GDNF Protects PC 12 cells from Oxidative Damage Induced Apoptosis

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Authors
Vettraino, Jason T.
Issue Date
1999
Type
Thesis
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en_US
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Abstract
Motor neuron Disease (MND) is a term which includes a variety of disorders characterized by progressive muscle weakness without sensory loss. Amyotrophic lateral sclerosis (AL8), the most common form of MND, is characterized by muscle atrophy, weakness, and loss of fine motor coordination, leading to paralysis, respiratory failure and premature death. The etiology of the disease is unknown. Current research is focused on abnormalities of neuronal cell metabolism involving glutamate and the role of potential excitotoxins and neurotrophic factors. Excitotoxicity describes the cellular conditions in which excitatory amino acids (EAAs) have a damaging effect on the central nervous system (CNS) due to over excitation and oxidative damage. Neurotrophic factors are specific proteins that are essential for the development, survival, and maintenance of both the peripheral nervous system (PNS) and the CNS. Neurotrophic factors have also demonstrated the ability to regenerate and/or save neurons from a variety of deaths. The goal of this experiment was to set up a simple, in vitro, neuronal model of ALS to study the ability of the neurotrophic factor, glia-derived neurotrophic factor (GDNF) to rescue neurons from apoptosis caused by oxidative damage. Results of this study conflrm prior studies from Oppenheim and colleagues (1995), and Gimenez and colleagues (1997) in that GDNF has therapeutic potentials. This study suggests that GDNF has the ability to prevent apoptosis induced by excitoxicity.
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iv, 28 p.
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U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder. All rights reserved.
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