ArticleNature neuroscience2020
Epigenomic analysis of Parkinson's disease neurons identifies Tet2 loss as neuroprotective.
Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Epigenome-wide association study of human frontal cortex identifies differential methylation in Lewy body pathology.Nature communications · 2022Pooled it
- Epigenomic Remodeling by Lipid Metabolism: A Cross-Disease Perspective on Cancer and Brain Disorders.Genes · 2026Review
- TET2 as a Context-Dependent Epigenetic Integrator in Clonal Hematopoiesis, Inflammation, Cancer, and Immunotherapy.Cell biochemistry and function · 2026Review
- Review
- Multi-omics approaches to parkinsonism: genomic, proteomic, and non-coding RNA perspectives.Molecular biology reports · 2026Review
- Neurobiology of exercise in Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Phosphorylated ubiquitin is a secondary messenger and an epigenetic mark mediating mitochondria to nucleus signaling.bioRxiv : the preprint server for biology · 2026Article
- Profiling of 5-hydroxymethylcytosine in blood reveals preferential enrichment at exon-intron junctions and predictive value for Parkinson's disease.NPJ Parkinson's disease · 2026Article
- DNA hydroxymethylation-mediated epigenetic modifications in alcohol use disorder.Frontiers in aging neuroscience · 2026Review
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Parkinson's disease-associated alterations in DNA methylation and hydroxymethylation in human brain.NPJ Parkinson's disease · 2025Article
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- DNA Methylation in Long-Term Memory.Physiology (Bethesda, Md.) · 2025Review
- Article
- Tet2 loss and enhanced ciliogenesis suppress α-synuclein pathology.Acta neuropathologica communications · 2025Article
- Mechanistic advances in factors influencing phenotypic variability in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a review.Frontiers in neurology · 2025Review
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- TET2 germline variants promote kidney disease by impairing DNA repair and activating cytosolic nucleotide sensors.Nature communications · 2024Article
- Repetitive transcranial magnetic stimulation alleviates motor impairment in Parkinson's disease: association with peripheral inflammatory regulatory T-cells and SYT6.Molecular neurodegeneration · 2024Article
- Parkinson's disease is associated with clonal hematopoiesis with TET2 mutation.NPJ Parkinson's disease · 2024Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) pathogenesis may involve the epigenetic control of enhancers that modify neuronal functions. Here, we comprehensively examine DNA methylation at enhancers, genome-wide, in neurons of patients with PD and of control individuals. We find a widespread increase in cytosine modifications at enhancers in PD neurons, which is partly explained by elevated hydroxymethylation levels. In particular, patients with PD exhibit an epigenetic and transcriptional upregulation of TET2, a master-regulator of cytosine modification status. TET2 depletion in a neuronal cell model results in cytosine modification changes that are reciprocal to those observed in PD neurons. Moreover, Tet2 inactivation in mice fully prevents nigral dopaminergic neuronal loss induced by previous inflammation. Tet2 loss also attenuates transcriptional immune responses to an inflammatory trigger. Thus, widespread epigenetic dysregulation of enhancers in PD neurons may, in part, be mediated by increased TET2 expression. Decreased Tet2 activity is neuroprotective, in vivo, and may be a new therapeutic target for PD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.