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Viral Therapy to Stabilize Mitochondria May Stall Parkinson’s

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www.ProHealth.com • December 20, 2011


The power-generating mitochondria in Parkinson’s disease patients are damaged – for complex reasons as yet unclear but perhaps related to genetic factors and toxic exposures. The resulting lack of cellular energy leads to a loss of dopaminergic neurons (dopamine-producing nerve cells in the brain that play an important role in voluntary movement and many behavioral functions including mood). The end result being the degeneration of brain function seen in Parkinson’s.

Therapy for PD (which affects 3% of the population) has often focused on raising dopamine levels in the central nervous system with L-DOPA, a dopamine precursor able to cross the blood-brain barrier.

Tackling the Destruction "Upstream"

But now a research team led by neurologist Roger Barker and virologist John Sinclair at the University of Cambridge may have found a way to address the problem “upstream” – by bolstering and stabilizing the mitochondria. They have done this successfully in a rat model of Parkinson’s using a strategy that viruses employ to sustain and ensure the survival of the cells they invade.

As detailed in their report published Dec 19 by the Journal of Experimental Medicine (www.jem.org), injections of a viral protein called http://www.ncbi.nlm.nih.gov/pubmed/20036157 beta2.7 – known to protect mitochondria without creating an immune response – into the PD rats have:

• Increased the number of dopaminergic neurons in the rat brains (both before and after PD-like brain lesions have formed),

• And produced better performance on tests of motor function and behavior.

Based on these exciting results, the researchers will embark on further work to determine if the therapy may provide a similar benefit in humans with Parkinson’s.

Sources: Based on Rockefeller University Press (Journal of Experimental Medicine publisher) news release, Dec 19, 2011; Parkinson's Disease Foundation; past research literature on Parkinson’s and beta2.7.



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