- Core epigenetic mechanisms: DNA methylation, histone modifications, chromatin remodelling and noncoding RNAs regulate gene expression without altering DNA sequence.
- Crosstalk among mechanisms and processes like X-chromosome inactivation and genomic imprinting establish long-term gene silencing and cell identity.
- Metabolic state and early environmental exposures shape epigenetic marks, influencing enzyme activity and contributing to lifelong brain function and disease susceptibility.
Handb Clin Neurol. 2026;219:3-17. doi: 10.1016/B978-0-443-19043-8.00026-8.
ABSTRACT
This chapter provides an introductory overview of epigenetic mechanisms, focusing on the molecular processes that regulate gene expression without altering the DNA sequence. It outlines the foundational concepts of DNA methylation, histone modifications, chromatin remodeling, and noncoding RNAs, with emphasis on their roles in cell identity and transcriptional regulation. The interactions between these epigenetic mechanisms, such as the crosstalk of histone acetylation and DNA methylation, are also discussed. Key mechanisms of long-term gene inactivation, like X-chromosome inactivation and genomic imprinting, are summarized. This chapter also highlights the relationships of epigenetic mechanisms with metabolic processes when the metabolite levels influence the activity of the writer and eraser enzymes. Environmental conditions experienced during development can have long-term impact on epigenetic marks, which in turn can play a significant role in disease susceptibility in adulthood. While the chapter’s primary focus is on the biochemical and structural basis of epigenetic regulation across cell types, it briefly touches on environmental epigenetic aspects and highlights a few brain-related epigenetic processes.
PMID:42880842 | DOI:10.1016/B978-0-443-19043-8.00026-8
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