Scientists just found a molecule that could stop Parkinson’s in its tracks

Alpha-synuclein is a protein found mainly inside brain cells (neurons), where it helps control the release of neurotransmitters such as dopamine, the chemical that allows neurons to communicate with each other.

In Parkinson’s disease, alpha-synuclein begins to stick together, forming toxic clusters that kill nerve cells. This cell loss leads to the hallmark symptoms of Parkinson’s, including tremors, muscle stiffness, and difficulty with movement. Although existing therapies can ease these symptoms, none currently stop or reverse the underlying damage.

In its normal or "native state," alpha-synuclein is a flexible strand, but when it becomes active it folds into a helix. This shape is crucial for its role in carrying and delivering dopamine within the brain.

The researchers designed a short peptide that locks alpha-synuclein into its healthy helical shape, preventing it from transforming into the harmful clusters that cause cell death.

Lab experiments revealed that the peptide remains stable, can enter brain-like cells, and reduces the buildup of toxic protein deposits while improving movement in a worm model of Parkinson’s disease.

Published in the journal JACS Au, the study highlights how rational peptide design can turn large, unstable proteins into smaller, more drug-like molecules.

The findings mark a significant step towards developing new peptide-based treatments for currently untreatable neurodegenerative conditions. Professor Jody Mason, from the Department of Life Sciences at the University of Bath, said: "Our work shows that it is possible to rationally design small peptides that not only prevent harmful protein aggregation but also function inside living systems.

"This opens an exciting path towards new therapies for Parkinson's and related diseases, where treatment options remain extremely limited."

Dr. Julia Dudley, Head of Research at Alzheimer's Research UK, which funded the research, said:

"Dementia isn't an inevitable part of ageing; it's caused by diseases like Alzheimer's. To make progress towards a cure for all forms of dementia, we need research focused on developing a broad range of treatments that can slow, stop and ultimately reverse these diseases.

"Although this is early research in an animal model, it's exciting to see that this new molecule can prevent the build-up of misfolded alpha-synuclein.

"By stabilizing alpha-synuclein in its healthy form, this could open the door to a new class of treatments that could slow progression in diseases like Parkinson's and dementia with Lewy bodies. We look forward to seeing this research taken to the next stage, potentially exploring how it would work in people.

"We're delighted to see such promising advances from Alzheimer's Research UK funded work opening up new avenues for treatments of the future, and the potential to change the lives of those affected by neurodegenerative diseases."

Further research is needed, but the team hopes that continued progress will enable these and similar molecules to advance towards clinical testing in the coming years.