Gloria E. Meredith, Ph.D., collaborated with D. James Surmeier, Ph.D. and other scientists at Northwestern University to study the drug, isradipine, and its possible effects on Parkinson's disease. The findings of this study were published this week in an article in Nature.
Dr. Meredith, Professor and Chair of the Department of Cellular and Molecular Pharmacology at Rosalind Franklin University of Medicine and Science, and an expert in Parkinson's disease, co-authored the article. She commented, "Parkinson's disease is a motor disorder caused by the death of dopamine-producing nerve cells in our brains. There is a big race to protect these neurons from dying. Currently available drugs only treat the symptoms."
Dr. Meredith, who studies a chronic mouse model that mimics the signs and symptoms of Parkinson's disease, said, "Isradipine is a common drug used to treat hypertension and stroke. Dr. Surmeier had developed the idea that this drug, a calcium channel blocker, may help protect dopamine neurons in humans. He also designed the basic study. We joined together to see if the drug could stop cells from dying in the mouse model. Our findings indicated that isradipine slowed the disease process and destruction of the dopamine-producing neurons. Results from the mouse model indicate that if the drug works in humans, then it could be used as a means to prevent the onset of this disease or slow its progression."
The next phase will be to develop clinical trials in humans. Dr. Meredith said, "It's exciting to think that if we can protect the dopamine neurons from dying, we may prevent the disease, and improve the quality of life for patients."
Dr. Meredith has been studying Parkinson's disease for over 15 years. Her research is currently funded by the National Institute of Neurological Disorders and Stroke (NINDS), a division of the National Institutes of Health (NIH), and the Department of Defense.
The above story is based on materials provided by Rosalind Franklin University of Medicine and Science. Note: Materials may be edited for content and length.
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