Researchers at La Trobe University in Australia have developed a world-first diagnostic blood test which could change the lives of people with Parkinson's disease.

Currently no clinical biomarker test exists for Parkinson's and the only means of diagnosis is through neurological tests. By the time patients develop symptoms and undergo the exam, large numbers of vital brain cells have already been destroyed. La Trobe's blood test will enable doctors to detect with unprecedented reliability the abnormal metabolism of blood cells in people with Parkinson's, which will allow them to provide treatment options much earlier. La Trobe Professor of Microbiology Paul Fisher said: 

This is a really exciting discovery. Parkinson's is a debilitating disorder and currently there is no cure. However, early diagnosis and treatment could enable better outcomes and a greater quality of life for people with the condition, which will be of great benefit to sufferers and their families.

It has long been recognised that mitochondrial dysfunction is critically involved in the demise of dopaminergic neurons in Parkinson’s disease.

CPT's Dr Richard Wyse said, "This discovery is potentially relevant to all our mitochondrial drug trials, as well as making it possible to start a range of therapeutic trials before motor symptoms appear."


About a decade ago, Professor Fisher's lab discovered that a permanently switched on 'alarm' at the cellular level could be responsible for symptoms in many incurable conditions involving defective mitochondria.

This led to an important new understanding of how mitochondrial defects damage cells – namely that it is a signalling disorder, rather than a fundamental energy insufficiency as previously thought.

'We realised this had important implications for understanding many different forms of mitochondrial disease, as well as most major neurodegenerative disorders,' he said.

Professor Fisher said he and his team demonstrated for the first time (using a laboratory organism called Dictyostelium, or Dicty) that an energy- and stress-sensing protein, known as AMPK, was permanently activated in mitochondrially diseased cells.

When energy production was compromised, this protein began signalling and interfering with other signalling pathways, causing cell functions to shut down.

Professor Fisher's team then joined forces with Dr Danuta Loesch-Mdzewska, Dr Sarah Annesley and other collaborators to extend their studies in Dicty to cells from Parkinson's disease patients.

The results were both dramatic and surprising.

Professor Fisher said in people with Parkinson's, something causes their cells to become 'hyperactive', which in turn increases the production of toxic oxygen by-products and over time damages vital cells in the brain - oxidative stress.

Apart from developing a definitive blood test, Professor Fisher said further work on differences in blood cells from Parkinson's patients and healthy control groups might also open a window to the underlying mechanisms of the disease.

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