Autophagy-associated non-coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra. The exact cause of PD remains unclear, but disrupted autophagy, a critical cellular process for maintaining protein and organelle integrity, is increasingly recognized as a key factor in its pathogenesis. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a significant role in modulating autophagy and contributing to PD pathophysiology. This review explores the regulatory impacts of ncRNAs in various PD models and patient samples, highlighting their potential in therapeutic strategies targeting autophagy-related mechanisms. Autophagy is crucial for the elimination of damaged proteins and dysfunctional organelles in eukaryotic cells. Dysregulation of autophagy has been linked to the accumulation of α-synuclein (α-syn), mitochondrial dysfunction, and neuroinflammation, which are key features of PD. The autophagy-lysosomal pathway (ALP) is involved in the degradation of α-syn and other proteins, and its dysfunction contributes to the progression of PD. ncRNAs, particularly miRNAs, lncRNAs, and circRNAs, regulate autophagy by modulating key signaling pathways and gene expression. For example, miR-3473b inhibits autophagy and participates in PD regulation, while lncRNAs such as NEAT1 and HOTAIR are involved in the progression of PD by stimulating autophagy. CircRNAs like ciRS-7 regulate miR-7, which limits α-syn expression and promotes autophagy. The review highlights the therapeutic potential of ncRNAs in addressing autophagy-related mechanisms in PD. Targeting ncRNAs could offer innovative strategies for developing therapies that enhance autophagy and reduce neuroinflammation. However, challenges remain in translating these findings into clinical practice. The study underscores the importance of ncRNAs in the molecular landscape of PD and their potential in novel treatment approaches. Understanding the role of ncRNAs in autophagy may provide new insights into the pathogenesis of PD and lead to the development of effective therapies.Autophagy-associated non-coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra. The exact cause of PD remains unclear, but disrupted autophagy, a critical cellular process for maintaining protein and organelle integrity, is increasingly recognized as a key factor in its pathogenesis. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play a significant role in modulating autophagy and contributing to PD pathophysiology. This review explores the regulatory impacts of ncRNAs in various PD models and patient samples, highlighting their potential in therapeutic strategies targeting autophagy-related mechanisms. Autophagy is crucial for the elimination of damaged proteins and dysfunctional organelles in eukaryotic cells. Dysregulation of autophagy has been linked to the accumulation of α-synuclein (α-syn), mitochondrial dysfunction, and neuroinflammation, which are key features of PD. The autophagy-lysosomal pathway (ALP) is involved in the degradation of α-syn and other proteins, and its dysfunction contributes to the progression of PD. ncRNAs, particularly miRNAs, lncRNAs, and circRNAs, regulate autophagy by modulating key signaling pathways and gene expression. For example, miR-3473b inhibits autophagy and participates in PD regulation, while lncRNAs such as NEAT1 and HOTAIR are involved in the progression of PD by stimulating autophagy. CircRNAs like ciRS-7 regulate miR-7, which limits α-syn expression and promotes autophagy. The review highlights the therapeutic potential of ncRNAs in addressing autophagy-related mechanisms in PD. Targeting ncRNAs could offer innovative strategies for developing therapies that enhance autophagy and reduce neuroinflammation. However, challenges remain in translating these findings into clinical practice. The study underscores the importance of ncRNAs in the molecular landscape of PD and their potential in novel treatment approaches. Understanding the role of ncRNAs in autophagy may provide new insights into the pathogenesis of PD and lead to the development of effective therapies.