Funded Studies
Study Rationale: Motor difficulties are not the only symptoms experienced by people with Parkinson’s disease (PD); up to 80% eventually develop dementia. This progression to dementia is associated with elevated levels of misfolded proteins in the brain, including both alpha-synuclein Lewy bodies and tangles of tau protein similar to those detected in Alzheimer’s disease. We still have minimal understanding of how alpha-synuclein Lewy bodies and tau tangles develop and influence each other in PD.
Hypothesis: We hypothesize that alpha-synuclein and tau pathologies together enhance disease progression and worsen behavioral outcomes in PD.
Study Design: We will develop a preclinical, mouse model of alpha-synuclein and tau co-pathologies as a means to understand disease progression in PD. We will systematically characterize pathology progression patterns and associated behavioral outcomes as a foundation for future evaluation of therapeutic interventions.
Impact on Diagnosis/Treatment of Parkinson’s disease: If the presence of tau co-pathology is a driving factor in the development of dementia in PD, multiple or broad-spectrum therapies may be necessary to halt disease progression.
Next Steps for Development: The preclinical model developed in this study can be used for future evaluation of potential therapeutic molecules for their efficacy in impacting the pathologies and behaviors associated with PD progression.