Since 2000, Team Parkinson has supported pilot study grants through the major Parkinson's organizations that have Scientific Advisory Boards. Typical grants are awarded in the range of $35,000 to $50,000. Researchers must have pilot data in preparation for applying for major funding from the National Institutes of Health (NIH). An example is Dr. Michael Jakowec from the University of Southern California. He received a pilot study grant through the Parkinson's Disease Foundation in New York, one of the organizations that Team Parkinson supports, and as a result of this grant applied to the NIH and received over one million dollars for research. It is crucial to fund promising pilot studies so that researchers can continue the important work of getting closer to finding a cure for Parkinson's disease.
Please come back and check this page occasionally, as we will have updates about new research that we will be funding.
We thank you for your dedication and commitment to this cause.
Grants Archive
2009 Grants
Team Parkinson is using its distribution to fund the following:
Project Title: Novel, small-molecule inhibitors of a-synuclein assembly and toxicity for disease-modifying therapy of Parkinson's disease.
Grant Awarded to: Dr. Gal Bitan
Project Description: The generous gift of The Parkinson Alliance and Team Parkinson will support exciting research in the Bitan Laboratory geared towards development of disease-modifying therapy for Parkinson's disease (PD). Current treatment of PD focuses on compensation for dopamine deficiency, predominantly by using L-dopa. Though this kind of treatment is successful in alleviating major symptoms, such as tremor, it does not address “non-dopaminergic” symptoms, including falling and freezing, which affect 80-90% of patients with PD and 100% of patients with early-onset PD, or dementia which afflicts ~30% of patients with PD. These non-dopaminergic symptoms are major causes of mortality and morbidity in PD. In addition, treatment with L-dopa causes complications such as “off-time” and dyskinesia (involuntary movement). To address these unmet needs, disease-modifying, rather than symptomatic, therapy is needed. We have discovered a new experimental drug that disarms what most researchers believe to be real culprit causing PD - toxic aggregates of a protein called alpha-synuclein. These toxic aggregates are the main component of Lewy bodies, the hallmark pathologic lesion in the brain of patients with PD. The new drug inhibits the formation of these toxic aggregates and thereby prevents the initial processes that lead to development of PD. Through collaboration with Dr. Bronstein's group, the new drug was found to block the toxic effect of alpha-synuclein aggregates in cultured cells and zebra fish. The fish, which without the drug are severely deformed and die within a few days, appear healthy and normal by simple addition of the drug to the water in which they swim. Related experiments in mice show that the drug can get into the brain and remove toxic protein aggregates.
With the help of The Parkinson Alliance and Team Parkinson, we will develop this promising research in pre-clinical studies in transgenic mice in collaboration with Dr. Chesselet. Specifically, we will use mice engineered to overexpress human alpha-synuclein. The mice develop alpha-synuclein aggregates in the brain and show motor deficits already at 2 months of age. We will conduct experiments to optimize dose and treatment duration examining the effect of the drug on clearance of alpha-synuclein aggregates in the brain and on the motor abilities of the mice. In addition, we will conduct pharmacological studies to determine the optimal route of administration of the drug. We expect that these pre-clinical experiments will lead to FDA approval of Investigational New Drug (IND) status for our lead compound, facilitate initiation of clinical trials, and hopefully result in effective treatment and cure for PD.
Grant Awarded to:
Giselle Petzinger, MD Assistant Professor Department of Neurology, USC Keck School of Medicine, Division for Movement Disorders. University of Southern California
Michael Jakowec, PhD, Assistant Professor Department of Neurology, USC Keck School of Medicine, Division for Movement Disorders, University of Southern California
Beth Fisher, PhD, PT, USC Keck School of Medicine, Division for Movement Disorders, University of Southern California
The following two sections describe allocation of funds to support two important research programs in our labs. Both research programs focus on understanding the underlying mechanisms by which exercise, in the form of intensive treadmill running, leads to improvement in motor behavior in both the MPTP rodent model for Parkinson’s disease and in patients with Parkinson’s disease. Together these projects are integrated in a translational research program where findings from the lab impact clinical studies in patients with PD, and vice versa, resulting in improved treatment for patients in the community.
(1) From The laboratories of Giselle Petzinger, MD and Michael Jakowec, PhD:
A fundamental aspect of studies in the mouse model of PD is to elucidate changes in protein expression within the basal ganglia, the region of the brain responsible for aspects of motor control affected in PD. Ongoing studies in our lab have shown that the electrophysiological properties of medium spiny neurons within the basal ganglia, a region affected in PD, are altered in a way consistent with our molecular studies showing that subunits of the AMPA receptor subtype of the glutamate receptor family, specifically the subunit GluR2, as well as the dopamine D2 receptor, are elevated with intensive treadmill running in animals rendered parkinsonian with MPTP. Currently we are investigating important aspects of this observation including (i) to determine if these changes are due to elevated expression of the genes and proteins encoding these receptors, (ii) what are the molecules that are responsible for trafficking these receptors to the synapses where they exert their effects, and (iii) are their morphological changes within the dendritic spines of medium spiny neurons that underlie these changes. To achieve many of the goals necessary to understand the mechanisms of motor behavior improvement we have purchased a spinning-disc confocal microscope from Olympus, Inc. This microscope will allow us to image and quantify changes in protein and genes expression at a high level of resolution within dendrites of neurons within the basal ganglia.
(2) From the laboratory of Beth Fisher, PhD, PT.
Ongoing studies in the Transcranial Magnetic Stimulation (TMS) Lab called the Neuroplasticity and Imaging Laboratory (NAIL) have shown beneficial changes in the brains of newly diagnosed individuals with Parkinson’s disease not yet on dopamine replacement therapy that had participated in intensive exercise. Specifically, we showed that exercise normalized the abnormal cortical excitability state consistently seen in Parkinson’s disease. We are the first group to demonstrate a brain effect in Parkinson’s disease from physical therapy, suggesting that exercise may have an important role in influencing the brain and potentially modifying disease progression. Findings from these studies are having direct impact on patient care as demonstrated by their influence on clinical practice within rehabilitation units for Parkinson’s disease now being established at sites such as Rancho Los Amigos National Rehabilitation Center here in Southern California, and at others around the country. To further our research studies we wish to purchase additional equipment from Jali Medical Inc., which will allow us to utilize an additional electrophysiological parameter called Paired-Pulse, and will enable us to demonstrate more robust changes in the brain in response to intensive exercise and provide insight into the mechanisms responsible for the beneficial effects of exercise on brain and behavior in individuals with Parkinson’s disease.
Project Title: Is there abnormal network activity in the motor cortex of 6-OHDA lesioned mice.
Grant Awarded to: Dr. Carlos Portera, M.D., PhD
Project Description: The current treatments for Parkinson disease (PD) offer some symptomatic relief, but often at the cost of serious side effects, including dyskinesias. The introduction of deep brain stimulation (DBS) in the treatment of PD two decades ago has arguably been the most effective treatment strategy since the discovery of levodopa. Understanding the exact mechanisms of how DBS helps PD patients will help improve this therapeutic strategy. A recent study using the 6-hydroxydopamine (6-OHDA) rodent model of PD (Gradinaru et al., 2009) suggests that DBS may help by reducing the activity of the subthalamic nucleus (STN) through its effects on the firing of neurons in motor cortex, which is the part of the brain that controls movement. This raises the possibility that neurons in the motor cortex of PD patients fire less than normal, leading to an overactive STN that produces some of the symptoms of PD. I propose to test the hypothesis that neurons are hypoactive in the motor cortex of mice that had been rendered parkinsonian by injection of the neurotoxin 6-OHDA into the substantia nigra. Specifically, I intend to examine the spontaneous activity of neurons in the motor cortex of mice before and after administering 6-OHDA. We will use the cutting-edge technique of two-photon calcium imaging to record the activity of large numbers of cortical neurons non-invasively.These experiments will shed light into the mechanisms of circuit dysfunction in PD and may lead to improved treatments for this devastating disorder.
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