Neurological Foundation awards over $1,020,000 in December 2010 grant round
The Neurological Foundation of New Zealand has today announced research grants, travel grants, fellowships and scholarships totalling more than $1,020,000 for its December 2010 funding round. This allocation brings the Foundation’s total neurological research and training funding for 2010 to over $2,000,000.
In this round, the Foundation awarded four project grants, two Miller PhD Scholarships, one Philip Wrightson Postdoctoral Fellowship, a one-year extension to the 2008 Philip Wrightson Fellowship recipient, one travel grant and two small project grants.
Executive Director Max Ritchie says “The calibre of applications was incredibly high - a sure reflection of the world-class neuroscience research being undertaken at universities and hospitals across the country. We’re thrilled to be able to fund crucial research at this level. Equally pleasing is the record number of young investigators applying for fellowship and scholarship grants in this round. The Foundation has supported career neuroscientists for nearly 40 years, so it is vital that we continue to nurture the talents of emerging scientists who have a passion for neuroscience.”
The first and largest incidence and outcome study of transient ischemic attack (TIA) in New Zealand is one of the four successful project grants. Neurological Foundation Chair of Clinical Neurology Professor Alan Barber will lead the study, which has great potential to play a central role in the planning of services and development of health policy in relation to TIA and stroke, both in New Zealand and internationally, and could be used to inform evidence-based recommendations for health care. TIA heralds the onset of stroke in a quarter of the 8,000 New Zealanders struck down with this devastating illness every year.
Jessie Jacobsen, nearing the completion of her two-year Philip Wrightson Fellowship awarded by the Neurological Foundation in 2008, has been granted a one-year extension to enable her to continue her research into Huntington’s disease at Massachusetts General Hospital and Harvard Medical School in the United States. Dr Jacobsen received the MacDiarmid Young Scientist of the Year Award in 2007 for her research into Huntington’s disease, and the University of Auckland’s Young Alumna of the Year 2010, and has been working in the laboratory of noted scientist Professor Marcy MacDonald at Harvard’s Centre for Human Genetic Research.
Mr Ritchie says still more investment needs to be made in neuroscience in this country. “In many areas of neurological research, including the exciting translation into clinical practice, New Zealand scientists are leading the way. There is an urgent need to maintain this level of research and a diminishing number of funding avenues for scientists. The Neurological Foundation will continue to promote and support neurological research at the highest level, and our objective for 2011 is to further increase our funding allocations so even more deserving research can be undertaken.”
Grant round December 2010 recipients:
For students who have already completed an Honours or Masters degree to allow them to undertake a PhD course at a New Zealand university.
Response control in Parkinson’s disease
Hayley MacDonald, Department of Sport and Exercise Science
University of Auckland, $100,224
About one to two percent of people over the age of 60 in New Zealand have Parkinson’s disease (PD), and although there are drugs designed to slow disease progression, these therapies need to be applied as early as possible in the disease process to be beneficial. This project aims to provide clinicians with a simple method to measure response control for early identification and monitoring of patients who may benefit from therapies for PD. It will also use non-invasive magnetic brain stimulation techniques to target areas of the brain to potentially improve response control in PD patients.
Autoregulatable gene expression in rat models of Parkinson’s disease
Jerusha Naidoo, Department of Pharmacology and Clinical Pharmacology
University of Auckland, $100,224
A major hurdle limiting widespread application of gene therapy in humans is the inability to target production of therapeutic protein to only diseased cells. Researchers in the Department of Pharmacology and Clinical Pharmacology at the University of Auckland have designed a novel gene regulation system that senses cell stress and switches on and express a therapeutic gene only in those cells at risk. This project will test whether this system can control expression of parkin, a neuroprotective molecule, at a level in stressed cells sufficient to prevent neuronal cell death and motor deficits in laboratory models of Parkinson’s disease. This system could limit the side-effects typically seen with traditional Parkinson’s disease pharmacotherapies.
Philip Wrightson Fellowships
For researchers who have completed a PhD and wish to develop their research careers. This work can be undertaken at either New Zealand or overseas universities or hospitals.
Stem cell production and molecular characterisation of a sheep model of Huntington’s Disease
Jessie Jacobsen, Department of Neurology
Massachusetts General Hospital and Harvard Medical School, $35,000
Extension of one year to existing Philip Wrightson Fellowship awarded in December 2008.
Huntington’s disease (HD) is a fatal, inherited neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. The ultimate goal of this research is to develop a treatment for Huntington’s disease (HD). The generation of transgenic sheep expressing the mutant HD gene has provided a unique tool through which researchers can help understand the underlying disease processes before cell death has occurred. Six sheep lines expressing the human HTT gene have been generated by the University of Auckland and initial molecular and neurochemical analysis demonstrate early disease changes that mimic HD. The animal husbandry is carried out at The South Australian Research and Development Institute (SARDI), however, the project is led by Professors Richard Faull and Russell Snell at the University of Auckland in New Zealand.
In collaboration with The University of Auckland, Dr Jacobsen has been undertaking her Philip Wrightson Fellowship at the Center for Human Genetic Research (CHGR) at Massachusetts General Hospital (MGH), working in a team that has been generating a well-characterised panel of cell lines from the HD transgenic (and normal) sheep that will serve as a permanent resource for the HD research community. This cell lines will also provide valuable insights into disease processes and will be used as a platform for cell-based assays to search for cures for HD. This postdoctoral fellowship extension will allow Dr Jacobsen to continue to advance this work, using state of the art technology in the MacDonald laboratory at MGH.
The effects of repetitive transcranial magnetic stimulation on swallowing neurophysiology
Phoebe Macrae, Department of Communication Disorders
University of Canterbury, $136,854
Fellowship will be undertaken at the Department of Physical Medicine and Rehabilitation, John Hopkins University.
Many patients who survive a stroke or other neurological damage are unable to eat or drink independently due to difficulty swallowing: instead they are reliant on a tube through the nose or stomach for nutrition. There are treatments for disordered swallowing, but clinicians cannot be confident in the outcomes that will be achieved, due to the lack of evidence in swallowing rehabilitation research. This study will investigate the effects of a novel treatment on swallowing recovery. The treatment alters the communication from the damaged parts of the brain during swallowing, therefore facilitating communication from the intact brain regions with the swallowing muscles.
Auckland Transient Ischemic Attack Study
Professor Alan Barber, Neurological Foundation Chair of Clinical Neurology,
Department of Medicine, Auckland City Hospital, and Faculty of Medical and Health Sciences, University of Auckland, $89,103
Of the 8,000 New Zealanders who have a stroke each year, a quarter will have previously experienced a transient ischemic attack (TIA). TIA is important as it indicates an increased risk of stroke and provides a window of opportunity for prevention. Little is known about the numbers of people having a TIA, or their outcomes and risk of stroke. In an age of aggressive stroke and heart disease risk factor management New Zealand is an ideal place to carry out this research because local researchers have a vast experience in performing these ‘incidence studies’ and because of our ethnically diverse population. This research aims to perform their first and largest TIA incidence and outcome study in New Zealand. Outcomes from this study will play a central role in the planning of services and development of health policy in relation to TIA and stroke, within New Zealand and internationally, and to inform evidence-based recommendations for health care.
Anatomy of the GABAergic synaptic innervation to dopaminergic neurons in the circuitry of non-reward: a three-dimensional ultrastructural study of somal intervention
Associate Professor Dorothy Oorschot, Department of Anatomy and Structural Biology
University of Otago, $182,739
The relation between the anatomy of neural circuits and their functions is central to understanding information processing in the brain. Dopaminergic neurons in the midbrain, a brain region responsible for the refinement of behaviour, have key roles in reward processing, learning and memory, and movement. Their dysfunction is implicated in a number of disorders, including Parkinson’s disease, schizophrenia and drug addiction. Aversive or negative stimuli alert neurons expressing the inhibitory neurochemical GABA in the midbrain to stop dopamine neurons firing, causing the animal to react appropriately to the stimulus. How this happens is poorly understood. The researchers will measure the structural and functional connectivity within the midbrain in a laboratory model. Single GABA-expressing neurons in the midbrain will be filled with a marker. Their connections onto dopamine neurons in the midbrain will be three-dimensionally mapped and analysed. These results will improve our understanding of how brain microcircuitry controls behaviour and contributes to neurological conditions.
Regulating macrophage and microglian effector functions during neuroinflammation
Professor Anne La Flamme, School of Biological Sciences
Victoria University of Wellington, $69,291
Multiple sclerosis (MS) is a disease characterised by nerve degeneration caused by a misguided attack by the immune system. MS may involve impaired vision, coordination and paralysis and affects one in every 1,500 New Zealanders. Although some treatments are available to help manage the disease, these treatments are not equally effective in all MS patients, and approximately 70 per cent do not respond well. Because MS is immune-mediated, the researchers propose to investigate one type of immune cell involved in causing neurological damage in the hope of identifying new targets and approaches to treat MS. Specifically, this project will determine how altering macrophages and microglia (brain-resident immune cells) can regulate the development of inflammation and damage in the central nervous system. (Macrophages are cells that act as the body’s first line of defence, and can recognise and engulf foreign substances.)
An examination of microRNA expression abnormalities as a result of maternal immune activation: a search for epigenetic abnormalities associated with increased risk for schizophrenia development
Dr Kathie Overeem, Departments of Anatomy and Structural Biology and Psychology
University of Otago, $190,352
Schizophrenia is a seriously debilitating neuropsychiatric disorder characterised by a number of deficits in thought and cognitive processing. It is thought that these symptoms are underpinned by altered gene expression in the brain that is caused, in part, by environmental events. Epidemiological research has demonstrated that maternal immune activation (infection during pregnancy) increases the risk of offspring developing schizophrenia in adulthood. In this study, the researchers will use the maternal immune activation model to examine the relationship between microRNA expression profiles in the brain and the expression levels of their putative gene targets as a result of this environmental event. This work will contribute to our understanding of the changes in the brain associated with increased risk of schizophrenia.
SMALL PROJECT GRANTS
Mechanisms of direct and indirect neuromodulation of tinnitus perception
Dr Grant Searchfield, Department of Audiology, School of Population Health
Tamaki Campus, University of Auckland, $9,164
Tinnitus (the phantom perception of sound) affects the quality of life of an estimated 400,000 New Zealanders. This research will examine the processes underlying tinnitus, and its treatment, by investigating the changes that occur following the use of hearing aids combined with low level electrical stimulation of the brain (transcranial Direct Current Stimulation [tDCS]). It is believed that tDCS will prime the auditory system for positive change that can be exploited by hearing aid use. This research may lead to an enhanced tinnitus treatment while at the same time allowing us to probe the mechanisms of tinnitus.
The genetic basis of Spinocerebellar Ataxia type 30 (SCA30)
Professor Robert Gardner, Dunedin School of Medicine
University of Otago, $9,750
There is a group of inherited brain disorders called the ‘spinocerebellar ataxias’. These mostly (but not always) come in adult life, and slowly progress, with increasingly disabling neurological symptoms: difficultly with balance, with coordination of movements, and with speech. Understanding the cause could pave the way to a treatment. About 30 different types are known, each due to a different gene. The researchers have studied a family with a type called SCA30, and believe they have identified the gene that causes it but need to confirm this by proving that the suspected gene operates at only ‘half-strength’.
Patterns of α-MSH-induced Neuronal Activation in the Pregnant Rat Brain
Erynne Scherf, Department of Anatomy and Structural Biology
University of Otago
During pregnancy, appetite is increased as the mother is “eating for two”. In fact, mother eats more than required for fetal growth, resulting in increased fat. This increased energy store helps the mother prepare for the future metabolic demands of lactation, and requires changes in the brain mechanisms that normally regulate eating. Such increased weight gain, however, also contributes to rising levels of obesity during pregnancy, which increases chances of obstetric complications. The aim of this study is to enhance understanding of neuroendocrine mechanisms controlling appetite during pregnancy, by measuring changes in neuronal activation in response to anorectic neuropeptides. (α-MSH is a hormone.)
Does depression predict conversion from mild cognitive impairment to dementia?
Nathan van Rij, Psychiatry Service for the Elderly, Older Persons Health Specialist Services
Canterbury District Health Board
‘Mild Cognitive Impairment’ (MCI) is a label given to the group of people who experience a definite, but relatively minor, decline in their cognitive abilities over time (such as memory). These people are at high risk of going on to develop a dementia such as Alzheimer’s disease – about half will convert over two years. A recent study indicated that MCI is more likely to progress to dementia if it occurs with depression. This study seeks to replicate this important finding in a sample of people diagnosed with MCI in Canterbury.