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Funded Studies

The Foundation supports research across basic, translational and clinical science to speed breakthroughs that can lead to the creation of new treatments and a better quality of life for people with Parkinson's disease.

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Previously funded studies appear chronologically, with the most recent appearing first.

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  • Parkinson’s Disease Therapeutics Pipeline Program, 2025
    Development of a Sequence Specific LRRK2-targeted Parkinson's Disease Splice Switching Oligonucleotide Drugs

    Study Rationale: Some forms of Parkinson’s disease are caused by inherited mutations in the LRRK2 gene, and these mutations change the LRRK2 protein in such a way that it becomes too active. The LRRK2...

  • Research Grant, 2025
    Measurement of 1-deoxysphingolipids in Parkinson’s Disease Plasma

    Study Rationale: The sphingolipid metabolic pathway is large and complex, comprising hundreds of lipids critical to normal cellular and brain function. Variants in multiple genes regulating...

  • T2T Validation - NOD2, 2025
    Characterizing NOD2 Genetic Landscape Driving Risk of Parkinson’s Disease

    Study Rationale: The NOD2 protein plays a key role in how the immune system detects bacteria and protects the gut. Recent research suggests that genetic variation in the NOD2 gene may be linked to...

  • T2T Validation - NOD2, 2025
    Development and Validation of Synthetic NOD2 Modulators for Parkinson’s Disease

    Study Rationale: The expression and activity of NOD2, an important immune pattern recognition receptor, is associated with neuroinflammation and Parkinson’s disease (PD) and promising therapeutic...

  • T2T Validation - NOD2, 2025
    Modulating Levels of NOD2 Ligands in the Gut Microbiota to Dampen Neuro-inflammation in Parkinson’s Disease

    Study Rationale: Recent research suggests that a protein in our cells involved in bacterial detection, called NOD2, may play a role in the development of Parkinson’s disease (PD) by triggering harmful...

  • T2T Validation - NOD2, 2025
    Investigating the Potential Role of NOD2 Activation in Reducing a-synuclein Aggregation and Toxicity in Human Cellular and Pre-clinical Models of Parkinson’s Disease
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