ArticleNature aging2024
A single-nuclei paired multiomic analysis of the human midbrain reveals age- and Parkinson's disease-associated glial changes.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Improving reproducibility of differentially expressed genes in single-cell transcriptomic studies of neurodegenerative diseases through meta-analysis.Nature communications · 2025Pooled it
- Single-cell transcriptomics of human brain disorders.Molecular psychiatry · 2026Review
- Injury-transduced oligodendrocytes modulate neuroinflammation and glial activation in diseased and non-diseased central nervous system.Nature communications · 2026Article
- Advances in sex-specific single-cell transcriptomic profiling in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- KOLF2.1J iTF-Microglia: A standardized platform to study microglial transcriptional regulatory networks in CNS disease.iScience · 2026Article
- Integrating dorsolateral prefrontal cortex multi-omics and GWAS summary data reveals genetic etiology of Parkinson's disease.Research square · 2026Article
- Integrating dorsolateral prefrontal cortex multi-omics and GWAS summary data reveals genetic etiology of Parkinson's disease.medRxiv : the preprint server for health sciences · 2026Article
- Regulator of G protein signaling 10: a critical regulator of chronic systemic inflammation in parkinson's disease.Journal of neuroinflammation · 2026Review
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- Single-nucleus multiomic profiling of the aging mouse substantia nigra reveals conserved gene alterations linked to Parkinson's disease.Genome research · 2026Article
- DNAJC6 Parkinson's disease: Endolysosomal dysfunction and emerging roles for oligodendrocytes.NPJ Parkinson's disease · 2026Review
- Synaptic effects of interleukin-6 on human iPSC-derived dopaminergic neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Massive-scale single-nucleus multi-omics identifies novel rare noncoding drivers of Parkinson's disease.bioRxiv : the preprint server for biology · 2026Article
- A Single-Cell Perspective on Remapping Human Adult Neurogenesis and Its Clinical Implications.Biomolecules · 2026Review
- Testing an inverse link between limbic alpha-synucleinopathy and myelin markers in mice and humans.NPJ Parkinson's disease · 2026Article
- Anti-TLR2 immunotherapy modulates neuron-to-oligodendrocyte propagation of α-synuclein in mouse and human models.Nature communications · 2026Article
- Microglia, Astrocytes, and Oligodendrocytes in Parkinson's Disease: Neuroinflammatory Crosstalk and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Transcriptional Heterogeneity Reveals a Synaptic Gene Program in Developing and Adult Human Oligodendrocyte Precursor Cells.bioRxiv : the preprint server for biology · 2026Article
- From cellular heterogeneity to precision medicine: single-cell multi-omics in CNS disease research.Frontiers in cellular neuroscience · 2026Review
- Integrating polygenic signals and single-cell multiomics identifies cell-type-specific regulomes critical for immune- and aging-related diseases.Nature aging · 2026Article
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Authors and funding
5 authors.
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Abstract
Age is the primary risk factor for Parkinson's disease (PD), but how aging changes the expression and regulatory landscape of the brain remains unclear. Here we present a single-nuclei multiomic study profiling shared gene expression and chromatin accessibility of young, aged and PD postmortem midbrain samples. Combined multiomic analysis along a pseudopathogenesis trajectory reveals that all glial cell types are affected by age, but microglia and oligodendrocytes are further altered in PD. We present evidence for a disease-associated oligodendrocyte subtype and identify genes lost over the aging and disease process, including CARNS1, that may predispose healthy cells to develop a disease-associated phenotype. Surprisingly, we found that chromatin accessibility changed little over aging or PD within the same cell types. Peak-gene association patterns, however, are substantially altered during aging and PD, identifying cell-type-specific chromosomal loci that contain PD-associated single-nucleotide polymorphisms. Our study suggests a previously undescribed role for oligodendrocytes in aging and PD.
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