCA affects neuronal function in regions not directly targeted for neurodegeneration in PD. To gain a better understanding of the consequences of excessive SNCA expression on basal ganglia function, we performed transcriptome analysis of striatal tissue from male Thy1-aSyn-mice and wt littermates. The present study investigated the consequences of SNCA overexpression on cellular processes and functions in the striatum of mice overexpressing wild-type, human SNCA under the Thy1 promoter (Thy1-aSyn mice) by transcriptome analysis. The analysis revealed alterations in multiple biological processes in the striatum of Thy1-aSyn mice, including synaptic plasticity, signaling, transcription, apoptosis, and neurogenesis. The present study investigated the consequences of SNCA overexpression on cellular processes and functions in the striatum of mice overexpressing wild-type, human SNCA under the Thy1 promoter (Thy1-aSyn mice) by transcriptome analysis. The analysis revealed alterations in multiple biological processes in the striatum of Thy1-aSyn mice, including synaptic plasticity, signaling, transcription, apoptosis, and neurogenesis.

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