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Glial cell signalling in Alzheimer’s Disease Supervisor: Dr Rhein Parri Email: [email protected] The project will investigate the role of glial cell function and dysfunction in Alzheimer’s disease. Alzheimer’s Disease is the most common of the devastating dementias affecting humans, and this project will use a transgenic model of Alzheimer’s Disease, the TG2576 mice which overexpress Amyloid. This is the most studied murine model of Alzheimer’s Disease. Glial cells are increasingly recognised as partners in CNS function and recent focus on astrocytes has implicated them in such diverse roles as synchronising neuronal activity to controlling cerebral blood flow. While it is known that astrocytic morphological changes occur in Alzheimer’s Disease and that they are involved in amyloid , nothing is known about changes in astrocytic transmitter release. This study will therefore focus on changes in glial glutamate and GABA release during the development of amyloid overexpression in these mice and determine the role of these changes in relation to known synaptic efficacy changes which parallel the cognitive decline in AD. The study will use electrophysiological recording from brain slice preparation to measure neuronal and glial signalling. This is an exciting project and will extend the knowledge of glial signalling in human disease. Dr.Parri’s group uses electrophysiological and calcium imaging techniques to investigate glial-neuron interactions and has close interactions with other electrophysiological groups at Aston in addition to those interested in Alzheimer’s Disease. Parri, H. R., Gould, T.M., Crunelli, V. (2001). Spontaneous astrocytic Ca2+ oscillations in situ drive NMDAR-mediated neuronal excitation. Nature Neuroscience 4(8): 803-12. Parri, H.R. and Crunelli, V. (2003). The role of Ca2+ in the generation of spontaneous astrocytic Ca2+ oscillations. Neuroscience. 2003;120(4):979-92. .