HOPE?

Media portrayal:

HOPE?

Scientific interpretation:

An anti-depressant and an experimental cancer drug may have potential as disease-modifying treatments for Parkinson’s.

Original article: Repurposed drugs targeting eIF2a-P-mediated translational repression prevent neurodegeneration in mice, Brain: April 20, 2017

The takeaway

Two drugs developed to treat other diseases—Trazodone, an antidepressant—and Dibenzoylmethane, an experimental cancer drug derived from licorice—prevented brain damage associated with neurodegeneration in mouse models. More research is needed to confirm the effect in humans.

Why is it important?

Current treatments for Parkinson’s only treat symptoms, not the disease’s underlying cause. These two drugs have shown promising early results as treatments that may actually interfere with the disease’s progression. Trazodone is already approved for the treatment of depression, potentially shortening its road to the clinic as therapy for Parkinson’s and other diseases.

%

IMPACT

  • Novelty 90% 90%
  • Proximity 60% 60%
  • Deliverability 60% 60%

Impact Opinion

“These results are extremely promising but must be confirmed in clinical trials prior to use in the clinical as a treatment for Parkinson’s.” Dr. Patrik Brundin

The details

Scientists screened more than 1,000 compounds in worm and cellular models to determine whether any of them could potentially interfere with neurodegeneration. After narrowing down the list, they identified two drugs—Trazodone and Dibenzoylmethane—as promising potential therapies for Parkinson’s using mouse models. Both drugs prevented brain damage, restored memory and reduced brain shrinkage in the models.

Next steps

Trazadone is already approved to treat depression and has a proven safety profile. A clinical trial is needed to examine its effect in humans.

Where can I learn more?

Original article: Halliday M, Radford H, Zents KAM, Molloy C, Moreno JA, Verity NC, Smith E, Ortori CA, Barrett DA, Bushell M, Mallucci G. April 20, 2017. Repurposed drugs targeting eIF2a-P-mediated translational repression prevent neurodegeneration in mice. Brain140(6):1768–1783.

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