July 2006 Research Grants
Neurological Foundation of New Zealand July 2006 Research Grants
Auckland neurological researcher heads for Cambridge University to take up Research Fellowship
Auckland doctor Dr Jennifer Somerfield will head to Cambridge University to study treatments for multiple sclerosis after receiving the VJ Chapman Research Fellowship in the latest Neurological Foundation grant round.
Dr Somerfield has been training as a neurologist at Auckland City Hospital as well as being involved in research. She was recently awarded the prize for the best presentation by a young researcher at the Australian Association of Neurology meeting for a study on stroke.
Neurologist Dr Barry Snow, chairman of the Foundation’s scientific advisory committee, said Dr Somerfield had been an excellent trainee neurologist, and now had a full set of skills to look after patients.
“With the Fellowship, she can now extend her research experience in a top overseas centre. We expect that she will return to New Zealand as a clinician-researcher. Clinician-researchers drive investigations into neurological diseases with direct relevance to people with the disorders. We expect that she will follow a line of Chapman Fellows who have brought the latest research back to clinical neurology in New Zealand.”
Another Chapman Fellowship holder, Dr Maurice Curtis, was awarded a further $57,000 to continue his research in Sweden. Dr Curtis has been working with world-renowned neuroscientist Professor Peter Eriksson at the Arvid Carlsson Institute for Neuroscience investigating stem cell migration within the brain.
In total, the Neurological Foundation awarded grants for more than $550,000 in the July 2006 round.
Other research projects funded included an University of Otago study on deep brain stimulation for Parkinson’s disease, how the thalamus affects spatial memory systems (also at Otago), and a Massey University study into the role protein synthesis plays in mental retardation.
Scientific secretary Dr Douglas Ormrod said a pleasing aspect of this round was a wider range of research groups applying for grants indicating the growing strength of neuroscience research in New Zealand.
Neurological Foundation executive director Max Ritchie said it was gratifying that the Foundation was able to foster emerging researchers as well as supporting established projects.
“With the incidence of neurological disorders set to rise as our population ages, it is crucial that investment continues to be made in research, but we need the support of New Zealanders to ensure it continues.”
Neurological Foundation of New Zealand
The Neurological Foundation’s annual appeal week will run from July 9 to 15.
The Neurological Foundation of New Zealand is an independent body that raises money to support neurological research and education in New Zealand.
The Foundation receives no government assistance, and is almost totally funded by individual New Zealanders, with more than 95 per cent of contributions coming from donations and bequests.
The funds are capitalised and the interest is used to fund research grants. This system provides ongoing funding for career scientists and long-term research projects. All grant applications are internationally peer-reviewed to ensure only high-quality research is funded.
Annually, the Foundation gives close to $1.5 million in grants to New Zealand researchers and students, covering the full neurological spectrum of disorders.
In the last ten years alone, the Foundation has funded more than 200 projects and currently supports more than 40 research projects being run at tertiary institutions throughout the country.
This unique dedicated funding body has helped New Zealand produce world-class neuroscientists and research. It also uses the combined expertise and detailed knowledge of this group to help keep the public informed of the advances made in neurological disorder prevention and cures.
Neurological Foundation of New Zealand July 2006 Research Grants
Agmatine and age-associated cognitive decline
Dr Ping Liu
Department of Anatomical and structural biology
University of Otago
We tend to learn slowly and forget quickly when we are old. Elevated level of an endogenous gas named nitric oxide (NO) has been shown to contribute to such age-related cognitive decline. Agmatine is a neurotransmitter and an endogenous regulator to control NO production. Our preliminary work has demonstrated a decreased agmatine level in the aged brain, which may account for increased NO production and poorer learning and memory ability during aging. This project will further test this possibility using multiple techniques. This work may lead to a future therapeutic intervention for cognitive impairments in normal aging and Alzheimer’s disease.
Finding the substrate upon which deep brain stimulation acts to relieve parkinsonian symptoms.
Professor Gordon W Arbuthnott, Assoc. Prof Brian I Hyland, Professor Jeffery R Wickens
Depts of Physiology and Anatomy and Structural Biology
University of Otago
Drug treatment for Parkinson’s disease works well initially, but becomes less effective as the disease progresses. Internationally, such patients are increasingly treated by deep brain stimulation, which involves inserting electrodes into the brain and applying continuous electrical stimulation to a structure deep in the brain. While effective, the mode of action of this invasive surgical procedure is not understood. This project aims to discover the mode of action of the stimulation in the hope of developing less invasive methods, which might have an equivalent efficacy.
Characterisation of the role of a novel RNZ binding protein (RBM3) in neuronal translation
Dr Armas Aschrafi
Institute of Molecular Biosciences
Dysregulated protein synthesis in the brain can result in mental retardation by altering synaptic connectivity between neurons. Protein synthesis is regulated by mRNA-binding proteins (mRNA-BPs). We have shown that the RNA-binding proteins RBM3 is a novel mRNA-BP. We also demonstrated that over-expression of these proteins in neuronal cell lines enhances protein synthesis. Based on their unique functional and structural characteristics, our proposed studies are designed to assess the general mechanisms by which RBM3 influences protein synthesis in neurons. The outcome of these investigations could provide important piece of evidence to support the idea that critical neuronal mechanisms disrupted in mental retardation are linked to regulation of neuronal protein synthesis by mRNA-BP’s such as RBM3.
How extended is the spatial memory system? Lessons from thalamus
Associate Prof John C. Dalrymple-Alford, Prof Raymond P. Kesner
Department of Psychology, University of Canterbury, Christchurch
Understanding the brain’s memory systems is a key goal in medical neuroscience. Amnesia in humans has long been know to be associated with damage or degeneration to brain structures in the thalamus, a complex region in the centre of our brain, as well as the medial temporal lobe, at the side of the brain. We know a considerable amount about the role of the medial temporal lobe and memory, but little about the thalamus and memory. The current study will extend our previous work on thalamus and memory and may initiate new work on recovery of function after thalamic injury.
Small Project Grants
Otolaryngological microscope for inner ear surgery
Dr. Yiwen Zheng, Prof. Paul F Smith
Dept. of Pharmacology and Toxicology
University of Otago
Our current Neurological Foundation-supported research involves examination of the effects of damage to the balance organs of the inner ear on a part of the brain that contributes to learning and memory, the hippocampus. In order to do these experiments, we need to be able to perform fine surgery on the inner ear and this requires the use of a specialised ear, nose and throat microscope.
Spike time dependent plasticity of the human motor cortex
Dr Natalie Mrachacz-Kersting, Dr Vanessa K Lim, Dr Jeff P Hamm
Department of Psychology and Department of Sport and Exercise
The University of Auckland
Stroke is the leading cause of disability in New Zealand, and strategies for the rehabilitation of motor function are required. This proposal will yield new data relating to possible therapeutic strategies that utilise state-of-the-art magnetic brain stimulation. Specifically, this study employs a brain stimulation technique with the aim of increasing the motor excitability of the legs by optimising the parameters for stimulation. Increasing excitability of the pathway from the muscles in the legs to the brain may be beneficial in the recovery of walking (and gait) in people who have suffered a stroke.
VJ Chapman Fellowship Award
Protective autoimmunity induced by Campath-1H treatment of multiple sclerosis
Department of Neurology
Auckland City Hospital
Dr Jennifer Anne Somerfield
Multiple sclerosis is a disease in which patients develop inflammation in the brain resulting in damage to nerves. Campath-1H is a known treatment for multiple sclerosis that reduces inflammation. New research suggests this treatment may also help repair damaged nerves. This project involves investigating the function of white blood cells from patients treated with Campath-1H. A series of laboratory techniques will be used to determine if the cells of treated patients work to enhance nerve growth. By clarifying the effect of Campath-1H on nerve growth and repair, this work will contribute to the development of future treatments for multiple sclerosis.
Progenitor cell migration in the rodent and human brain
Arvid Carlsson Institute, Medicinaregat 11
Suburb Box 432 s-40530
City Göteborg, Sweden
Neuron-forming migratory progenitor cells in the human brain have long been thought absent. However, our recent finding that new neurons are produced from progenitor cells in response to Huntington’s disease indicates that these progenitors may migrate to areas of cell loss. We have tested this hypothesis by looking at the region in which most species have migratory progenitors, the rostral migratory stream (RMS). The human brain also has a RMS and we are using it to find the cues that progenitor cells use to migrate. The application is to direct progenitor cells toward brain regions affected by neurodegenerative disease.