New Insights into Parkinson’s Treatment

Cardiolipin molecule found inside nerve cells ensures that alpha-synuclein protein folds properly. Misfolding of alpha-synuclein protein leads to protein deposits that are the hallmark of Parkinson's disease, a fatal neurodegenerative disorder. "Identifying the crucial role cardiolipin plays in keeping these proteins functional means cardiolipin has a role in the development of therapies against Parkinson's disease," said Scott Ryan, Professor at the University of Guelph in Ontario, Canada.

"Currently there are no treatments that stop nerve cells from dying," Ryan added.

These deposits are toxic to nerve cells that control voluntary movement. When too many of these deposits accumulate, nerve cells die, the researchers said.

For the study, published in the journal Nature Communications, researchers used stem cells collected from people with the disease. The team studied how nerve cells try to cope with misfolded alpha-synuclein.

"We thought if we can better understand how cells normally fold alpha-synuclein, we may be able to exploit that process to dissolve these aggregates and slow the spread of the disease," Ryan said.

The study revealed that, inside cells, alpha-synuclein binds to mitochondria, where cardiolipin resides. Cells use mitochondria to generate energy and drive metabolism.

Normally, cardiolipin in mitochondria pulls synuclein out of toxic protein deposits and refolds it into a non-toxic shape, the researchers added.

The researchers found that, in people with Parkinson's disease, this process is overwhelmed over time and mitochondria are ultimately destroyed.

"As a result, the cells slowly die. Based on this finding, we now have a better understanding of why nerve cells die in Parkinson's disease and how we might be able to intervene," the researchers noted.

Source-IANS