Parkinson’s disease is one of the most complicated diseases that humans suffer from and while studies continue towards finding more definite causes and possible therapies, one study has brought us closer to understanding what causes nerve cell death in the disease.
Parkinson’s disease is the most common degenerative movement disorder in Canada, affecting about 100,000 people. Published in the journal Nature Communications, the study used stem cells collected from people with the disease. The research team studied how nerve cells try to cope with misfolded alpha-synuclein.
Through the study, a University of Guelph researcher has possibly unlocked the potential for treatment to slow the progression of this fatal neurodegenerative disorder. Prof. Scott Ryan’s research has led to discovery that a molecule inside nerve cells called cardiolipin helps ensure that a protein called alpha-synuclein folds properly. Misfolding of this protein leads to protein deposits that are the hallmark of Parkinson’s disease.
These deposits are toxic to nerve cells that control voluntary movement. When too many of these deposits accumulate, nerve cells die. This is a crucial find considering that the discovery may represent a new target for development of therapies against Parkinson’s disease.
Normally, cardiolipin in mitochondria pulls synuclein out of toxic protein deposits and refolds it into a non-toxic shape. The U of G researchers found that, in people with Parkinson’s disease, this process is overwhelmed over time and mitochondria are ultimately destroyed, said Ryan.
He said understanding cardiolipin’s role in protein refolding may help in creating a drug or therapy to slow progression of the disease.