A researcher from the University of Guelph has discovered an important factor behind nerve cell death that leads to Parkinson’s disease, illuminating a potential target for future treatment of the disease. The study was published today in Nature Communications.
Using stem cells collected from patients with Parkinson’s, the research team sought to understand how cells normally fold alpha-synuclein. Misfolding of alpha-synuclein is a hallmark of Parkinson’s disease.
The study found that alpha-synuclein binds to mitochondria in nerve cells. In healthy cells, a protein called cardiolipin pulls synuclein out of toxic protein deposits and refolds it into a non-toxic shape. In Parkinson’s, however, the process is overwhelmed over time and mitochondria are ultimately destroyed.
Identification of the role of cardiolipin’s role in protein folding provides a better understanding of the disease and may offer a target for creating treatments that slow the disease’s progression. The team’s next steps will be to test a treatment in animal models using cardiolipin as a target.