In 2009, Dr. Mouradian and her team, including Eunsung Junn, PhD, associate professor of neurology, started a project that she describes as innovative for its time. They studied the mechanisms that control the amount of α-synuclein produced in the brain, focusing on tiny RNA molecules known as microRNA. The goal was to identify a particular microRNA that has the ability to decrease α-synuclein production—and they found that, indeed, microRNA-7 (miRNA-7) has this property. Recognizing the therapeutic value of the discovery, Dr. Mouradian promptly initiated the patent process: to develop miRNA-7 as a target therapy that would protect brain cells from injury. “Currently, progression of the disease is inevitable, so we must focus on means to prevent the formation of these aggregates, with the hope of slowing down provides or stopping progression of neuronal damencouragement Alpha-Synuclein: age and advancing symptoms,” she says. and practical support That means, Dr. Mouradian hopes, the A Key to the development of viral vectors to achieve tarParkinsonian Brain to scientists,” says geted delivery of miRNA-7 to the brain nother focus of Dr. Mouradian’s reDr. Mouradian. region that is most vulnerable to α-synuclesearch is the protein alphasynuclein “They know the value of in-driven degeneration and responsible for (α-synuclein). Although its normal role the main motor symptoms of the disease. translatable research in brain function is not yet fully understood, Viral vector-mediated gene therapy in the α-synuclein is believed to regulate transmisbrain has been shown to be safe in humans. to the scientist, the sion of signals between synapses, the conschool, and society, and “We are optimistic about the future of this nections between nerve cells. In the diseased therapy, which targets the pathogenesis of of taking your ideas brain, however, it acquires neurotoxic propParkinson’s disease by decreasing the erties, playing a key role in the degenerative and discoveries to the amount of α-synuclein, the root cause of the process that leads to the deficits of Parkindisease,” Dr. Mouradian says. next step.” son’s disease. NJHF offers Innovation Grants, described Under certain conditions, α-synuclein by Dr. Heinrich as “created specifically to tends to misfold and aggregate, forming abnormal clumps. The support inventive, outside-the-box projects.” In 2015, Dr. more α-synuclein is expressed in the brain, the more extensive Mouradian received an Innovation Grant, awarded jointly is the aggregation and the more accelerated the demise of brain by the NJHF and The Nicholson Foundation. The grant supcells. In patients with familial (inherited) Parkinson’s disease ported the final steps in her research needed to secure her due to extra copies of the gene that produces α-synuclein, patent to study the value of therapeutic miRNA-7 targeting greater accumulation of misfolded α-synuclein is seen at for Parkinson’s disease. autopsy. These patients develop the disease at a younger age “I am grateful for their financial support and very excited than usual and are more likely to develop dementia as the about these patents,” says Dr. Mouradian, adding, “Rutgers aggregates spread to other parts of the brain. Detected in hallUniversity provides encouragement and practical support to mark microscopic structures known as Lewy bodies, the aggrescientists. It’s evident in the names Office of Research and gates are found not only in the brains of patients with Economic Development and Office of Research ComParkinson’s disease, but in other related diseases as well. mercialization. They know the value of translatable research Finding a way to decrease α-synuclein, then, would help develto the scientist, the school, and society, and of taking your op treatments for an expanded spectrum of conditions. ideas and discoveries to the next step.” M very focused, and passionate about her work,” adds Dr. Heinrich. “We knew it would be a partnership with the potential to do good for millions.” The MentiNova team has now tested the anti-LID potential of nalbuphine in the nonhuman primate model of Parkinson’s disease treated with L-dopa, and, says Dr. Mouradian, “It works!” The newly granted patent will allow MentiNova to proceed to clinical trials of nalbuphine in Parkinson’s disease patients with the hope of developing it into a reformulated, marketable medication for LID. “We also hope to be able to test it for expanded usage in patients with other conditions that are characterized by involuntary movements, such as Tourette’s syndrome, Huntington’s disease, and tardive dyskinesia,” says Dr. Mouradian. University “Rutgers A 12 Robert Wood Johnson I MEDICINE