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Featured Research

What can we learn by studying genetics and Parkinson's? PDF-funded researchers Drs. Mata and Zabetian share their progress six years after launching the first large-scale survey of PD genetics in Latin America.

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2012 Investigator-Initiated Abstracts

2012 | 2011 | 2010 | 2009 | 2008 | 2007 | 2006 | 2005 | 2004 | 2003

 

Among PDF's research awards of $5.3 million in 2012, we awarded $1.55 million for 17 novel investigator-initiated research projects.

Abstracts of these projects appear below.  Most projects are funded  the International Research Grants program and the Research Fellowships program, which both seek to encourage novel ideas by respectively funding “high-risk/high-reward” projects and supporting scientists in the early stages of their careers.

The applications by members of our Grants Review Committee comprising members of our Scientific Advisory Board, our Parkinson’s Advocates in Research program as well as other leading Parkinson’s scientists. This committee has selected this year’s projects - which represent only five percent of those submitted for funding - as the best science that is most likely to impact the lives and futures of people touched by Parkinson’s.

 

International Research Grants

Stability of Tetrameric α-synuclein as a Biomarker in Parkinson’s Disease
Tim Bartels, M.Sc., Ph.D., and Dennis J. Selkoe, M.D.
Harvard Medical School and Brigham and Women’s Hospital
Boston, MA
Total Award Amount: $165,000 over two years

A hallmark of Parkinson’s is the clumping together of a protein known as α-synuclein (α-Syn) in certain cells of the brain.  Although scientists don’t know exactly how or why α-Syn forms clumps, abnormally shaped forms of the protein may be to blame.  The laboratory of Dr. Bartels and Dr. Selkoe recently discovered that in normal cells, four copies of the α-Syn protein associate with each other to form a structure that is called a tetramer.  In people with PD, however, the α-Syn tetramer doesn’t assemble properly, which may make the protein more vulnerable to clumping.  Currently, researchers do not have a method for detecting these abnormal forms of α-Syn in the blood or brains of people with PD.  Therefore, the researchers plan to develop a test, known as an Enzyme-linked Immunosorbant Assay (ELISA), to detect different forms of α-Syn.  The ELISA will use antibodies that can discriminate between normal and abnormal α-Syn forms to determine which forms of α-Syn are present in blood or brain tissue samples.  They will use this ELISA to characterize α-Syn forms in many blood samples and brains of humans and mice with PD.  Being able to do so may help scientists better understand how α-Syn forms clumps, as well as aid PD diagnosis and the search for more effective therapies.

Evaluating the Role of Mitochondrial Dynamics in Parkinson's Disease in an In Vivo Vertebrate Model: Real-time Live Imaging of Mitochondrial Dynamics in Dopamine Neurons in Whole Zebrafish*
Sarah B. Berman, M.D., Ph.D., and Edward Burton, M.D., D.Phil., F.R.C.P.
University of Pittsburgh
Pittsburgh, PA
Total Award Amount: $165,000 over two years

Mitochondria are energy-producing structures found inside all cells of the body.  Many studies have shown that mitochondria are damaged early in Parkinson’s disease.  Drs. Berman and Dr. Burton have developed methods to study mitochondria in dopamine neurons — the cell type affected by PD — in live zebrafish.  Zebrafish are the fish equivalent of the lab mouse, yet are also transparent early in life.  Using genetic tools to make the mitochondria in zebrafish fluorescent, they will be able to record images of individual mitochondria as they move within the axons of dopamine neurons — a feat that has proven very difficult in the past.  They will first examine mitochondrial movements in normal zebrafish, and then compare these to zebrafish with mutations in α-synuclein (a gene implicated in PD), as well as zebrafish exposed to mitochondrial toxins.  They also will engineer zebrafish in which certain mitochondrial proteins can be tracked over a long period of time, and in which potential PD therapies aimed at protecting mitochondria could be tested.

Impact of Low- and High-frequency Electrical Stimulation on the Inputs, Integrative Properties, and Output of the Subthalamic Nucleus
Mark Bevan, Ph.D.
Northwestern University
Evanston, IL
Total Award Amount: $165,000 over two years

Nerve cells communicate by both chemical and electrical signals.  In people with Parkinson’s the loss of dopamine, a chemical signaling molecule, leads to overactive electrical signaling in an area of the brain called the subthalamic nucleus (STN).  One therapy for PD — deep brain stimulation (DBS) — delivers an electric current to the STN and helps restore normal patterns of signaling.  But how this works at the level of individual nerve cells and their connections is still not well understood.  Dr. Bevan will study patterns of electrical signaling of STN neurons in slices of brain tissue from mice that have dopamine loss and PD symptoms.  He will compare the effects of low- and high-frequency DBS on the STN and try to determine how the stimulation actually restores normal function.  A better understanding of the mechanisms underlying brain stimulation may lead to refinements in DBS therapy or to drug or gene therapies that mimic its effects.

Dissecting the Different Properties of Human α-synuclein Between Dopamine and Nondopamine Neurons in Vivo
Linan Chen, M.D., Ph.D., and Xiaoxi Zhuang, Ph.D.
University of Chicago
Chicago, IL
Total Award Amount: $165,000 over two years

Recently, scientists discovered that α-synuclein (α-Syn) — a protein that when damaged forms clumps called Lewy bodies in the brains of people with Parkinson’s disease (PD) — exists in cells as a complex of four α-Syn proteins bound together, known as a tetramer.  In people with PD, this tetramer may fall apart into four single α-Syn proteins, which are then more prone to clumping.  Researchers don’t know why certain brain cells, called dopamine neurons, are more vulnerable to Lewy body formation than other cell types. One possibility is that dopamine neurons contain less α-Syn tetramer and more single α-Syn proteins than other brain cells. However, comparing the levels of α-Syn tetramer in different cell types is very difficult: When researchers purify α-Syn from dissected brain tissue, they can’t tell which α-Syn proteins came from dopamine neurons and which came from non-dopamine neurons. Therefore, they have genetically engineered mice to produce large amounts of human α-Syn specifically in dopamine neurons.  When they isolate human α-Syn from the brains of these mice, they will know that it was produced exclusively by dopamine neurons.  Likewise, they generated mice that produce high amounts of human α-Syn in non-dopamine neurons.  They will compare the forms of human α-Syn in the brains of these two groups of mice. These experiments may shed light on the vulnerability of dopamine neurons to Lewy bodies and how α-Syn is toxic for these neurons.

The Cellular Mechanisms of Semaphorin 3E-Plexin-D1 Signaling in Basal Ganglia Circuitry Formation and Neurodegenerative Diseases
Chenghua Gu, D.V.M., Ph.D.
Harvard Medical School
Boston, MA
Total Award Amount: $165,000 over two years

People with neurological diseases such as Parkinson’s often suffer from uncoordinated, involuntary body movements.  This impaired motor function may result from an imbalance in the transmission of nerve signals within the brain. If one set of neurons are too stimulated or, alternatively, too inactive, they could cause either involuntary or impaired muscle movement.  An important part of achieving the correct balance requires proper “wiring” of brain circuits during development.  Currently, scientists don’t know exactly how neurons make specific connections with other neurons to achieve the proper balance in the brain regions affected by Parkinson’s.  Recently, however, Dr. Gu discovered that a protein called semaphorin 3E (Sema3E) that is secreted by certain neurons helps guide circuit formation.  She and her colleagues found that Sema3E interacts with another protein called Plexin-D1.  This interaction between these two proteins helps determine how neurons connect to each other. She plans to further explore the importance of the Sema3E–Plexin-D1 interaction in maintaining the proper balance between stimulatory and inhibitory circuits that control movement.  By understanding how neuronal circuits maintain the proper balance, Dr. Gu hopes to use this information to help find ways to rebuild neural circuits that have been destroyed by cell death in PD, thereby improving the motor control of people affected by PD.

Identification and Characterization of a Novel Gene for Parkinsonism
Paul Lockhart, Ph.D., and Gabrielle Wilson, Ph.D.

Bruce Lefroy Centre, Murdoch Childrens Research Institute, Royal Children's Hospital
Parkville, Victoria, Australia
Total Award Amount: $165,000 over two years

Parkinson’s disease is a common neurodegenerative disorder with symptoms that predominantly result from the loss of a specific type of neuron, called dopamine neurons, within the brain.  These neurons make up less than one percent of the more than 50 million neurons in the brain, and scientists do not know why they are the ones lost during disease development.  Therefore, identifying what causes dopaminergic neurons to die is a crucial step in understanding PD.
 Genetic studies and modern genomic technologies provide a powerful approach to identify genes and disease-causing events associated with PD.  Dr. Lockhart and Dr. Wilson have studied two families with early onset parkinsonism and identified a shared underlying genetic cause.  They will now characterize the gene responsible and determine what role the gene plays in PD.  This study will help to understand what causes dopamine neurons to die and may identify new therapies to prevent PD or slow its onset and progression.
 
Small Aromatic Molecules as Novel Inhibitors of α-synuclein Aggregation*
Daniel Segal, Ph.D.
Tel Aviv University
Tel Aviv, Israel
Total Award Amount: $165,000 over two years

The hallmark of Parkinson’s is the accumulation and clumping together of α-synuclein protein in certain brain cells.  Such protein aggregation is typical of other neurodegenerative diseases, as well.  In Alzheimer’s disease, for example, a protein called β-amyloid accumulates in brain cells.  In previous studies, Dr. Segal synthesized a small molecule that, because of its shape, prevents β-amyloid molecules from sticking together.  When administered to fruit flies and mice in laboratory tests, it inhibited β-amyloid clumping, reversed cognitive problems in the laboratory animals, and reduced amyloid deposits in their brains.  Applying these ideas to PD, Dr. Segal has also shown that this synthetic molecule inhibits the aggregation of α-synuclein in cells in a Petri dish. His goal is to extend this research to studies with fruit flies and mice, and to use the results to refine the structure of the molecule.  Ultimately, this research may lead to a therapy that alters the progression of PD.

Cyclic GMP Signaling and Experimental Parkinsonism

Anthony R. West, Ph.D., and Kuei-Yuan Tseng, M.D., Ph.D.
Rosalind Franklin University
North Chicago, IL
Total Award Amount: $165,000 over two years

Dr. West and Dr. Tseng plan to identify new strategies to treat Parkinson’s disease by interfering with specific signaling pathways inside brain cells.  Like a signal to turn on a light switch can illuminate an entire room, these pathways take small signals and turn them into large responses.  The pathway Drs. West and Tseng are investigating is called the soluble guanylyl cyclase (sGC) – cyclic GMP (cGMP) signaling pathway, where sGC is the switch and cGMP is the light.  Mice and rats with PD-like conditions have elevated levels of cGMP in cells of the striatum of the brain.  Dr. West and Dr. Tseng recently found that a drug that can block activation of the sGC switch can reverse various cellular and behavioral abnormalities in animal models of PD.  Now they will determine the effects of administering the drug for a long period of time to rats with a PD-like condition. They hypothesize that selectively blocking the sGC–cGMP activity with the drug will ease the rats’ symptoms and enhance their response to levodopa therapy.  These studies will provide valuable information on the effects of this signaling pathway in the brain and may reveal promising new therapies for PD that could be used alone or in combination with levodopa treatment.

Identification of Genes for Parkinson's Disease in an isolated Greek Community and a Greek Population Cohort*
Georgia Xiromerisiou, M.D., Ph.D.
University of Thessaly
Thessaly, Greece

Henry Houlden, M.D., M.R.C.P., Ph.D.
University College London
London, England
Total Award Amount: $165,000 over two years

Scientists have recently identified several genes that, when mutated, cause rare inherited forms of Parkinson’s disease.  In an effort to identify new PD mutations, Dr. Xiromerisiou and Dr. Houlden will study the DNA of people who live in and around the isolated village of Rapsani in central Greece, where the prevalence of PD is high.  Study participants with PD do not have any of the genetic variants that are known to contribute to PD.  Using standard techniques for genome sequencing, they will analyze the DNA of 30 people from the village who have PD, unaffected members of families with many cases of PD, and healthy individuals.  In addition, they will analyze DNA from people in the surrounding region of Thessaly, including 385 people with unexplained PD and 335 healthy people of similar age, gender, and ethnicity.  The goal is to discover regions of DNA shared by people with PD but not by healthy people.  A genetic answer as to why this group is susceptible to PD is likely to further focus how scientists approach PD research.

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Research Fellowship Grants

Regulation of α-Synuclein mRNA Translation in SNCA-expressing Neurons
Ianai Fishbein, Ph.D.

Institute for Human Genetics, University of California, San Francisco
San Francisco, CA
Total Award Amount: $47,500 over one year

Current therapy for Parkinson’s disease treats symptoms, rather than slowing or halting progression of the disease.  To develop more effective therapies, scientists must understand why dopamine neurons in the brain die and cause PD.  Important information can be gained from studying inherited forms of PD.  People with hereditary PD often inherit extra copies of the SNCA gene, which encodes the protein α-synuclein (α-Syn).  The extra copies of SNCA cause overproduction of the α-Syn protein.  Too much α-Syn protein can clump together in neurons, forming toxic Lewy bodies that are a hallmark of PD.  Dr. Fishbein recently discovered that although cells with extra copies of SCNA overproduce α-Syn, the amount of protein is not as high as expected based on the levels of α-Syn messenger RNA (mRNA) in the cell.  mRNA carries a working copy of the genetic blueprint for a protein from the nucleus, where most genes permanently reside, to the cytoplasm, where proteins are made in a process called “translation.”  Their observation suggests that neurons have ways to cope with excess α-Syn mRNA by reducing its translation into protein.  Identifying these cellular coping mechanisms may enable researchers to exploit them to reduce α-Syn protein in people’s cells.  Dr. Fishbein will study these mechanisms by measuring the efficiency of α-Syn protein production from mRNA in neurons with different levels of α-Syn mRNA.  He will analyze where in the cell the α-Syn mRNA accumulates, what elements of the RNA control its translation into protein, and what proteins bind to the mRNA to regulate it.  With these experiments, he hopes to find new ways to reduce the production of α-Syn protein in neurons, protecting them from cell death that leads to Parkinson’s.

Dopaminergic Neuron Subtype Differences in OXPHOS Capacity and Mitophagy in Response to mtDNA Damage
Alicia Pickrell, Ph.D.

Division of Intramural Research, National Institute of Neurological Disorders and Stroke (NINDS)
Bethesda, MD
Total Award Amount: $47,500 over one year

Adenosine triphosphate (ATP) is the major energy source for cells, allowing them to survive and function.  This important chemical is produced by the “cellular power plants,” or mitochrondria, in a process called oxidative phosphorylation (OXPHOS). Mitochondria are tiny cellular compartments that contain their own, separate DNA that encode some of the proteins necessary for OXPHOS.  Other mitochondrial proteins are encoded by DNA in the nucleus.  People with Parkinson’s often have deletions in their mitochondrial DNA, compromising the OXPHOS process and reducing ATP production. In addition, some inherited forms of PD are caused by mutations in genes in the cell’s nucleus that encode mitochondria-related proteins, such as Parkin and Pink1.  In a process called “mitophagy,” Parkin and Pink1 help recycle defective mitochondria that aren’t functioning properly or have harmful mutations in the mitochondria DNA.  Scientists think that PD may develop when defective mitochondria aren’t removed from the cell, as is the case for people with mutations in Parkin or Pink 1 genes.  Dr. Pickrell plans to investigate: 1) how deficiencies in OXPHOS impact different types of dopamine neurons (the neurons affected by PD), 2) if mitophagy occurs in dopamine neurons with defective mitochondria, and 3) whether calcium in the cell cytoplasm influences mitophagy.

The Role of Parkin in Regulating Mitochondrial Dynamics and Homeostasis in Cortical and Dopaminergic Neurons
Victor Van Laar, Ph.D.
University of Pittsburgh
Pittsburgh, PA
Total Award Amount: $47,500 over one year

Increasing evidence suggests that exposure to environmental toxins can contribute to Parkinson’s development.  For example, scientists have linked the pesticide rotenone to PD in animals and humans.  Rotenone may promote PD by damaging structures called mitochondria, which produce energy, in certain cells of the brain.  A gene known as Parkin helps keep cells healthy by getting rid of damaged mitochondria.  Mutations in Parkin are one of several rare, inherited causes of PD.  Dr. Van Laar and others have been examining how Parkin targets damaged mitochondria for degradation.  He unexpectedly discovered that Parkin regulates mitochondria in neurons differently under normal conditions than under conditions of chronic rotenone exposure.  This finding suggests that environmental toxin exposure may affect PD-related gene and protein function.  Building on this work with his PDF grant, he will now examine the effects of chronic pesticide exposure on Parkin's ability to regulate mitochondrial proteins in neurons.  This research will provide important clues as to how environmental exposures can interact with genes to promote PD development.

The Locus Coeruleus as a Substrate of Cognitive Inflexibility in Parkinson's Disease
Elana Vazey, Ph.D.
Medical University of South Carolina
Charleston, SC
Total Award Amount: $47,500 over one year

In addition to movement symptoms such as tremor and rigidity, many people with Parkinson’s experience cognitive changes.  These can include slowed thinking and trouble shifting between tasks, or multi-tasking.  Medications that raise the level of the chemical dopamine in the brain help movement, but are not effective against cognitive symptoms. This study focuses on a part of the brain stem called the locus coeruleus, which produces a different chemical messenger—norepinephrine.  Research suggests that degeneration of the locus coeruleus in PD contributes to cognitive symptoms as well as changes in sleep and mood.  In studies with rats, Dr. Vazey will investigate the cognitive effects of raising and lowering levels of norepinephrine in the locus coeruleus.  This will lead to an improved understanding of the role of the locus coeruleus in cognitive function, and assess the potential of regulating norepinephrine as a therapy for cognitive symptoms in PD.

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Lucien Côté Early Investigator Award in Clinical Genetics

Parkinson Disease in a Minority Inner City Population: Clinical Phenotypes and Genetic Etiologies, Focus on Afro-Caribbean Populations
Jose C. Cabassa, M.D.
SUNY Downstate Medical Center
Mentor: Rachel Saunders-Pullman, M.D., M.P.H.
Beth Israel Medical Center, Einstein College of Medicine
Total Award Amount: $55,000

Most studies on the genetics and symptoms of Parkinson’s disease have focused on people of European ancestry.  However, the limited data available on non-European minority populations suggests differences in PD features among various ethnic and racial groups.  The goal of this study is to examine symptoms and genetic causes of PD in a diverse inner city population, with a focus on people of Afro-Caribbean descent, to better understand and treat PD in this growing but understudied population.  Researchers will characterize PD symptoms and collect DNA from people with PD who are of African descent.  The collected DNA will help identify families with inherited forms of PD and will lay the foundation for screening European and US populations for mutations associated with PD.  This study will be one of the largest to characterize PD in a predominantly black US population.

 

Localization of Alpha-synuclein in Mitochondrial-associated ER Membranes (MAM): A New Insight into the Pathogenesis of PD
Cristina Guardia-Laguarta, Ph.D.
Mentor: Serge Przedborski, M.D., Ph.D.
Columbia University Medical Center
Total Award Amount: $55,000

Some people with inherited forms of Parkinson’s disease (PD) have mutations in a gene that makes a protein called α-synuclein (α-syn). Scientists do not yet understand the responsibilities of α-syn in the brain.  However, they know that in Parkinson’s, there is too much of it.  It forms toxic clumps in brain cells in both inherited and non-inherited forms of PD.  If researchers can understand α-syn, they may be able to develop treatments for all forms of PD. To find clues, Dr. Guardia-Laguarta will look at α-syn and something called “MAM” or mitochondria-associated ER membranes.  MAM forms a bridge that connects important cell structures. MAM may be important for the success of cell processes such as metabolism, signaling, and energy production.  Dr. Guardia-Laguarta will study how α-syn affects MAM and how PD-related genetic mutations might damage or affect this role.  These studies should increase scientists’ understanding of how PD develops and may suggest new treatments for the disease.

Mutant Glucocerebrosidase Causes Dysfunctional Chaperone-mediated Autophagy and Alpha-synuclein Accumulation in Patient Fibroblast-derived Dopaminergic Neurons
Sheng-Han Kuo, M.D., Ph.D.
Mentor: David Sulzer, Ph.D.
Columbia University Medical Center
Total Award Amount: $55,000

The most common cause of inherited Parkinson’s disease is a mutation in the glucocerebrosidase (GBA) gene.  However, scientists do not yet know how these mutations cause PD.  Several studies have suggested that GBA mutations may cause the toxic build-up of alpha-synuclein in brain cells that is the hallmark of PD.  Dr. Kuo and Dr. Sulzer’s initial experiments suggest that one way the mutation could cause alpha-synuclein to build up is by interfering with the cell’s recycling process.  This process, called chaperone-mediated autophagy (CMA), helps the cell to stay healthy – to get rid of unneeded proteins, including alpha-synuclein.  It may prevent too much alpha-synuclein from accumulating in cells and becoming toxic.  However, this observation needs to be confirmed in human neurons.  Therefore, Dr. Kuo will use “artificial” stem cell technology to study dopamine neurons that have created from the skin cells of people with PD (who also have mutations in GBA gene).  In these cells, he will measure levels of GBA enzyme and alpha-synuclein proteins and study whether CMA is working properly.  He hopes to find out whether CMA is works properly in human neurons with GBA mutations.  If it does not, he will also investigate whether improving CMA might provide an effective treatment for PD.

Identifying Genetic Causes Underlying Early-onset Parkinson’s Disease
Coro Paisán-Ruiz, Ph.D.
Mentor: Joseph D. Buxbaum, Ph.D.
Mount Sinai School of Medicine
Total Award Amount: $55,000

Although most cases of PD are sporadic, meaning that they have no known cause, scientists have identified at nearly two dozen gene or gene regions that, when mutated, cause inherited forms of PD.  Growing evidence indicates that genetics plays an important role in the development of both inherited and sporadic PD.  Dr. Paisán-Ruiz seeks to identify new genes associated with PD by using the latest gene sequencing technology and comparing the DNA of families with inherited forms of the disease.  In this way, researchers can identify new gene mutations linked to PD.  To confirm that mutations in these genes contribute to PD development, the genes will be sequenced in additional families with inherited PD, people with the sporadic form of PD, and individuals who are healthy.  The proposed studies should identify new PD genes, which will increase scientists’ understanding of PD development and possibly help them devise more effective treatments.

Conference Awards

Fighting the Law of Gravity:  Exploring Approaches to Address Postural Instability and Falls in PD
Lee Dibble, P.T., Ph.D., University of Utah, Colleen Canning, P.T., Ph.D., University of Sydney, Gammon M. Earhart, P.T., Ph.D., Washington University, Terry Ellis, P.T., Ph.D. Boston University
Total Award Amount: $16,500

Postural instability is one of the most disabling motor aspects of Parkinson disease. Additionally, approximately 70 percent of older adults with PD fall each year – more than double the number of elders in the general community who fall annually (30 percent).  These profound statistics have led some to proclaim that postural instability and falls are an inevitable consequence of PD.  Common treatments for Parkinson’s disease, such as dopamine replacement medication and deep brain stimulation (DBS) surgery, which are effective in reducing bradykinesia, rigidity and tremor, may have limited effect in easing postural instability.  In fact, increases in movement speed without similar improvement of protective postural responses have been theorized to contribute to increased falls in the PD population. Despite the magnitude of this problem and the enormous impact on disability, most studies have only examined the cross sectional alterations in postural instability in persons with PD relative to controls and few studies have followed these mechanistic studies with interventions specifically targeted at the identified deficits.  This conference will strategy this unmet need in Parkinson's research and treatment, by gathering leaders in physical therapy in 2013.

West Coast Conference on Parkinson’s Disease: Determining Factors in PD Progression Rate –The Next Translational Challenge
Marie-Françoise Chesselet, M.D., Ph.D., UCLA
Total Award Amount: $10,000
Over the past few years, focus of PD research has shifted from the loss of dopaminergic cells, to the widespread pathology both within and outside the brain. Strong evidence has pointed to dysfunction of neurons outside the substantia nigra (the area of the brain impacted by PD) long before the loss of dopaminergic cells in the brain and motor symptoms of PD.   As we enter the next promising translational phase for PD treatments based on these findings, a major problem remains the difficulty of predicting the rate of disease progression in individuals living with Parkinson’s disease. This issue plagues the design of clinical trials. Trials generally include mixed patient populations with very different rates of disease progression. This limits the chance of detecting positive effects of new treatments, and necessitates large numbers volunteers living with Parkinson’s disease, making clinical trials cost-prohibitive and unattractive to industry. If researchers could more effectively focus on subpopulations of people with Parkinson’s, who have similar uniform progression rates, it would considerably accelerate efforts towards identifying effective disease-modifying treatments, by potentially cutting down the time and costs associated with bringing novel therapies to market. We propose to address this critical issue with leaders in PD research by hosting a multi-institutional conference at UCLA in early November 2013, focused on developing ways to identify the key determinants of disease progression, and modifying the mechanisms of this progression, leading to enhanced quality of life and improved prognosis.

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*Denotes second year of funding