eng Oriental Scientific Publishing Company Biomedical and Pharmacology Journal 0974-6242 2025-10-22 18 October Spl Edition 68563 article Ritika Sharma 1 Hitesh Dewangan 1 Kundan Bora 2 Department of Pharmacy, University Institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India Department of Pharmacy, University Institute of Pharma Sciences and Research, Chandigarh University, Mohali, Punjab, India Parkinson's disease (PD) is a neurodegenerative condition that worsens with time and is defined by the buildup of defective mitochondria and the selective loss of neurons that are dopaminergic. Neuronal homeostasis relies on the delicate symphony of events involving mitophagy, the selective autophagic elimination of damaged mitochondria, and mechanistic target of rapamycin (mTOR) signaling. The intricate interplay between mitophagy and mTOR pathways is discussed in this review, drawing attention to the fact that both pathways play a dual role in neuronal survival and degeneration in PD. Hyperactivation of mTOR signaling suppresses mitophagy, which can lead to mitochondrial malfunction and increased neurodegeneration, in contrast to nutrient-rich situations when mTOR signaling promotes cell development and inhibits autophagy. On the flip side, removing damaged mitochondria and avoiding oxidative stress depend on proper mitophagy activation through the PINK1/Parkin pathway. Cellular energy shortages and neuronal death can also be caused by excessive or dysregulated mitophagy. Here, we go over the molecular processes that control the interaction of mTOR complexes, AMPK, ULK1, and autophagy-related proteins, and how dysregulation of this interaction contributes to the development of PD. In order to restore mitochondrial quality control and attenuate neurodegeneration in PD, it is promising to understand this bidirectional regulation and find treatment pathways that modulate mTOR and mitophagy. https://biomedpharmajournal.org/vol18octoberspledition/crosstalk-between-mtor-signaling-and-mitophagy-pathways-a-double-edged-sword-in-pd/ Autophagy Mitophagy Mitochondrial dysfunction mTOR signaling Neurodegeneration PD PINK1/Parkin