Epigenetic Regulation in Neuronal Development, Neurodegeneration and Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 28 December 2025 | Viewed by 831

Special Issue Editor


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Guest Editor
Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-7088, USA
Interests: epigenetics; gene expression; DNA methylation; neural stem cell differentiation; adult brain function; somatic cell reprogramming
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Special Issue Information

Dear Colleagues,

The intricate interplay between epigenetic mechanisms and neuronal processes has emerged as a cornerstone of modern neuroscience, offering transformative insights into how the nervous system develops, adapts, and repairs itself. This Special Issue invites researchers to contribute cutting-edge work exploring the dynamic role of epigenetic regulation—spanning DNA methylation, histone modifications, non-coding RNAs, and chromatin remodeling—in shaping neuronal development and regeneration.

Recent advances in technologies such as single-cell sequencing, CRISPR-based epigenome editing, and high-resolution imaging have revolutionized our understanding of how epigenetic landscapes guide neural stem cell differentiation, synaptic plasticity, and axon regeneration. Yet, critical questions remain: How do environmental cues, aging, or disease states interact with epigenetic machinery to influence neurodevelopment or repair? Can we harness epigenetic targets to promote recovery in neurodegenerative diseases or traumatic injuries?

This issue aims to bridge fundamental discoveries with translational applications, fostering dialog across disciplines including molecular biology, neurobiology, and clinical research. We welcome original research articles, reviews, and clinical studies addressing topics such as the following:

  • Epigenetic control of neural stem cell fate and neurogenesis;
  • Chromatin dynamics in synaptic plasticity and cognitive function;
  • Epigenetic barriers to neuronal regeneration and strategies to overcome them;
  • Cross-talk between metabolism, inflammation, and epigenetic pathways;
  • Therapeutic interventions targeting epigenetic modifiers in neurodegeneration (e.g., Alzheimer’s, Parkinson’s) or spinal cord injury.

We encourage researchers to share their breakthroughs to advance this rapidly evolving field and inspire future therapeutic paradigms.

Prof. Dr. Guoping Fan
Guest Editor

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Keywords

  • epigenetic regulation
  • neuronal development
  • neuronal regeneration
  • chromatin remodeling

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Published Papers (1 paper)

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Research

29 pages, 23179 KiB  
Article
Oligodendrocyte-Specific STAT5B Overexpression Ameliorates Myelin Impairment in Experimental Models of Parkinson’s Disease
by Yibo Li, Zhaowen Su, Jitong Zhai, Qing Liu, Hongfang Wang, Jiaxin Hao, Xiaofeng Tian, Jiamin Gao, Dandan Geng and Lei Wang
Cells 2025, 14(15), 1145; https://doi.org/10.3390/cells14151145 - 25 Jul 2025
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Abstract
Background: Parkinson’s disease (PD) involves progressive dopaminergic neuron degeneration and motor deficits. Oligodendrocyte dysfunction contributes to PD pathogenesis through impaired myelination. Methods: Single-nucleus RNA sequencing (snRNA-seq) of PD mice revealed compromised oligodendrocyte differentiation and STAT5B downregulation. Pseudotemporal trajectory analysis via Monocle2 demonstrated impaired [...] Read more.
Background: Parkinson’s disease (PD) involves progressive dopaminergic neuron degeneration and motor deficits. Oligodendrocyte dysfunction contributes to PD pathogenesis through impaired myelination. Methods: Single-nucleus RNA sequencing (snRNA-seq) of PD mice revealed compromised oligodendrocyte differentiation and STAT5B downregulation. Pseudotemporal trajectory analysis via Monocle2 demonstrated impaired oligodendrocyte maturation in PD oligodendrocytes, correlating with reduced myelin-related gene expression (Sox10, Plp1, Mbp, Mog, Mag, Mobp). DoRothEA-predicted regulon activity identified STAT5B as a key transcriptional regulator. Results: Oligodendrocyte-specific STAT5B activation improved myelin integrity, as validated by Luxol Fast Blue staining and transmission electron microscopy; attenuated dopaminergic neuron loss; and improved motor function. Mechanistically, STAT5B binds the MBP promoter to drive transcription, a finding confirmed by the luciferase assay, while the DNMT3A-mediated hypermethylation of the STAT5B promoter epigenetically silences its expression, as verified by MethylTarget sequencing and methylation-specific PCR. Conclusions: DNMT3A inhibited the expression of STAT5B by affecting its methylation, which reduced the transcription of MBP, caused oligodendrocyte myelin damage, and eventually led to dopamine neuron damage and motor dysfunction in an MPTP-induced mouse model. This DNMT3A-STAT5B-MBP axis underlies PD-associated myelin damage, connecting epigenetic dysregulation with oligodendrocyte dysfunction and subsequent PD pathogenesis. Full article
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