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Targeting PARP1 Is Effective In Protecting HD Cells from Damage

t assays examined whether blocking PARP1 activity with K245-14 could reduce energy depletion in cells with the HD genetic mutation. Using cells from human HD patients and from a mouse model of the disorder, the MIND researchers compared the reactions of HD cells to oxidative stress caused by the application of hydrogen peroxide with the reactions of normal cells.

Although all of the cells reacted with a loss of ATP, a key source of cellular energy, the HD cells – which had much lower ATP levels to begin with – were much more vulnerable to stress-induced energy loss. Inhibiting PARP1 by means of K245-14 reduced ATP loss in all tested cells and significantly protected against both energy loss and cell death in the HD cells. ‘While we were pleased to observe these predicted protective effects in our experiments, validation of PARP1 as a useful HD drug target will require the testing of inhibitors in animal trials,’ Kazantsev explains.

The process of identifying the best candidates for trials will be very complex, since any drug treating a central nervous system disorder needs to penetrate the blood-brain barrier. We will be working with our collaborators at the Scripps Research Institute – world leaders in computational chemistry – to conduct a more comprehensive virtual screen and select additional promising candidates for drug development. ‘Inhibition of PARP1 activity is thought to be potentially beneficial for treatment of cancer, neurodegenerative conditions such as Parkinson's disease, and over twenty other human disorders,’ he adds. ‘We envision broad therapeutic applications for small molecule inhibitors of PARP1.’ Kazantsev is an assistant professor of Neurology at Harvard Medical School.

Souce: Eurekalert
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