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Omics data integration suggests a potential idiopathic Parkinson’s disease signature

ABSTRACT: Omics data integration suggests a potential idiopathic Parkinson’s disease signature

PROVIDER: PRJNA853627 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19882208.fastq.gz	Fastqsanger.gz
	SRR19882209.fastq.gz	Fastqsanger.gz
	SRR19882210.fastq.gz	Fastqsanger.gz
	SRR19882211.fastq.gz	Fastqsanger.gz
	SRR19882212.fastq.gz	Fastqsanger.gz

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Omics data integration suggests a potential idiopathic Parkinson’s disease signature

Project description:Identification of early transcriptomic and metabolic alterations consistent across different idiopathic Parkinson’s disease (IPD) patients might reveal the potential basis of increased dopaminergic neuron vulnerability and primary disease mechanisms. In this study, we combine systems biology and data integration approaches to identify differences in transcriptomic and metabolic signatures between IPD patient and healthy individual-derived midbrain neural precursor cells. Characterization of gene expression and metabolic modeling reveal pyruvate, several amino acid and lipid metabolism as the most dysregulated metabolic pathways in IPD neural precursors. Furthermore, we show that IPD neural precursors endure mitochondrial metabolism impairment and a reduced total NAD pool. Accordingly, we show that treatment with NAD precursors increases ATP yield hence demonstrating a potential to rescue early IPD-associated metabolic changes.

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Omics data integration suggests a potential idiopathic Parkinson's disease signature.

Project description:The vast majority of Parkinson's disease cases are idiopathic. Unclear etiology and multifactorial nature complicate the comprehension of disease pathogenesis. Identification of early transcriptomic and metabolic alterations consistent across different idiopathic Parkinson's disease (IPD) patients might reveal the potential basis of increased dopaminergic neuron vulnerability and primary disease mechanisms. In this study, we combine systems biology and data integration approaches to identify differences in transcriptomic and metabolic signatures between IPD patient and healthy individual-derived midbrain neural precursor cells. Characterization of gene expression and metabolic modeling reveal pyruvate, several amino acid and lipid metabolism as the most dysregulated metabolic pathways in IPD neural precursors. Furthermore, we show that IPD neural precursors endure mitochondrial metabolism impairment and a reduced total NAD pool. Accordingly, we show that treatment with NAD precursors increases ATP yield hence demonstrating a potential to rescue early IPD-associated metabolic changes.

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Autophagy impairments in directly reprogrammed neurons in patients with idiopathic Parkinson’s disease

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Project description:Establishing reliable biomarkers for assessing and validating clinical diagnosis at early prodromal stages of Parkinson’s disease is crucial for developing therapies to slow or halt disease progression. Here, we present the largest study to date using whole blood gene expression profiling from over 500 individuals to identify an 87-gene blood-based signature. Our gene signature effectively differentiates between idiopathic PD patients and controls in both a validation cohort and an independent test cohort, and further highlights mitochondrial metabolism and ubiquitination/proteasomal degradation as potential pathways disrupted in Parkinson’s disease.

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Project description:Patients with Parkinson’s disease (PD) exhibit differences in their gut microbial community compared to healthy subjects. Although alterations have been most commonly described as differential abundance of bacteria, fewer studies have focused on the functionnal aspect of these changes. Causal and mechanistic connections between the gut microbiome and PD pathogenesis remain elusive, but could include molecules that influence inflammation or neuronal α-synuclein aggregation. Here, we perform an integrated multi-omic analysis of fecal samples from patients with PD or a prodrome thereof (idiopathic REM sleep behaviour disorder, iRBD) compared to healthy controls. We reveal 11 metabolites significantly different between the three groups, amongst which β-glutamate was increased in PD and prodromal PD, and correlated with the transcriptional activities of Methanobrevibacter smithii and Clostridium spp. In addition, we identified a decrease in transcript for motilty and flagellar assembly pathways in keystone bacteria such as Roseburia and Agathobacter. Our study highlights the apparent disruption of microbial gene expression in PD, in particularly gene associated to mobility which can impact the immune system, and the neuro-inflammation involved in PD.

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Early-to-mid stage idiopathic Parkinson’s disease shows enhanced cytotoxicity and differentiation in CD8 T-cells in females

Project description:Neuroinflammation in the brain contributes to the pathogenesis of Parkinson’s disease (PD), but the potential dysregulation of peripheral immunity has not been systematically investigated for idiopathic PD (iPD). Here we showed an elevated peripheral cytotoxic immune milieu, with more terminally-differentiated effector memory (TEMRA) CD8 T, CD8+ NKT cells and circulating cytotoxic molecules in fresh blood of early-to-mid iPD, especially in females, after analyzing >700 innate and adaptive features. This profile, also reflected by fewer CD8+FOXP3+ regulatory T cells, was confirmed in another subcohort. Co-expression between cytotoxic molecules was selectively enhanced in CD8 TEMRA and effector memory (TEM) cells. Single-cell RNA-sequencing analysis demonstrated the accelerated CD8 differentiation within CD8 compartments, enhanced cytotoxic pathways in CD8 TEMRA and TEM cells, while CD8 central-memory (TCM) and naïve cells were already more-active and transcriptionally-reprogrammed. Our work provides a comprehensive map of dysregulated peripheral immunity in iPD, proposing previously-unrecognized candidates for early diagnosis and treatments.

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