Evidence indicates that leucine-rich repeat kinase 2 (LRRK2) controls multiple processes in neurons and glia cells. Deregulated LRRK2 activity due to gene mutation represents the most common cause of autosomal dominant Parkinson's disease (PD). Protein kinase A (PKA)-mediated signaling is a key regulator of brain function. PKA-dependent pathways play an important role in brain homeostasis, neuronal development, synaptic plasticity, control of microglia activation and inflammation. On the other hand, a decline of PKA signaling was shown to contribute to the progression of several neurodegenerative diseases, including PD. In this review, we will discuss the accumulating evidence linking PKA and LRRK2 in neuron and microglia functions, and offer an overview of the enigmatic cross-talk between these two kinases with molecular and cellular implications.
Skip Nav Destination
Review Article| February 15 2017
Cross-talk between LRRK2 and PKA: implication for Parkinson's disease?
Publisher: Portland Press Ltd
Received: October 28 2016
Revision Received: December 12 2016
Accepted: December 19 2016
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2017 The Author(s); published by Portland Press Limited on behalf of the Biochemical Society
Elisa Greggio, Luigi Bubacco, Isabella Russo; Cross-talk between LRRK2 and PKA: implication for Parkinson's disease?. Biochem Soc Trans 8 February 2017; 45 (1): 261–267. doi: https://doi.org/10.1042/BST20160396
Download citation file:
Don't already have an account? Register
Get Access To This Article
Buy This Article