Epigenetic Regulation in Neuroplasticity: Key to Understanding and Treating Neurological Diseases.

Abstract

Epigenetic mechanisms-DNA methylation, histone modifications, and non-coding RNAs-integrate genetic programs with environmental cues to shape neural development, plasticity, and pathology. During neurogenesis, methylation patterns and histone marks direct stem cell fate and synapse formation, while microRNAs fine-tune gene expression. In the adult brain, rapid, reversible histone acetylation and activity-dependent non-coding RNAs underlie learning, memory, and injury responses. Environmental stressors, toxins, and diet can trigger maladaptive epigenetic changes, linking exposures to cognitive deficits and psychiatric risk. Aberrant methylation and histone landscapes are implicated in autism, Alzheimer's, and Parkinson's-altering synaptic scaffolding, amyloid processing, and neuronal survival-while dysregulated microRNAs serve as both biomarkers and intervention targets. Advances in single-cell methylome sequencing, ChIP-seq, and multi-omics are clarifying cell-type specificity, and emerging therapies (HDAC inhibitors, methyl donors, RNA-based tools) offer promise, pending precise delivery and safety optimizations.