Funded Studies
Study Rationale:
Methods are needed for imaging early pathological changes in the brain. With such brain imaging, we would be able to determine whether medications are protecting against progression of Parkinson’s disease (PD) or even reversing it. Evidence suggests that dysfunction of the ‘energy’ organelles of brain cells — mitochondria — may be an early initiation of PD neurodegeneration.
Hypothesis:
We hypothesize that a novel positron emission tomography (PET) agent that binds the mitochondrial component Complex I will detect changes in the brain of those with PD, with the potential for monitoring disease progression or neuroprotection.
Study Design:
Participants with PD without cognitive difficulties, PD with cognitive difficulties or a diagnosis of dementia with Lewy Bodies, and control participants without neurologic disease (18/group) will undergo neurologic evaluation and brain imaging using the novel PET agent, [18F]BCPP-EF, which binds to an important component of mitochondrial function termed Complex I (mito-C1). We will compare the amount of mito-C1 signal in each group, across different regions of the brain, and will analyze whether differences exist.
Impact on Diagnosis/Treatment of Parkinson’s Disease:
If successful, PET imaging with this agent may 1) provide an early and accurate biomarker of PD; 2) monitor disease progression (indicated by progressive loss of mitochondrial function); and, importantly, 3) detect a slowing or even reversal of this decrease in mitochondrial function during disease-modifying drug trials.
Next Steps for Development:
If this is successful, next steps would more fully evaluate whether brain imaging with this PET agent is able to stage progression of disease, and is able to detect early disease, in order to determine its utility as a biomarker for neuroprotection trials.