A newly discovered protein could hold the key to stopping the progression of Parkinson’s disease, a new study has found.

Scientists, from the University of Sheffield, found that by blocking the protein, Tigar, nerve cells usually lost in the progression of Parkinson’s could be saved — potentially halting the spread of the condition.

The ground breaking research was conducted by Dr Oliver Bandmann and his team who looked at the cell death of dopamine-producing nerve cells in zebrafish with a mutation in a gene called PINK1.

PINK1 is linked to a rare, inherited form of early—onset Parkinson’s in humans.

The team discovered that Tigar became overactive in the PINK1 zebrafish suggesting that it may be involved in causing the death of nerve cells, triggering the start of Parkinson’s.

By blocking the activity of Tigar, the researchers were able to save the dopamine—producing nerve cells. It is these precious cells which are also lost in people with Parkinson’s.

If blocking Tigar activity has the same effect in people it could have the potential to stop the spread of Parkinson’s, scientists said.

“These results suggest that we may have unearthed a promising new target for developing treatments that can actually protect dopamine—producing nerve cells lost in Parkinson’s,” lead researcher Bandmann said.

“The first stage of our study was in tiny fish brains which are in many ways both very similar and very different to ours,” Bandmann said.

“As a result of these exciting findings we will now look at brain tissue from people with early-onset Parkinson’s as well as people with late-onset Parkinson’s, to see whether the Tigar protein is involved in all forms of the condition. We will also study Tigar in other model systems of Parkinson’s,” he said.

“This new research, holds real promise in helping to slow down, or even stop the spread of Parkinson’s. This could move our search for better treatments, which are desperately needed, another step forward,” Claire Bale, Research Communications Manager at Parkinson’s UK, added.

The study was published in the journal Annals of Neurology.

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