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Subtype-specifieke dendritische herstructurering in retinale ganglioncellen

Year: 2025
Type: dissertation
Abstract: Neurodegenerative disorders affect an ever-larger group of people. Moreover, they lead to a drastically reduced quality of life, to a large extent because the central nervous system of adult mammals has only a limited capacity to repair itself. Retinal ganglion cells are the neurons that majorly affected in glaucoma and other optic neuropathies. Unraveling the mechanisms involved in the natural ganglion cells developmental growth and the differences and similarities between it and the lack of regrowth in neurodegeneration can provide new insights that are essential to develop new therapeutic strategies for axonal regeneration in the central nervous system. In this project we want to empower in the mouse our innovative hypothesis, which states that dendritic shrinkage contributes to axonal regeneration in order to recapitulate the developmental order and hence attain successful repair. We also want to investigate whether energy transfer via mitochondrial transport could be at the basis of this interaction. First, we will characterize the rules of dendritic growth in retinal ganglion cells during development and their relationship with axonal growth. Next, we will use the retina as a model to investigate similarity between development and recovery from disease, we will demonstrate that the axonal regeneration after optic nerve injury process mimics the events during development, by a correlation between dendrite remodelling and axonal growth. Finally, mitochondrial morphology and transport will be analyzed, and its possible role in stimulating axonal growth will be studied in mouse retinal neurons. This work will unravell mechanisms involved both in development and in neurodegeneration, allowing us to be a step closer to find new therapeutic strategies for axonal regeneration in central nervous system.
Source: Lirias
Author: Faneca Santos, Joana
Language: English
Open Access status: green
OpenAlex ID: W7112896166
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