Parkinson’s is a variable disease — different in age of onset, experience of symptoms and cause — but a new study points to a potential common link.
“Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it,” said Marco Baptista, PhD, MJFF director of research programs in an interview with Scientific American.
A study recently published in Cell Stem Cell identified dysfunction of the Miro protein and mitochondria (powerhouse of the cell that makes energy) as that shared mechanism.
The Michael J. Fox Foundation (MJFF) funded part of this study, led by Stanford University, which examined cells from people with a mutation in the LRRK2 gene, the greatest known genetic contributor to Parkinson’s disease (PD). The scientists found that both LRRK2 cells and cells from “sporadic” (cause unknown) PD showed Miro and mitochondria dysfunction.
Miro is taken away when mitochondria isn’t working well and needs to be recycled by the cell. LRRK2 dysfunction prevents that Miro removal, which slows the recycling process and may harm the cell.
These findings present another piece of the LRRK2 puzzle. Our Foundation is leading an effort to learn more about this top therapeutic target. Read more about another finding in this area.
And these results are a key example of how studying genetic dysfunction in PD — though not many cases are genetic — can uncover traits shared across the disease. Another example is how researchers discovered that clumps of the protein alpha-synuclein are in cells of nearly all people with PD by identifying mutations in the SNCA gene among a small group.
MJFF’s landmark biomarkers study, the Parkinson’s Progression Markers Initiative (PPMI), is studying people with LRRK2 mutations to learn more about this subset of Parkinson’s.
Article Source: The Michael J. Fox Foundation