Abstract
The need to better understand the cellular and biochemical mechanisms
contributing to brain injury following stroke/cerebral ischemia is essential for the
development of new treatments in order to reduce the massive impact this
devastating disease has on patients and on our social, economic and health
systems. One of the major instigators leading to neuronal cell death and brain
damage following cerebral ischemia is calcium dysregulation. The neuron’s
inability to maintain calcium homeostasis is believed to be a result of increased
calcium influx and impaired calcium extrusion across the plasma membrane.
The focus of this project is to characterise the role of the transmembrane
protein, the sodium-calcium exchanger (NCX) in response to cerebral ischemia.
The NCX’s main function is transporting calcium in and out of the cell. The
main hypothesis from this study is that increased NCX activity will enable cells
to better maintain calcium homeostasis and potentially be neuroprotective
following stroke/cerebral ischaemia, To this end, it is anticipated that the results
obtained in this study will provide important information regarding the role of the
NCX protein following cerebral ischaemia and aid the development of any future
NCX related therapeutics for stroke.
contributing to brain injury following stroke/cerebral ischemia is essential for the
development of new treatments in order to reduce the massive impact this
devastating disease has on patients and on our social, economic and health
systems. One of the major instigators leading to neuronal cell death and brain
damage following cerebral ischemia is calcium dysregulation. The neuron’s
inability to maintain calcium homeostasis is believed to be a result of increased
calcium influx and impaired calcium extrusion across the plasma membrane.
The focus of this project is to characterise the role of the transmembrane
protein, the sodium-calcium exchanger (NCX) in response to cerebral ischemia.
The NCX’s main function is transporting calcium in and out of the cell. The
main hypothesis from this study is that increased NCX activity will enable cells
to better maintain calcium homeostasis and potentially be neuroprotective
following stroke/cerebral ischaemia, To this end, it is anticipated that the results
obtained in this study will provide important information regarding the role of the
NCX protein following cerebral ischaemia and aid the development of any future
NCX related therapeutics for stroke.
| Original language | English |
|---|---|
| Qualification | Doctor of Philosophy |
| Publication status | Unpublished - 2012 |