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WHY DO DIFFERENT PARKINSON’S DISEASE MUTATIONS CONVERGE ON SIMILAR OUTCOMES, WHILE IDENTICAL MUTATIONS DO NOT?
Li Zhang
Johannes Gutenberg University Mainz
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-081
Presentation
Date TBA
Board: PS03-08AM-081
Event Information
Poster Board
PS03-08AM-081
Poster
View posterAbstract
Parkinson’s disease (PD) is defined by the selective degeneration of dopaminergic neurons, yet its genetic architecture reveals two seemingly opposing features. On one hand, diverse PD-associated mutations converge on remarkably similar pathological outcomes, suggesting shared cellular constraints underlying neuronal vulnerability. On the other hand, identical mutations can lead to markedly different clinical and cellular trajectories, highlighting the phenomenon of reduced penetrance and neuronal resilience.
My work addresses this apparent paradox by shifting the analytical focus from binary cell loss to graded neuronal function. Using a comparative framework, I interrogate PD-associated neuronal dysfunction along two complementary dimensions: across distinct disease-associated perturbations to assess convergence, and within the same perturbation across multiple phenotypic scales to capture variability in disease expression.
Applying this comparative framework points to a shared vulnerability axis. Across models, distinct disease-associated perturbations converge on this axis, while within a single model, its engagement correlates with phenotypic severity. Together, this framework reframes PD as a disorder of graded neuronal dysfunction shaped by shared vulnerability and context-dependent resilience.
My work addresses this apparent paradox by shifting the analytical focus from binary cell loss to graded neuronal function. Using a comparative framework, I interrogate PD-associated neuronal dysfunction along two complementary dimensions: across distinct disease-associated perturbations to assess convergence, and within the same perturbation across multiple phenotypic scales to capture variability in disease expression.
Applying this comparative framework points to a shared vulnerability axis. Across models, distinct disease-associated perturbations converge on this axis, while within a single model, its engagement correlates with phenotypic severity. Together, this framework reframes PD as a disorder of graded neuronal dysfunction shaped by shared vulnerability and context-dependent resilience.
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