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

## TL;DR

This paper explores how c-Abl inhibitors could help treat Parkinson’s disease by targeting alpha-synuclein and protecting dopamine neurons.

## Contribution

The paper proposes c-Abl kinase as a novel therapeutic target for Parkinson’s disease based on its role in neurodegeneration and α-synuclein regulation.

## Key findings

- c-Abl activation is linked to neurodegeneration in Parkinson’s disease.
- c-Abl inhibitors may improve motor function and prevent dopamine neuron loss.
- These inhibitors could regulate α-synuclein phosphorylation and clearance.

## 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 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.