Tabriz University of Medical Sciences Advanced Pharmaceutical Bulletin 2228-5881 15 1 2025 04 15 c-Abl Inhibitors in Parkinson’s: Exploring Hypotheses on Alpha-Synuclein Modulation 7 10 10.34172/apb.42806 EN Jyutia Nargish https://orcid.org/0009-0002-6848-3961 Hirok Jyoti Baishya https://orcid.org/0009-0007-6094-9647 Piyong Sola https://orcid.org/0000-0003-3503-7316 EDITORIAL 10.34172/apb.42806 2024 02 19 2025 02 03 Parkinson’s disease (PD) stands as the second most prevalent neurodegenerative disorder, impacting a global population estimated between 6 to 10 million individuals. The condition primarily arises from a dopamine deficiency and the presence of α-synuclein, forming Lewy bodies in the substantia nigra pars compacta (SNcp). Despite the ongoing quest to unravel the precise pathophysiological mechanisms underlying PD, recent literature reviews posit that heightened activation of the Abelson non-receptor tyrosine kinase(c-Abl), in brain tissues plays a pivotal role in neurodegeneration observed in PD patients. Notably, these studies put forth compelling evidence suggesting that c-Abl inhibitors’ interventions exhibit notable therapeutic potential. The potential benefits encompass enhancements in motor function, prevention of dopamine neuron loss, and the meticulous regulation of α-synuclein phosphorylation and clearance. These findings collectively advocate for the exploration of c-Abl as a prospective therapeutic target, thereby presenting inhibitors of this kinase as promising candidates for intervention in the management of PD.