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The Parkinson’s Foundation supports three research centers with $2.36 million. Our support allows groups of scientists to collaborate, advancing our understanding of Parkinson’s disease (PD).

Columbia University Medical Center

We’ve supported Columbia University Medical Center’s research efforts since 1957. The center's researchers and doctors are leaders in Parkinson’s science and training. They have developed scales to assess the severity of Parkinson's, tested new drugs to treat the disease and are leaders in uncovering the pathogenesis of the disease.

Recent grants have supported research in neuroinflammation, genetics, programmed cell death/GDNF in development of dopamine neurons, animal models using toxins and gene alterations, molecular alterations of nerve terminal dopamine pools, neuropsychology, behavioral effects, epidemiology, clinical trials and evaluation of surgical procedures. 

Highlight: Finding Potential Targets for Preventing or Treating Parkinson’s

Although the vast majority of Parkinson’s cases have no known genetic cause, among those that do run in families, the most common mutations occur in the LRRK2 gene (leucine-rich repeat kinase-2). Now, researchers led by Ana Maria Cuervo, M.D., Ph.D., at Albert Einstein College of Medicine and David Sulzer, Ph.D., of the Parkinson’s Foundation Research Center at Columbia University Medical Center (funded in part by the foundation) have shown for the first time why the faulty LRRK2 protein is harmful, and how it can block the normal cell recycling process. The online edition of Nature Neuroscience published this research in 2013. It builds upon earlier Parkinson’s Foundation-funded work.

Normal cells, including those in the brain, use a recycling and waste disposal system to stay healthy. The process — known as chaperone-mediated autophagy — begins when molecules called chaperones patrol for damaged proteins and then transport them to a recycling center (the lysosome). After arriving there, the damaged proteins travel to the interior region of the lysosome, where they break down into reusable components.

Drs. Cuervo and Sulzer showed that chaperone-mediated autophagy was capable of recycling healthy LRRK2 proteins, but it was not as successful in breaking down those LRRK2 proteins that had the mutation found in people with Parkinson’s. These faulty LRRK2 proteins also prevent other proteins, such as alpha-synuclein (a protein that causes PD), from breaking down and getting recycled.

The studies of Drs. Cuervo and Sulzer over the years have spotlighted the need for developing therapies that can help restart or speed up cellular recycling — therapies that could potentially help people whose PD has no known genetic cause as well as those who have LRRK2 mutations.

Highlight: Scientists Discover Most Common Genetic Risk Factor for Parkinson’s

Lorraine N. Clark, Ph.D., and Karen Marder, M.D., M.P.H., two scientists supported at the Columbia University Medical Center Research Center, have collaborated with a team led by Ellen Sidransky, M.D., of the National Human Genome Research Institute, to create one of the largest clinical investigations of the genetics of Parkinson’s ever undertaken.

Results of the study, published in the New England Journal of Medicine, showed that people who carry a mutation in a gene known as GBA have a significantly increased risk — over five-fold — for developing Parkinson’s. (GBA gene mutations can also cause Gaucher’s disease.) This makes the newly identified genetic risk factor for Parkinson’s the most common among the dozen or so genetic factors that have been found to date. Mutations in the GBA gene most likely increase susceptibility to PD, which when combined with other factors, results in disease. We need further research to understand how this happens.

Weill Cornell Medical Center

Weill Medical Center, headed by Dr. M. Flint Beal is another New York institution with an important Parkinson's research program. The Parkinson’s Foundation has supported the research efforts of this group with grants since 2003.

Highlight: New Tool Will Improve Testing of New Treatments

In foundation-funded labs at Weill Cornell Medical Center and Columbia University Medical Center, M. Flint Beal, M.D., and Robert Burke, M.D., have made progress finding a new and powerful tool for testing new Parkinson’s therapies and studying the underlying causes of the disease.

Working with Chenjian Li, Ph.D., at Weill Medical College and Tinmarla Francis Oo at Columbia University, Drs. Beal and Burke have created a unique “mouse model” that expresses a mutated form of the LRRK2 gene — the gene most commonly implicated as a cause of Parkinson’s. Nature Neuroscience published the results. Their model will help scientists create and test new Parkinson’s treatments in the lab. Scientists did not have a model that accurately mimicked the natural course of PD in humans prior to this development, hampering progress in Parkinson’s research.

Rush University Medical Center

The Parkinson’s Foundation has supported the Rush Parkinson's Disease and Movement Disorder program in Chicago since 1999. Basic and clinical research scientists at Rush work closely together in planning and executing projects dealing with Parkinson's. Dr. Christopher Goetz directs the clinical program and Dr. Jeffrey H. Kordower heads the basic science program.

Highlight: Using MRI to Better Understand Cognitive Impairment

Cognitive impairment is a common and troublesome non-motor Parkinson’s complication that can range from mild dysfunction to advanced dementia. People living with Parkinson’s and their caregivers feel the impact of cognitive impairment. Jennifer Goldman, M.D., M.S., of Rush University Medical Center has developed a research program that uses Magnetic Resonance Imaging (MRI) to examine whether there are brain stricture changes that may accompany mild cognitive impairment and dementia in Parkinson’s.

With the Parkinson’s Foundation’s support, she conducted a pilot study of 30 people with Parkinson’s and found shrinkage in the brain regions implicated in memory function among individuals who had the greatest cognitive impairment. By helping to identify those individuals who are most at risk for developing dementia, Dr. Goldman's research may provide leads to developing new therapeutic interventions for these people.

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