ArticleNPJ Parkinson's disease2025
Longitudinal multi-omics in alpha-synuclein Drosophila model discriminates disease- from age-associated pathologies in Parkinson's disease.
Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Knockouts of Sulfur Metabolism Genes Induce Chronic Inflammation and Immune Dysregulation inAntioxidants (Basel, Switzerland) · 2026Article
- Spatial multi-omics reveals region-specific molecular signatures in a 6-OHDA model of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Massive-scale single-nucleus multi-omics identifies novel rare noncoding drivers of Parkinson's disease.bioRxiv : the preprint server for biology · 2026Article
- Immune crosstalk in Alzheimer's and Parkinson's disease: insights from Drosophila models into the brain-peripheral immune axis.Frontiers in immunology · 2026Review
- Modelling Neural Disorders with theBiomolecules · 2025Review
- Article
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Authors and funding
16 authors.
Funding
Abstract
Parkinson's disease (PD) starts decades before symptoms appear, usually in the later decades of life, when age-related changes are occurring. To identify molecular changes early in the disease course and distinguish PD pathologies from aging, we generated Drosophila expressing alpha-synuclein (αSyn) in neurons and performed longitudinal bulk transcriptomics and proteomics on brains at six time points across the lifespan and compared the data to healthy control flies as well as human post-mortem brain datasets. We found that translational and energy metabolism pathways were downregulated in αSyn flies at the earliest timepoints; comparison with the aged control flies suggests that elevated αSyn accelerates changes associated with normal aging. Unexpectedly, single-cell analysis at a mid-disease stage revealed that neurons upregulate protein synthesis and nonsense-mediated decay, while glia drive their overall downregulation. Longitudinal multi-omics approaches in animal models can thus help elucidate the molecular cascades underlying neurodegeneration vs. aging and co-pathologies.
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