In a new paper from the lab, Claudia Manzoni studies how fibroblast cells from people with Parkinson’s disease caused by mutations in LRRK2 react to starvation. Although the changes are quite subtle, there are differences between the way that fibroblasts that contain mutant LRRK2 respond to being starved – suggesting that there may be changes in the way that these cells regulate a key process called autophagy (a term which comes from the greek meaning to eat yourself, and is one of the ways that cells get rid of waste and recycle proteins and organellles). One important bit of information that comes out of this study is that all of the mutations that Claudia looked at, no matter where in the LRRK2 protein they are found, seem to have a similar impact on autophagy. This is important because, up until now, there hasn’t been a clear cellular symptom linked to all these mutations and might indicate that disrupted autophagy is a common feature of LRRK2 mutations. A lot more work is needed in order for us to really understand how mutations in LRRK2 alter autophagy, but this study provides an intriguing hint that autophagy might be very important in Parkinson’s disease.
Read more about our study at Biochemical and Biophysical Research Communications: