Finland researchers correct Parkinson’s motor symptoms in mice
Researchers in Finland, led by University of Helsinki Docent Timo Myöhänen, have successfully corrected the motor symptoms associated with Parkinson’s disease in mice in a study that offers promising results in terms of treatment for the disease.
Parkinson’s disease is a degenerative disease of the motor system, in which the nerve cells in the brain areas which regulate voluntary movement are destroyed for an unknown reason. It is practically always diagnosed only after motor symptoms appear, which may be alleviated with drug treatment, but there is currently no known cure.
Up to 2% of people aged over 60 contract Parkinson’s. Although the exact cause of the disease is not known yet, during the past 15 years, research has focused on a protein called alpha-synuclein, which has several functions in the brain areas that regulate motor functions.
This protein is involved in neurotransmission in the brain, for example in the areas that regulate voluntary movements. It is prone to defective structures and when mis-folded will clump together with other alpha-synuclein proteins to form large aggregated pieces which damage brain cells.
In Parkinson’s disease, aggregated alpha-synuclein proteins accumulate within nerve cells, damaging them. They can also propagate from one cell to the next and spread the impairment of nerve cells in the brain.
Researchers had previously known that the PREP enzyme, which occurs naturally in the body, can promote the formation of such harmful alpha-synuclein aggregates in the brain. Now researchers wanted to determine the connection that the enzyme and protein have to the symptoms of Parkinson’s disease by blocking PREP in the brain.
In the study, Myöhänen’s group set up a mouse model for Parkinson’s disease, in which the brain’s motor areas were made to produce large amounts of alpha-synuclein. This led to the accumulation of mis-folded proteins in the brains of the mice as expected, resulting in the associated motor symptoms.
Only when the mice began manifesting motor symptoms did the researchers started treatments with a PREP blocker. This situation would be similar in a human case of Parkinson’s which is typically diagnosed only once the symptoms have appeared.
The researchers managed to clear the brains of mice of alpha-synuclein aggregates by blocking the PREP enzyme, curing them of the motor symptoms which characterize Parkinson’s disease.
“After as little as two weeks of treatment, the motor symptoms in the mice had practically disappeared. And they did not reappear until after the experiment was over,” explains Myöhänen.
A detailed analysis established that the PREP blocker treatment had stopped the motor areas from becoming further damaged and had cleared the brain of nearly all accumulations of alpha-synuclein.
“We have a long way to go from animal models to human trials, but these results are extremely encouraging in terms of future drug development,” says Myöhänen.
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