The growth factor that may slow Parkinson's disease

By LabOnline Staff
Monday, 30 January, 2017

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Australian researchers have found that a naturally occurring molecule in the brain may hold the key to stopping the progression of Parkinson’s disease.

The study was led by Professor Bryce Vissel and Dr Sandy Stayte from the Garvan Institute of Medical Research, with the latter noting that a significant obstacle in treating Parkinson’s patients is the lack of any therapy that can prevent or slow the disease.

“Often, sufferers have lost 70% or more of their dopamine neurons and have serious movement problems by the time they’re diagnosed,” said Dr Stayte. “The gold standard treatment, levodopa, works on those symptoms but it does nothing to arrest the progress of the disease.

“Our goal is to try to slow down or halt further degeneration in the brain by protecting the surviving neurons.”

One promising avenue of research has been the administration of growth factors to promote the survival of midbrain neurons, although the mechanism by which these growth factors provide neuroprotection has not yet been understood. Professor Vissel, Dr Stayte and their team decided to take one such growth factor, activin A, and apply it into the brains of mice to see what would happen.

“Activin A, a member of the transforming growth factor β superfamily, has been shown to be a potent anti-inflammatory following acute brain injury and has been demonstrated to play a role in the neuroprotection of midbrain neurons against MPP+-induced degeneration in vitro,” the researchers explained in the journal PLOS ONE.

Having hypothesised that activin A may offer similar anti-inflammatory and neuroprotective effects in Parkinson’s disease, the researchers found that the growth factor did indeed offer the mice protection against the loss of dopamine neurons. According to Professor Vissel, this provides a possible approach to slowing progression of the disease.

“An exciting aspect of our previous research is that we’ve shown the activin A molecule has the potential to trigger regeneration in the nervous system,” said Professor Vissel. “It raises the question as to whether this could lead to a treatment that could also repair the damaged brain areas in Parkinson’s disease.”

The study is additionally expected to tie in with current research into early indications of Parkinson’s disease, such as identifying pre-motor symptoms and biomarkers. As noted by Dr Stayte, “There is a much higher chance of being able to deliver a therapeutic strategy that will halt the cell-death process if we can identify the disease earlier.”

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