Ryan McLaughlin, 15, will welcome Health Secretary Nicola Sturgeon to the conference in Clydebank, where she is to give a keynote speech.

The event will bring together academics from across the world to consider the possible links between vitamin D deficiency and various health problems, including MS.

It is taking place after Ryan, who watched his mother Kirsten struggle with MS, launched his Shine on Scotland campaign. The teenager has already taken a petition on the issue to the Scottish Parliament.

He said: “It’s fantastic that all of these very important and very busy people have taken the time to come to Glasgow and consider the issues raised by my campaign.”

Vitamin D can be created naturally in the body by exposure to the sun but in Scotland there is only enough sunlight of the right UVB wavelength to create vitamin D in the required manner for about half the year.

Johns Hopkins scientists found this mechanism that may lead to important new targets for drugs already known to inhibit it, thus controlling symptoms of the disorder.

Previous research demonstrated that a protein called parkin protects brain cells by ‘tagging’ certain toxic elements that are then destroyed naturally.

However, the results of the new study have indicated that an over-activation of a protein called c-Abl- can shut down the activity of parkin and contribute to a build-up of toxic proteins that kill brain cells and enables the progression of PD.

C-Abl contributes to the regulation of cell death and is implicated in a host of diseases. It has already proven to be a target for certain types of cancer-killing drugs, such as imatinib (Gleevec) said Ted Dawson.

“Our new appreciation of c-Abl’s role in sporadic PD suggests that we can give brain-permeable inhibitors of c-Abl to maintain parkin’s normal protective function.

“The testing of these already approved, well-tolerated drugs for a new use – as a neuro-protective treatment for PD – is a potentially exciting therapeutic arc that should be pursued,” said Dawson.

The researchers first used a test called the Western blot to label certain proteins in neuron-like human cells in culture. They could see that c-Abl shut down the activity of parkin by measuring the levels of chemical tags on proteins that, in a healthy system, are marked for destruction.

These “garbage” proteins, when overabundant, have been shown previously by Dawson’s lab to be selectively toxic to neurons. When c-Abl was active, parkin’s ability to tag those proteins was significantly decreased.

Next, using a mouse, which had been given drugs, that cause Parkinson’s-like traits, the team proved that when c-Abl is activated, parkin’s function shuts down and as a result, garbage proteins accumulate and lead to a significant loss of neurons.

Finally, the scientists turned to human brain tissue to look for evidence that c-Abl are a major regulator of parkin function. By comparing brain tissue of patients who died with Parkinson’s disease with those who died of other causes, they established that when c-Abl shuts down Parkin, the “garbage” proteins accumulate and result is the death of neurons.

The findings were published in the Proceedings of the National Academy of Sciences (PNAS)