LRRK2 function on actin and microtubule dynamics in Parkinson’s disease

Abstract

The mutations in the LRRK2 gene cause clinically typical, late-onset Parkinson’s disease, strengthening the idea that the familial forms of the disease represent an important tool for the study of the idiopathic forms. Despite the great effort to describe and functionally characterize the LRRK2 gene product, its physiological role remains elusive. In this article, we will discuss along with other references, our recent findings that assigned a critical role of LRRK2 protein on cytosleketal dynamics and how this direction could provide a valuable platform to further appreciate the mechanism underlying LRRK2-mediated pathophysiology of the disease.

Acknowledgements

This work was supported in part by the intramural research program of the National Institute on Aging/NIH (NIA, AG000944-01). We thank Ms. Natalie K. Cygan for her editing this manuscript.