Dataset Information

Epigenetic resetting in the Parkinson's disease entail histone modification remodeling.

ABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons (DN) in the substantia nigra and disrupted cellular maintenance. Here, we demonstrate that NDST3-mediated epigenetic reprogramming halts neuronal degeneration and restores motor function in a PD animal model. Following NDST3 administration, DN and associated circuits in the substantia nigra and striatum show marked revitalization, accompanied by significant alleviation of PD-like motor deficits. Integrative single-cell and spatial RNA sequencing with ChIP sequencing reveal that NDST3-driven reactivation of pathways linked to neuronal survival, synaptic integrity, steering compromised cells toward a resilient phenotype. By recalibrating the epigenetic landscape, NDST3 fosters cellular maintenance and functional recovery within key motor circuits. These findings highlight NDST3’s therapeutic potential as epigenetic modulator in PD. Our findings provide insights into the mechanisms underlying neuronal revitalization and underscore the promise of NDST3 as a novel agent for restoring brain function in neurodegenerative conditions.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Neuronal Stem Cell

DISEASE(S): Parkinson's Disease

SUBMITTER: Yongwoo Na

LAB HEAD: Jong-Seo Kim

PROVIDER: PXD067971 | Pride | 2026-03-16

REPOSITORIES: Pride

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Publications

NDST3-Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease.

Chang Yujung Y Na Yongwoo Y Im Hyeonjoo H Yang Garam G Yang Seungseon S Shim Hyun Soo HS Kim Chunggoo C Kim GyeungYun G Park Hyeok Ju HJ Kim Hee Young HY Lee Seung Eun SE Lee Wonwoong W Ha Yoon Y Park Sungho S Kim Jieun J Cho Won-Young WY Sun Woong W Kim Jong-Seo JS Yoo Junsang J

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20251121

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons (DN) in the substantia nigra and disruption of cellular maintenance. Here, we demonstrate that NDST3-mediated epigenetic reprogramming halts neuronal degeneration and restores motor function in an animal model of PD. Following NDST3 administration, the DN and its associated circuits in the substantia nigra and striatum showed marked revitalization, accompanied by a considerable ...[more]

PMID: 41268696

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Project description:Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder that is clinically defined in terms of motor symptoms. These are preceded by prodromal non-motor manifestations that prove the systemic nature of the disease. Identifying genes and pathways altered in living patients provide new information on the diagnosis and pathogenesis of sporadic PD. We study changes in gene expression in the blood of 40 sporadic PD patients and 20 healthy controls (Discovery set?) by taking advantage of the Affymetrix platform. Patients were at the onset of motor symptoms and before initiating any pharmacological treatment. By applying Ranking-Principal Component Analysis, PUMA and Significance Analysis of Microarrays, gene expression profiling discriminates patients from healthy controls and identifies differentially expressed genes in blood. The majority of these are also present in dopaminergic neurons of the Substantia Nigra, the key site of neurodegeneration. Together with neuronal apoptosis, lymphocyte activation and mitochondrial dysfunction, already found in previous analysis of PD blood and post-mortem brains, we unveiled transcriptome changes enriched in biological terms related to epigenetic modifications including chromatin remodeling and methylation. Candidate transcripts were validated by RT-qPCR in an independent cohort of 12 patients and controls (?Validation set). Our data support the use of blood transcriptomics to study neurodegenerative diseases. It identifies changes in crucial components of chromatin remodeling and methylation machineries as early events in sporadic PD suggesting epigenetics as target for therapeutic intervention. Analyzed samples include blood samples from 40 PD patients and 20 healthy controls. Of the original 60 samples, one (a control sample) did not pass the microarray hybridization quality controls and was excluded from further analyses. All results of bioinformatics analyses shown in this study refer to this set of 59 samples (reported here).

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