Abstract
Stroke is the leading cause of disability in the Australian community. We can prevent stroke and even treat an occlusion within the cerebral circulation with thrombolysis. The future challenge is how to improve functional outcome post-stroke when the brain has been irretrievably damaged. There is controversy as to the role of stem cell therapy in the answer to this challenge. Although many stem cell populations exist the optimum for neuro-regeneration is unknown. We have published extensively on the discovery and neural potential of a stem cell population derived from human teeth, i.e. the Dental Pulp Stem Cell (DPSC). In this study we used a reversible middle cerebral artery occlusion method to
generate an ischaemic stroke in Sprague-Dawley rats. 24 hours poststroke
500,000 DPSCs were transplanted into the peri-infarct region of the rodent brain. Cyclosporin was administered daily to DPSC treated and media-only treated, control animals. Multiple neuro-behavioural assessments were undertaken weekly on all animals before and following treatment and the assessor was blinded to treatment. At four weeks following treatment we found enhanced improvement in function in the DPSC treated animals (n=9) in comparison to the control animals (n=5). By this time a majority of DPSC had not survived in the stroke brain, when immunohistochemically labelled for human mitochondrial antigen, suggesting functional improvement may not depend upon direct neural replacement. All experiments were authorised through the University of Adelaide, Animal Ethics Committee.
generate an ischaemic stroke in Sprague-Dawley rats. 24 hours poststroke
500,000 DPSCs were transplanted into the peri-infarct region of the rodent brain. Cyclosporin was administered daily to DPSC treated and media-only treated, control animals. Multiple neuro-behavioural assessments were undertaken weekly on all animals before and following treatment and the assessor was blinded to treatment. At four weeks following treatment we found enhanced improvement in function in the DPSC treated animals (n=9) in comparison to the control animals (n=5). By this time a majority of DPSC had not survived in the stroke brain, when immunohistochemically labelled for human mitochondrial antigen, suggesting functional improvement may not depend upon direct neural replacement. All experiments were authorised through the University of Adelaide, Animal Ethics Committee.
Original language | English |
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Publication status | Published or Issued - 31 Jan 2010 |
Event | Australasian Neuroscience Society 2010 - Sydney, Australia Duration: 31 Jan 2010 → 3 Feb 2010 |
Conference
Conference | Australasian Neuroscience Society 2010 |
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Country/Territory | Australia |
City | Sydney |
Period | 31/01/10 → 3/02/10 |