Project: SUF
Investigating neuro-glial metabolic coupling in optic atrophies
Optic atrophies, including hereditary conditions like ADOA and glaucoma, are neurodegenerative disorders characterized by the progressive loss of retinal ganglion cells (RGCs). While mitochondrial dysfunction is a recognized hallmark of RGC degeneration, the contribution of non-neuronal cells in maintaining metabolic homeostasis remains a critical knowledge gap. This project investigates the role of inter-cellular mitochondrial quality control, specifically the metabolic crosstalk between RGCs and astrocytes, in the pathogenesis of optic neuropathies.
We hypothesize that RGC mitochondrial stress triggers a compensatory metabolic response in astrocytes, and that the failure of this neuron-glia metabolic unit accelerates axonal degeneration. By integrating advanced live-cell imaging with sophisticated co-culture systems, this research aims to characterize how dysfunctional organelles are managed within this neuro-glial interface.
The project will establish whether enhancing glial-mediated clearance pathways can mitigate RGC vulnerability. Our findings will provide fundamental insights into the mechanisms of mitochondrial homeostasis in the retina, potentially identifying novel metabolic checkpoints that serve as therapeutic targets for preserving vision in optic neuropathies.
Key Methods
- Cellular models of genetic optic atrophy
- Advanced live-cell super-resolution microscopy to monitor organelle dynamics
- Molecular manipulation of mitochondrial quality control pathways
- Quantitative morphological and metabolic profiling of neuro-glial interactions.
