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Submitted: 19 Feb 2024
Revision: 25 Jan 2025
Accepted: 03 Feb 2025
ePublished: 09 Feb 2025
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Adv Pharm Bull. Inpress.
doi: 10.34172/apb.42806
  Abstract View: 9

Editorial

c-Abl Inhibitors in Parkinson's: Exploring Hypotheses on Alpha-Synuclein Modulation

Jyutia Nargish ORCID logo, Hirok Jyoti Baishya ORCID logo, Piyong Sola* ORCID logo
*Corresponding Author: Email: piyongsola@yahoo.com

Abstract

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 interventions involving c-Abl inhibitors exhibit notable therapeutic potential. The potential benefits encompass enhancements in motor function, prevention of dopamine neuron loss, and the meticulous regulation of alpha-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.
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