The therapy is based on the MCC950 molecule and the researchers hope to carry out human clinical trials of drugs based on this molecule by 2020.
IANS
Researchers have developed a new therapy using a molecule that has been found to stop the development of Parkinson's disease in several animal models.
The therapy is based on the MCC950 molecule and the researchers hope to carry out human clinical trials of drugs based on this molecule by 2020.
The molecule works by cooling the "brains on fire", turning down inflammatory activity caused by immune cells in the brain called microglia, and allowing neurons to function normally, according to the study published in the journal Science Translational Medicine.
"Parkinson's disease is the second-most common neurodegenerative disease worldwide, with 10 million sufferers, whose control of body movements is affected," said one of the researchers Trent Woodruff, Associate Professor at University of Queensland in Australia.
The disease is characterised by the loss of brain cells that produce dopamine, which is a chemical that co-ordinates motor control, and is accompanied by chronic inflammation in the brain.
"We found a key immune system target, called the NLRP3 inflammasome, lights up in Parkinson's patients, with signals found in the brain and even in the blood," Woodruff said.
"MCC950, given orally once a day, blocked NLRP3 activation in the brain and prevented the loss of brain cells, resulting in markedly improved motor function," Woodruff added.
There are no medications on the market that prevent brain cell loss in Parkinson's patients, with current therapies focusing on managing symptoms rather than halting the disease.
The drug companies had traditionally tried to treat neurodegenerative disorders by blocking neurotoxic proteins that build up in the brain and cause disease, said Professor Matt Cooper from University of Queensland.
"We have taken an alternative approach by focusing on immune cells in the brain called microglia that can clear these toxic proteins," he said.
COMMENTS