Hawkes Bay-born Dr Erin Cawston has been named the 2011 Neurological Foundation Repatriation Fellow. Erin will return from her position as Research Fellow at the Mayo Clinic Arizona next month, in order to further her research into Huntington’s disease at the Centre for Brain Research.
The Repatriation Fellowship ensures outstanding young researchers who have completed postdoctoral studies overseas can return home and continue to develop their research careers in their specialist area. Dr Cawston says “I am incredibly grateful to the Neurological Foundation for this Repatriation Fellowship allowing me to come home to New Zealand. I look forward to working with Associate Professor Michelle Glass and Professor Mike Dragunow on such an exciting project as well as being back amongst the New Zealand scientific community.” Dr Cawston begins her Fellowship at The University of Auckland in February.
Alongside this exciting research, the Neurological Foundation has also funded a number of exciting new research projects at the CBR.
Optimising a novel induced neural precursor-like cell line Associate Professor Bronwen Connor, Department of Pharmacology and Clinical Pharmacology, Centre for Brain Research University of Auckland, $136,862
The generation of ‘embryonic-like’ stem cells from adult human skin was first demonstrated in 2007. This project will advance this capability by directly generating immature brain cells (neural precursor cells) from adult human skin. Of major significance is that this will avoid the need to generate an intermediate embryonic-like stem cell phase, providing neural precursor cells for therapeutic applications without risk of tumour formation from stem cells. This project provides a unique opportunity to establish a novel technology which is likely to have wide-reaching applications for future research in the areas of neurological disease modeling, drug development, and potentially cell replacement therapy.
A genetic mechanism underlying late-onset Alzheimer’s disease Professor Russell Snell, School of Biological Sciences University of Auckland, $86,875
Alzheimer’s disease is a debilitating disorder affecting up to 50 per cent of those aged over 80 years old. Despite decades of research and innumerable clinical trials, there are no treatments that prevent or reverse the progression of the disease. There is currently some evidence that patients have a small proportion of brain cells with three copies of chromosome 21 instead of the normal two, leading to an increased production of the toxic protein amyloid-beta peptide. This study aims to confirm this observation, determine the pathological consequences of these cells and look for markers that make these cells different, which may lead to new therapies.
Immodulation of stroke with risperidone Associate Professor Bronwen Connor, Department of Pharmacology and Clinical Pharmacology, Centre for Brain Research, University of Auckland, $11,999
Stroke is a leading cause of disability in New Zealand and the burden associated with this neurological disorder is increasing. Treatment of stroke represents a large, unmet medical need. Neuroinflammation is an important pathophysiological mechanism involved in stroke and impacts profoundly on the extent of cell loss, as well as injury progression. Neuroinflammation therefore offers an exciting therapeutic target for the treatment of stroke. It has been recently demonstrated that the anti-psychotic drug, risperidone, is effective at reducing neuroinflammation and disease progression in a model of multiple sclerosis. This project will now explore whether the anti-inflammatory properties of risperidone can reduce the progression and severity of stroke.
Do BMP antagonists play a role in directing the fate of adult neural progenitor cells following neural cell loss?
Shwetha George, Department of Pharmacology and Clinical Pharmacology, Centre for Brain Research, University of Auckland, $4,000
The ability for adult neural stem cells to migrate to areas of brain damage and generate replacement brain cells may provide a unique mechanism by which to develop novel therapeutic strategies for the treatment of brain injury or neurological disease. However, the local environment appears to be critical for directing the final fate of adult stem cells in the damaged brain. This study will investigate whether brain injury alters the expression of a group of compounds known as bone morphogenic protein antagonists to promote adult neural stem cells to form glial rather than neuronal cells. The results of this study will enhance our knowledge as to how stem cells respond to brain cell loss and may assist in the development of novel therapeutic strategies for the treatment of brain injury or disease.