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Identifier 000443887
Title BNN27 therapeutic effects on optic nerve injury
Alternative Title Τα θεραπευτικά αποτελέσματα του BNN27 μετά από τραυματισμό του οπτικού νεύρου
Author Σαριδάκη, Ερασμία Αγγελική
Thesis advisor Γραβάνης, Αχιλλέας
Χαραλαμπόπουλος, Ιωάννης
Τζεράνης, Δημήτριος
Abstract Traumatic optic neuropathy (TON) is a condition, induced when an injury occurs within the optic pathway and results in complete vision loss. TON is caused by falls, car accidents or even attacks and affects thousands of people every year, mainly young people aged between 11-30 years old. The optic pathway consists of the retina, optic nerve, optic tracts, optic radiation and finally of theprimary visual cortex. At a cellular level TON leads to Retinal Ganglion Cell (RGC) death, inflammation/astrogliosis, demyelination and axon degeneration. Due to CNS incapacity to promote axon regeneration, TON tends to be an irreversible situation. There is still no appropriate treatment that promotes CNS axons to regenerate effectively, reversing the vision loss effect caused by TON. Clinical treatments emphasize mainly to corticosteroid administration, whereas experimental approaches include: eye drops, injections, biomaterials’ implantation, Peripheral Nervous System grafts, cell transplantation and also gene therapy. Neurotrophins secreted from the neurons or from the glial cells within the retina and the optic nerve are promising molecules for TON therapy, as generally exert neuroprotective properties to neurons, increase their proliferation and their differentiation. In this study, a synthetic analog of DHEA, a microneurotrophin, named BNN27 that mimics NGF is administered in Optic Nerve Crushed mice either 2 weeks or 10 weeks after injury. BNN27 is administered by two strategies: 1. Eye drops (1 eye drop/day or 2 eye drops/day) and 2. through biomaterial-implantation. In the latter approach, BNN27 at the day of the surgery, is entrapped in a scaffold/peptide that is placed around the lesion site of the Optic Nerve. This strategy assures steady release of the drug in the lesioned tissue. Our results prove that unilateral Optic Nerve Crush model is reproducible as it results in a 40% RGC loss within the first week after injury and a 60% RGC death within 2 weeks after injury. The results of the 2- weeks study prove that BNN27 delivered either by eye drops or by biomaterial reduces significantly Retinal Ganglion cell death caused by Optic Nerve Crush. Furthermore, BNN27 does not exert anti-inflammatory properties to Muller cells and does not inhibit demyelination in the Optic Nerve. Concerning the 10 -week study, BNN27 does not minimize Retinal Ganglion Cells loss and does not promote axon regeneration within the Optic Nerve. Taking these results into account, an important finding of this research is that BNN27 delays RGC death in the retina 2 weeks after injury, whereas it does not exert any neuroprotective properties in RGCs within 10 weeks after injury, resulting in RGC loss and eventually in lack of axon regeneration.
Language English
Subject Neuroprotection
Issue date 2021-12-01
Collection   School/Department--School of Medicine--Department of Medicine--Post-graduate theses
  Type of Work--Post-graduate theses
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