Researchers in Dundee (Scotland) and Stanford (USA) have identified a novel method of reducing LRRK2 activity in Parkinson's.

Mutations in the gene that codes for the leucine-rich repeat kinase 2 or the LRRK2 gene are a major cause of familial and sporadic (non-familial) Parkinson's. LRRK2 is a complex protein, a part of which acts as an enzyme catalyst and interacts with a number of other cellular processes. Gene mutations lead to a toxic increased response of this enzyme, with multiple detrimental knock-on effects.

There are currently clinical trials evaluating drugs that directly inhibit this 'run-away train' of a protein, but there are concerns regarding the potential toxicity of such treatments because LRRK2 is involved in many cellular processes in different parts of the body.

Given these concerns, scientists have been searching for indirect methods of putting the brakes on LRRK2 activity. In a collaboration between Dundee and Stanford Universities, researchers have identified a protein called PPM1H which efficiently suppresses LRRK2 activity.

Based on their results, PPM1H appears to act as a key modulator of LRRK2 signalling and the investigators are now searching for PPM1H activators which could be tested as a new treatment for slowing the progression of Parkinson's.

Further reading:

Read the research report here.

Read the full press release here.

Read more about the genetics of Parkinson's