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The role of glia in protein misfolding diseases

The role of glia in protein misfolding diseases
The role of glia in protein misfolding diseases
The astrocytes, oligodendrocytes and microglia make up a significant proportion of the cells of the CNS. In recent years, there has been a burgeoning interest in the role of glial cells, in neurodegenerative disease. These cell types have been shown to play diverse roles in neuroinflammation, bioenergetics, signalling and intracellular oxidative balance, amongst others. Studies on Parkinson's, Alzheimer's, Huntington's and prion diseases suggest that the misfolded intra- or extra-cellular proteins that characterize these diseases could interfere with glial cell functions. I have developed and characterized an in vitro astrocyte primary cell culture. I have used this to look at the changes in glial glutamate transporter levels in the presence of mutant htt and to conduct a set of calcium experiments. These experiments provide essential tools for future studies into glial biology in neurodegeneration.
Samson, Ben
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Samson, Ben
50bdd1c7-e9c6-4207-8e62-f014446c0fdc
Wyttenbach, Andreas
05019897-52b1-4bb6-b259-5d51abae7540
Perry, V. Hugh
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Samson, Ben (2010) The role of glia in protein misfolding diseases. University of Southampton, School of Biological Sciences, Masters Thesis, 83pp.

Record type: Thesis (Masters)

Abstract

The astrocytes, oligodendrocytes and microglia make up a significant proportion of the cells of the CNS. In recent years, there has been a burgeoning interest in the role of glial cells, in neurodegenerative disease. These cell types have been shown to play diverse roles in neuroinflammation, bioenergetics, signalling and intracellular oxidative balance, amongst others. Studies on Parkinson's, Alzheimer's, Huntington's and prion diseases suggest that the misfolded intra- or extra-cellular proteins that characterize these diseases could interfere with glial cell functions. I have developed and characterized an in vitro astrocyte primary cell culture. I have used this to look at the changes in glial glutamate transporter levels in the presence of mutant htt and to conduct a set of calcium experiments. These experiments provide essential tools for future studies into glial biology in neurodegeneration.

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Published date: 1 June 2010
Organisations: University of Southampton

Identifiers

Local EPrints ID: 168311
URI: http://eprints.soton.ac.uk/id/eprint/168311
PURE UUID: f7dfee79-1782-490f-8d12-f33643fdade5

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Date deposited: 03 Dec 2010 16:08
Last modified: 14 Mar 2024 02:17

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Contributors

Author: Ben Samson
Thesis advisor: Andreas Wyttenbach
Thesis advisor: V. Hugh Perry

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