<p>Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic neurons in the substantia nigra, resulting in hallmark motor symptoms such as tremor, bradykinesia, rigidity, and postural instability. Beyond these classical features, emerging evidence highlights the critical role of RNA modifications, particularly N6-methyladenosine (m⁶A), in regulating neuronal health and disease. The m⁶A modification is dynamically controlled by writers (METTL3, METTL14, WTAP), erasers (FTO, ALKBH5), and readers (e.g., YTHDF2, HNRNPC), which together influence RNA splicing, stability, and translation. Dysregulation of the readers HNRNPC and YTHDF2 has been implicated in oxidative stress, neuroinflammation, and dopaminergic neurodegeneration, positioning the HNRNPC/YTHDF2 axis as a central regulator of RNA metabolism and as a potential therapeutic target. In the healthy brain, HNRNPC ensures proper splicing and stabilizes transcripts essential for neuronal function, while YTHDF2 promotes the degeneration of deleterious m⁶A-modified RNAs to maintain neuronal homeostasis. In PD, their downregulation disrupts these processes, leading to transcript accumulation, impaired splicing, heightened neuroinflammation, oxidative stress, and apoptosis, contributing to dopaminergic neuron susceptibility and degeneration. We further highlight their role in α-synuclein regulation, dopaminergic signaling, and neuroimmune interactions, underscoring their promise as biomarkers and therapeutic targets. Finally, we discuss emerging therapeutic strategies targeting the m⁶A landscape, including antisense oligonucleotides (ASOs), RNA interference (RNAi), CRISPR-Cas13-based epitranscriptomic editing, and small-molecule modulators of m⁶A regulators. This review integrates molecular insights with therapeutic perspectives to elucidate how HNRNPC and YTHDF2 contribute to PD pathophysiology and explore novel avenues for interventions.</p>