Neurological Foundation announces July 2012 grant round recipients; $40 million committed to neurological research in 40 years
The Neurological Foundation announced today that funding of over $800,000 for neurological research and educational scholarships has been approved in its July 2012 grant round. This brings the total funding committed to neurological research in New Zealand to over $40 million since the Foundation’s first grants were allocated in 1972. The Neurological Foundation is the primary non-government sponsor of neurological research in New Zealand.
Neurological Foundation Executive Director Max Ritchie says “In 1972, five grants totaling $28,500 were made. The annual budget for research is now $2 million. The Foundation has an efficient research evaluation system managed by the Scientific Secretary and carried out by the Scientific Advisory Committee. If the selection is right, then the quantity of research becomes as effective as any measure of progress. Improvement in patient care – both for treatment and rehabilitation – is directly related to that figure, so as we progress into the future, we will see a commensurate improvement in outcomes for people with neurological disorders.”
The July grant round showcases the breadth of world-class neurological research being carried out at universities and research institutions across New Zealand. In this round, the Foundation awarded seven project grants, a training grant, the Neurological Foundation VJ Chapman Research Fellowship and the Neurological Foundation Repatriation Fellowship.
Research projects granted funding include the identification of genetic traits in Autism Spectrum Disorders, understanding and preventing long-term disability in multiple sclerosis, the efficacy of a stroke risk-reduction tool, the management of subarachnoid haemorrhage and a study that will identify the prevalence of Parkinson’s Disease in New Zealand.
Dr Wallace Brownlee has been awarded the 2012 Neurological Foundation V J Chapman Research Fellowship. Dr Brownlee will undertake his three year Fellowship at the Institute of Neuroinflammation at the University College London under the supervision of leading multiple sclerosis authority Professor David Miller who is also a New Zealander.
Dr Jessie Jacobsen, the 2008 Neurological Foundation Postdoctoral Fellow, has been awarded the 2012 Neurological Foundation Repatriation Fellowship. See attached story for details of her repatriation.
The Neurological Foundation is an independent body and charitable trust and its funding has facilitated many of New Zealand’s top neuroscientists’ pioneering breakthroughs. Without the ongoing support of individual New Zealanders, the Foundation could not commit to progressing research to the high level that it does. Ninety eight per cent of funding comes from donations and bequests.
For further information or interviews please contact Sue Giddens, General Manager Marketing and Fundraising on 021 650 906 or firstname.lastname@example.org
Research grants totalling $809,608 have been approved by the Neurological Foundation Council in the July 2012 grant round.
NEUROLOGICAL FOUNDATION 2012 REPATRIATION FELLOWSHIP
Dr Jessie Jacobsen
School of Biological Sciences
The University of Auckland
See the press release on Dr Jessie Jacobsen for more details
NEUROLOGICAL FOUNDATION V J CHAPMAN RESEARCH FELLOWSHIP
The Neurological Foundation V J Chapman Research Fellowship is awarded to a medical graduate committed to a career in neurology, to give him or her the opportunity of spending a period in clinical or biomedical research. This may be combined with advanced clinical training in neurology, but the research component should be at least 50%, and is designed to provide a unique training experience to clinicians with an interest in a career in clinical investigation.
Dr Wallace Brownlee
Auckland City Hospital
Understanding and preventing long-term disability in multiple sclerosis: a 14-year follow-up study of patients with clinically isolated syndrome (CIS)
Multiple sclerosis (MS) is an autoimmune disease that usually starts with an attack called a clinically isolated syndrome (CIS). Currently there is no cure for MS, and it affects one in every 1400 New Zealanders. Most people have permanent disability ten to fifteen years after the CIS from the effects of relapsing/remitting MS or a gradual deterioration called secondary progressive MS. To manage MS effectively, clinicians need to know who will develop disability. Dr Brownlee will follow up people who had a first CIS attack 14 years ago and who were last seen seven years ago. Dr Brownlee will undertake advanced MRI scans at the 14 year stage to clarify the causes and predictors of disability and identify new treatment targets.
Dr Wallace Brownlee completed the Royal Australasian College of Physicians written and clinical exams in 2010. Later that year he began his advanced training in Neurology and will finish his core training requirements at the end of 2012. Dr Brownlee’s Neurological Foundation V J Chapman Research Fellowship will be undertaken at the Institute of Neuroinflammation at the University College London under the supervision of leading multiple sclerosis authority Professor David Miller who is also a New Zealander.
Dr Annemarei Ranta
Department of Neurology
MidCentral Health/University of Otago
Efficacy and safety of a TIA/Stroke Electronic Decision Support Tool in the primary care setting to improve patient access to secondary services and overall stroke care in New Zealand
Of the 8,000 New Zealanders who have a stroke each year, a quarter will have previously experienced a transient ischemic attack (TIA). TIAs identify high-risk patients and rapid best medical management reduces stroke risk by 80 per cent. The TIA/Stroke Electronic Decision Support Tool (EDS) is designed to help general practitioners to achieve this potential risk reduction. The project aims to test the efficacy of the EDS tool with regard to stroke reduction, assess any risks associated with EDS use, and establish costs of EDS use compared with usual management. This is the first formal evaluation of a TIA/Stroke EDS tool and, within three years of study commencement, its results will inform policy and practice relating to use of the tool in New Zealand. The information from this study will be compiled with a number of studies into a PhD thesis.
Dr Johanna Montgomery
Department of Physiology
University of Auckland
Role of zinc in reversing synaptic deficits in autism
Autism Spectrum Disorders (ASD) are a set of neurodevelopmental disorders characterised by impaired communication and social behaviour, learning difficulties, and by repetitive or stereotyped behaviours. The estimated number of people with Autism Spectrum Disorders in New Zealand is 40,000. The cause is unclear, and no treatments have been developed. Dr Montgomery’s team has recently shown that mutations that occur in autistic patients result in weakening of communication at the connections (synapses) between neurons. In this research, Dr Montgomery aims to determine whether enhancing the functions of certain proteins at synapses can recover synapse function in autism. Specifically, the impact of zinc in reversing the synaptic effects of genes which are altered in autism will be assessed. Zinc is a metal ion known to stabilise synapse proteins. The research has the potential to identify a unifying link to normalise synaptic changes in autism. This information can then be used to identify cellular mechanisms that could be used to develop treatments for the cognitive symptoms associated with ASD.
Dr Toni Pitcher
Department of Medicine
University of Otago, Christchurch
Parkinson’s disease in New Zealand: Prevalence and medication consumption
Parkinson’s disease (PD) is a neurodegenerative disease which causes disabling motor (movement) and non-motor disturbances. Currently, there is a distinct lack of information regarding the impact of PD in New Zealand, with the most recent estimate of prevalence being a regional one from the early 1990s. Up-to-date information on the numbers of people living in New Zealand with PD is important: our population structure is changing, and as the proportion of the population aged over 65 years increases, the number of people living with age-related disorders such as PD will also increase. Dr Pitcher will utilise the national prescription database to analyse PD drug dispensing data and provide an up-to-date estimate of the number of Parkinson’s disease patients living in this country and the trends of anti-parkinsonian medication use. Improved information will contribute to better planning and provision of appropriate patient-directed information and support services.
Dr Patries Herst
Malaghan Institute of Medical Research and
University of Otago, Wellington
Effect of high dose ascorbate on brain tumour progression
Glioblastoma multiforme (GBM) brain tumours are highly aggressive and invasive due to their extreme resistance to radiation and chemotherapy. As a result, the prognosis of patients with GBM brain tumours is poor with a median survival time of 19 months. In the presence of free metals, high-dose vitamin C produces free radicals that kill cells by damaging their DNA. Solid tumours, but not normal tissues, produce the acid and free metals necessary for this to occur. Dr Herst’s team has previously shown that high-dose ascorbate kills significantly more GBM cells isolated from patient tumours, than normal glial cells. This project will validate these findings by determining the effect of high-dose ascorbate progression in a GBM model.
Mr Edward Mee
Consultant Neurosurgeon/Clinical Director
Department of Neurosurgery
Auckland City Hospital
Temporal changes in post subarachnoid haemorrhage
Subarachnoid haemorrhage (SAH) occurs when an aneurysm (weakened blood vessel) bleeds into the space around the brain, resulting in a life-threatening situation requiring immediate treatment. This study aims to utilise unique New Zealand stroke data to evaluate the effectiveness of current practices on patient outcomes, and compare management changes and their effectiveness from 1981 to the present. It is anticipated that this comparison will provide a better understanding of the merits of the new management strategies to reduce the impact of the devastating outcomes of subarachnoid haemorrhage including death and ongoing disability.
Professor Neil McNaughton
Department of Psychology
University of Otago
Brain stimulation parameters for optimal memory recovery
Memory dysfunction results in brain disorders ranging from traumatic brain injury to dementia. In the brain, the hippocampus and surrounding cortex are implicated in disorders of memory and show slow rhythmic activity (known as theta). Professor McNaughton’s team has recently shown that deep brain stimulation reinstates theta and can repair memory deficits in models of dementia. There is evidence that such stimulation also ameliorates the effects of traumatic brain injury. The effectiveness of the stimulation appears to depend on its parameters and Professor McNaughton and team will optimise these parameters and test their range. This will provide a basis for the transfer of the technique to deep brain stimulation in traumatic brain injury and subsequently to disorders such as dementia and vestibular (inner ear) dysfunction.
Professor Paul Smith
Department of Pharmacology and Toxicology
University of Otago
Novel GABAB receptor agonists for the treatment of chronic tinnitus
Chronic tinnitus is a debilitating condition affecting approximately ten per cent of the population. There are very limited drug treatment options, mainly due to a lack of systematic, well-controlled preclinical drug studies and a lack of understanding of the underlying mechanisms of the condition. It has been suggested that tinnitus is generated in the brain by the hyperactivity of brain cells involved in hearing. This project will investigate a novel drug, which can reduce this brain cell activity, in a model of tinnitus. The goal of this study is to determine whether this drug is a potential new treatment for severe chronic tinnitus.
Associate Professor Cynthia Darlington
Department of Pharmacology and Toxicology
University of Otago
The effects of fluctuating and non-fluctuating vestibular dysfunction on cognition
Damage to the vestibular portion of the inner ear has been demonstrated to produce deficits in spatial memory and cognition. These deficits manifest as an inability to navigate in complex settings (such as supermarkets), and loss of ability to use spatial information (such as map reading). These cognitive deficits have been associated with an increased incidence of anxiety and depression. The aim of this research is to determine if there is a difference between the effects of constant chronic inner ear damage, and fluctuating damage as seen in Meniere’s disease and benign paroxysmal positional vertigo. This will contribute to a better understanding of the symptoms that patients with vestibular disorders experience, and suggest ways that such symptoms might be treated effectively.