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Doctoral thesis

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New Approaches to Modify the Proliferating Glia in an environment of Spinal Cord Injury

Spinal Cord Injuries

Doctoral student: Lucila Maite Pérez Gianmarco

Sinopsis

About half a million people suffer spinal cord injury (SCI) every year. But the therapies for SCI are very limited, and many patients remain in the wheel-chair life-long. Therefore, there is a need to search for new molecular targets to promote regeneration and functional recovery of the patients. A key molecule in the pathophysiology of SCI is glutamate.

Glutamate is often considered as a negative player during injury because it is released in excess and may induce excitotoxic cell death via activation of ionotropic glutamate receptors of AMPA and NMDA type. However, a big puzzle remains: astrocytes, oligodendroglial progenitors, and microglia also express ionotropic glutamate receptors, but they do not die out after SCI; they get activated, proliferate, and contribute to scar formation. Why this occurs remains unknown. We hypothesize that subunit composition and Ca2+-permeability of AMPARs play an important role for triggering proliferation rather than death of glial cells after SCI, and may modulate their cell fate upon differentiation.

To test this hypothesis, we will use a clinically relevant mouse model of SCI and manipulate properties of AMPARs in proliferating glial cells using viral gene delivery approach in vivo. We will then investigate how AMPA manipulations affect survival and properties of neurons and glia after SCI, and which genes and molecular signaling pathways may be involved. The expected results have a potential to highlight new molecules that may be of interest for pharmaceutical companies and clinicians, and over the long-term may lead to the generation of new drugs for management of SCI.

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