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Single-cell transcriptomic and proteomic analysis of Parkinson’s disease brains

ABSTRACT: Single-cell transcriptomic and proteomic analysis of Parkinson’s disease brains

PROVIDER: PRJNA835055 | ENA |

REPOSITORIES: ENA

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Single-cell transcriptomic and proteomic analysis of Parkinson’s disease brains

Project description:Parkinson’s disease (PD) is a prevalent neurodegenerative disorder where recent evidence suggests pathogenesis may be mediated by inflammatory processes. The molecular architecture of the disease remains to be fully elucidated. We performed single-nucleus transcriptomics and unbiased proteomics using postmortem tissue obtained from the prefrontal cortex of 12 individuals with late-stage PD and age-matched controls. We analyzed ~80,000 nuclei and identified eight major cell types, including brain-resident T cells, each with distinct transcriptional changes in line with the known genetics of PD. By analyzing Lewy body pathology in the same postmortem tissue, we found that α-synuclein pathology is inversely correlated with chaperone expression in excitatory neurons. Examining cell-cell interactions, we found a selective abatement of neuron-astrocyte interactions and enhanced neuroinflammation. Proteomic analyses of the same brains identified synaptic proteins in prefrontal cortex that were preferentially downregulated in PD. Strikingly, comparing this dataset to a regionally similar published analysis for Alzheimer’s disease (AD), we found no common differentially expressed genes in neurons, but identified many shared differentially expressed genes in glial cells, suggesting that disease etiology in PD and AD are likely distinct. These data are presented as a resource for interrogating the molecular and cellular basis of PD and other neurodegenerative diseases.

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Project description:Despite the advance of genetic and genomic analysis of Parkinson’s disease (PD), our understanding of PD pathophysiology remains limited due to unclear etiology of idiopathic PD and unavailable integrated approach for large-scale multi-dimensional data. Herein we report a novel multiscale network approach to establish transcriptomic network from postmortem PD brain data. The analysis delineates structures of gene-gene regulatory networks in PD and identifies novel network regulators that are functionally connected to previously identified PD risk genes. We identify STMN2, encoding a neuron-specific stathmin family protein and down-regulated in PD brains, as the top regulator of the transcriptomic network underlying PD. Knock-down of Stmn2 in mice validates its regulatory role, and Stmn2 deficient mice show dopaminergic neuron vulnerability, phosphorylated a-synuclein elevation, and locomotor function deficits. As predicted from the network analysis, reduced STMN2 expression impairs synaptic vesicle trafficking in midbrain neurons. Our approach sheds light on the complexity of PD pathogenic network and thus facilitates identification of novel PD therapeutic targets.

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