Researchers transmit Parkinson disease variant from humans to mice

November 12, 2013

New research using tissue from the Parkinson's UK Brain Bank suggests that a protein called alpha-synuclein causes the spread of nerve cell death in multiple system atrophy (MSA), a Parkinson's-like condition.

Researchers injected a misshapen human version of the into the brains of healthy mice and saw the symptoms of MSA develop and slowly worsen.

These new findings are published in the scientific journal PNAS.

This follows on from a study last year that showed very similar results for Parkinson's.

What is multiple system atrophy?

Multiple system atrophy (MSA) is a progressive neurological disorder that affects around 3,000 people in the UK.

It's caused by the death of nerve cells in the brain which can result in problems with movement, balance and automatic functions of the body such as bladder and .

MSA is a form of parkinsonism - an umbrella term that describes many conditions which share some of the symptoms of Parkinson's.

In the early stages, people with MSA can sometimes be wrongly misdiagnosed with Parkinson's.

And, like Parkinson's, sticky clumps of misshapen alpha-synuclein protein are found in the brains of people with MSA.

What this study found

First, the researchers took misshapen alpha-synuclein from donated to the Parkinson's UK Brain Bank by people who had lived with MSA.

Next, the team injected the protein into the brains of healthy mice.

The researchers began to notice changes in the behaviour of the mice around 90 days after the injection.

And when they looked inside their brains they found that the misshapen had spread through many areas and caused nerve cell death.

Important insights into a complex condition

Claire Bale, our research communications manager, comments:

"Multiple system atrophy is a very complex condition and at the moment the treatments available to people living with it are limited.

"This study offers hope that developing treatments that can stop the spread of alpha-synuclein could have huge potential for treating both Parkinson's and .

"It also provides a new animal model that can be used to study how the condition develops over time, and for testing new treatments.

"Finally, this study also demonstrates the vital role that human brain tissue plays in Parkinson's and MSA research. We simply couldn't understand these conditions without it."
- See more at:

Explore further: Absence of the SMG1 protein could contribute to Parkinson's and other neurological disorders

More information: "Transmission of multiple system atrophy prions to transgenic mice," by Joel C. Watts et al.

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1 / 5 (2) Nov 12, 2013
As some forms of multiple sclerosis have been linked to the bacterium Chlamydophila pneumoniae & it's toxin found in the Cerebrospinal fluid (CSF) then its entirely possible a viral or bacterial vector could find a way in past the blood brain barrier & set up home, small enough not to be discovered but large enough to feed out toxins causing the type of 'infection' over time as suggested in this article.

CSF may well not be as sterile as expected & a form of equilibrium may occur allowing any number of pathogens to continue to exist albeit at low levels not sufficient for contemporary levels of detection.

Also pathogens may not be free floating in the CSF but bound in any number of cerebral habitats, the only means therefore to detect them is by their toxins & even then those toxins may be at a much lower level than otherwise expected as some will doubtless be metabolised to varying degrees & unlikely to accumulate, low levels could still do damage over extended time periods.

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