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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.
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