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Auckland Medical Research Foundation Awards close to $4.5m

Auckland Medical Research Foundation Awards close to $4.5m to Medical Researchers

The Auckland Medical Research Foundation (AMRF) has recently announced $3,064,496 in funding to medical researchers in the final three funding rounds for 2013, raising the distribution of grants in 2013 to $4.48m.

Foundation Executive Director, Kim McWilliams says, “More research is the only way we can ensure genuine advances in medicine and outcomes for patients. From our beginnings, we have promoted research of high scientific value and purpose across the full spectrum of medical science. This round we acknowledge Guardian Trust, a strategic partner that has enabled us to distribute more funds to the research sector this year ”.

The successful grants included 12 research projects ($1,340,308), 4 Doctoral Scholarships ($504,000) 2 Postdoctoral Fellowships ($382,640), 1 Ruth Spencer Medical Research Fellowship, ($257,333), 1 Sir Harcourt Caughey Award $20,294), 2 Jean Cathie Tinnitus Research Awards ($165,484), 7 travel grants ($18,000) for researchers to present their research overseas and 1 Goodfellow Repatriation Fellowship ($376,437). Grants were awarded over a variety of medical and clinical research areas including cell biology; nutrition; tinnitus; pre-term birth complications; bone and joint diseases; cancer; kidney disease; exercise following heart attack; and neurodegenerative diseases.

See Below for Project Summaries

The Auckland Medical Research Foundation is a major independent funding agency and charitable trust that provides contestable funding for medical research across the complete spectrum of modern medicine. Over the last 58 years we have distributed over $50 million in funding to a wide range of research activities – currently around $3-4 million annually.

Our Foundation is unique in the charity sector, in that every dollar donated from within the community goes directly and fully (100%) to research. Our administration costs are generously supported by a benefactor.

For further information on the current grants awarded and application forms for future grant rounds see our website at


URATE AND BONE ($157,475 – 2 years) 1113015
A/Prof Nicola Dalbeth, Dr Jacquie Harper, Prof Jillian Cornish
Dept of Medicine, University of Auckland

Elevated urate levels in the blood are present in approximately 20% of the adult population. Recent observational studies have reported that high urate levels are protective in the development of thin bones (osteoporosis) and fractures. This laboratory study aims to understand how urate exerts this protective effect. We will study the effects of urate on the function of bone-forming cells (osteoblasts) and cells that control the breakdown of bone (osteoclasts). We will also study the effects of medications that reduce urate levels on bone structure. If urate does indeed directly act on bone cells to increase bone density and reduce fracture risk, these observations may have important clinical implications in guiding blood urate targets in people treated for gout (the most common form of inflammatory arthritis), understanding patterns of bone disease in people with gout, and, in the long-term, identifying new therapeutic strategies for prevention of osteoporosis.

OXYGEN IN DISEASE KIDNEYS ($160,000 – 2 years) 1113016
Prof Simon Malpas, Dr Maarten Koeners
Dept of Physiology, University of Auckland

Kidney disease is a growing global public health problem. Low tissue oxygen and kidney disease are associated although the mechanisms responsible and their time course are ill-defined. We hypothesize that low oxygen levels in the kidney is central in the pathogenesis of kidney disease. This project will examine how and when low oxygen levels in the kidney can play a major role in driving disease progression and whether improving kidney oxygenation can prevent kidney disease. Investigation of kidney oxygen regulation has been hindered because of an inability to measure tissue oxygen for long periods of time. Using our world first technology which allows wireless measurement of kidney tissue oxygen in unrestrained rats we have solved this problem. We will investigate, using this technology and unique expertise, the sequence of events that lead to reduced kidney tissue oxygen in kidney disease. We aim to identify when and which mediators/controllers of long-term regulation of kidney oxygen precedes and/or is a prerequisite for the progression of disease. This will reveal causation that will assist in optimising the appropriate, and novel, treatment strategies. We believe this will ultimately have a major impact in clinical practice, making it a very promising and timely subject

Dr Donald Love, Dr Jonathan Skinner, Dr Ivone Un San Leong
Diagnostic Genetics, LabPlus

Congenital long QT syndrome and hypertrophic cardiomyopathy are life-threatening cardiac disorders that are the most common causes of sudden death in 1 – 40 year olds in New Zealand, with an incidence of 1 in 4,500 and 1 in 500, respectively. These diseases commonly present in childhood and young athletes, and are characterised by unexplained fainting episodes and dangerously fast heart rates that could cause sudden death. The genotyping of patients with these disorders has greatly assisted both with family screening and individualizing clinical management. The current sequence-based screening strategy for mutations in patients is labour intensive. Critically, developments in Massively Parallel Sequencing (MPS) technology has made it possible to screen scores of genes for mutations, or the entire coding potential of the human genome (termed whole-exome sequencing, WES), in parallel. This project will establish MPS technology in the clinical diagnostic arena of New Zealand (with a focus on cardiac disorders), and will therefore improve the current method and provide an enhanced national service for patients.

THE SYNAPTIC BASIS OF AUTISM ($21,048 – 1 year) 1113018
Dr Charlotte Thynne
Dept of Physiology & Centre for Brain Research
University of Auckland

Autism Spectrum Disorders are complex disorders that are diagnosed based on behavioural symptoms including social and cognitive impairments, communication difficulties and repetitive behaviours. Interestingly, many of the genes that have been implicated in Autism encode proteins found at excitatory synapses in the brain. These include genes which encode postsynaptic scaffolding proteins as well as presynaptic calcium channels and calcium dependent mechanisms. This work aims to determine if there is a functional sub-cellular link between postsynaptic scaffolding proteins and presynaptic calcium channels, which could explain the shared features observed in Autism patients carrying mutations in the genes which encode these separate entities. Using electrophysiology techniques, I will examine how ProSAP2, a postsynaptic scaffolding protein implicated in Autism, regulates presynaptic calcium channel function and how autism-associated mutations in this protein affect this regulation. These experiments have the potential to determine how the function and plasticity of excitatory synapses may be disrupted in Autism, leading to interference with cognitive function and behaviour.

ACELERATED BEP STUDY ($59,105 – 2 years) 2113019
Dr Fritha Hanning, Dr Peter Fong, Dr Reuben Broom
Auckland Regional Cancer & Blood Service, Auckland City Hospital

Testicular cancer and closely related cancers called germ cell tumours are the most common cancer in men aged 16 to 45. Despite this, it receives very little attention or publicity, in part due to an understandable reluctance of men in this age group to discuss their cancer journeys. Thankfully for those men who are able to detect their cancer early, there are excellent outcomes with treatment ranging from 98-99% cure rates for men with stage one disease (confined within the testicle) to 90-95% for men with good prognosis metastatic cancer (cancer which has spread to other parts of the body). Unfortunately for men whose disease is more extensive and aggressive, there is still a significant chance of dying from the cancer. The research study ‘Accelerated BEP’ aims to improve outcomes for men whose cancer was not diagnosed before it reached this more serious stage. It is looking at whether changing the timing of an established chemotherapy treatment will improve survival. A positive outcome from this study would mean an increased cure rate for this group of young men and an increased chance of them living full and productive lives.

A/Prof Ralph Maddison, Dr Robyn Whittaker, Dr Anna Rolleston, Hon Prof Ralph Stewart, Dr Nicholas Grant, Dr Ian Warren, Mr Jonathan Rawstorn
National Institute for Health Innovation, School of Population Health, University of Auckland

Exercise is essential to aid recovery from a heart attack, however adherence to regular exercise is low. In this trial we will compare the effectiveness of home-based monitored exercise using mobile phones and monitoring technology to existing supervised exercise cardiac rehabilitation. 230 participants will be allocated at random to 12 weeks standard supervised exercise cardiac rehabilitation or to the new mobile phone programme. Assessments will compare physical fitness, and change in risk factors associated with heart disease between the two groups. This approach has potential to improve the delivery of cardiac rehabilitation services in New Zealand for those who need it.

Dr Justin Dean
Dept of Physiology, University of Auckland

The white matter regions of the brain are important for transferring signals between different brain structures. For rapid movement of these brain signals, cells in the white matter called oligodendrocytes produce an insulating material called myelin. In preterm born babies, oligodendrocytes show a particular vulnerability to injury resulting from low brain blood flow, leading to loss of myelin and cerebral palsy, a devastating lifelong movement disorder for which there is no cure. Therefore, there is a need for new therapies. In humans, although oligodendrocytes are easily killed, we now know that they rapidly grow back. Strikingly, for unknown reasons these new oligodendrocytes fail to properly mature, and do not produce myelin, in areas of injury. We have new evidence that a molecule called hyaluronan is highly up-regulated in preterm ischemic white matter injury, and that hyaluronan may be the cause of failure of oligodendrocytes to produce myelin. In this proposal, we will examine how hyaluronan triggers myelin deficits in the preterm brain. This new knowledge will further our understanding of the causes of cerebral palsy in preterm infants, and determine whether blocking hyaluronan is a potential treatment strategy in this large group of children.

SHON RECEPTOR IDENTIFICATION ($159,960 – 2 years) 1113022
Dr Dong-Xu Liu, Dr Christopher Squire
Liggins Institute, University of Auckland

Breast cancer is a major health issue, being the most common malignancy and the leading cause of cancer deaths among New Zealand women. Each year approximately 3,000 women are diagnosed with breast cancer and more than 650 die from the disease. We have identified a novel secreted oncoprotein, called SHON, in the blood. SHON plays an important role in breast cancer. Its expression status in breast tumours predicts the response of patients to anti-estrogen therapies. We will identify the mechanism by which SHON regulates cellular function by finding proteins to which it binds and signalling pathways that it activates. These studies will provide an important contribution to our understanding in the area of secreted oncogenic proteins and is likely to lead to better treatment for breast cancer in the future.

Dr Anthony Phillips, Dr Cherie Blenkiron
School of Biological Sciences, University of Auckland

The use of maggots for a medicinal purpose is age-old. The maggots, from the green bottle blow-fly, secrete a potent cocktail of molecules which kill infecting bacteria, digest away dead tissue and even directly promote wounds to heal. We intend to look at the activity of maggot secretions on a range of target cells to give us a greater understanding of its biological effects. With better understanding of its bioactivity we hope to exploit specific components for use in the clinic as new classes of treatment for a range of surgical wounds.

A/Prof David Christie, A/Prof Nigel Birch
School of Biological Sciences, University of Auckland

This is produced by mitochondria, organelles that act as the power generator. Many neurodegenerative diseases have an energy deficit due to a loss of mitochondrial function. As a result, agents that promote mitochondrial activity have the potential to protect neurons. Creatine, a commonly used dietary supplement, is one such molecule as it enhances and maintains cellular energy levels. To be effective creatine must first be taken up into neurons and then be converted to phosphocreatine. These processes require a group of creatine system proteins. In this research we will investigate how the levels of creatine system proteins are controlled and how they contribute to the energy levels and function of neurons. If ways can be found to up-regulate creatine system proteins this may lead to new strategies to enhance the neuroprotective effects of creatine for the treatment of human neurodegenerative diseases.

Dr Maurice Curtis, Prof Richard Faull
Centre for Brain Research, University of Auckland

Alzheimer’s disease (AD) causes severe memory loss and progressive dementia that directly affects 48,000 people in New Zealand and has a significant impact on the lives of a further 300,000 people in New Zealand. What causes this devastating disease is currently unknown in most instances with only approximately 10-15% of cases having an obvious genetic susceptibility. In brains affected by AD there is major cell death in the temporal and frontal lobes, however 8-10 years before this is evident the olfactory system (the smell centre) has already suffered significant cell death. To overcome the problem of major cell loss in AD, it will be important to intervene early before major cell loss has occurred but to date the major studies of AD have focussed on end stage disease and not the initial brain changes. In the current project we aim to study the human olfactory system (where the disease begins), to determine what cell type are affected the most and to compare it with the textbook regions where damage occurs in AD. We will identify the earliest changes that occur in AD in the hope that future treatments might be helpful before depletion of brain cells has occurred in the brain.

A/Prof James Paxton, Dr Zimei Wu, Dr Yan Li
Dept of Pharmacology & Clinical Pharmacology, University of Auckland

A major factor responsible for the failure of chemotherapy in pancreatic cancer is the development of multi-drug resistance due to up-regulation of various efflux pumps in the cancer cells. The latter can efficiently remove the drug from the cell, thus causing the drug to lose its effect. Our aim is to investigate a novel bi-functional liposomal delivery system which contains the anticancer drug plus curcumin, an inhibitor of the efflux pump. This combinational liposome will more effectively target and retain the active drug within the cancer cell, thus overcoming multidrug resistance, and also minimising any toxic side effects.


MATERNAL THERAPY AND THE FETUS ($126,000 – 3 years) 1213003
Mr Christopher Lear
Dept of Physiology, University of Auckland

Brain injury after preterm birth now contributes more than a third of all cases of cerebral palsy. We now know that even babies born prematurely without brain injury have a high risk of long-term disability and learning difficulties. Mothers who are about to deliver prematurely are almost universally given treatments such as steroids and magnesium sulphate to reduce the risk of death and many newborn complications after preterm birth. Given how often our youngest and most vulnerable infants are exposed to these treatments, it is vital to understand their effects on the preterm brain. We have recently shown that a clinical course of maternal steroids triggers transient abnormal brain activity in preterm animals, and can worsen injury during exposure to low oxygen levels. The long-term effects are unknown. In this study, I will examine the long-term impact of exposure to maternal steroids on brain activity and structure, how timing of treatment affects the response to low oxygen, and finally, whether magnesium sulphate treatment can alleviate the adverse effects of steroids on the brain. This will be providing critical new information to help guide the clinical treatment of women at risk of preterm delivery.

Funded by: Barbara Basham Medical Charitable Trust – Guardian Trust

MOLECULAR IMAGING OF LENS CATARACT ($126,000 – 3 years) 1213004
Mr Mitchell Nye-Wood
School of Medical Sciences, University of Auckland

Cataract is primarily a disease of old age and Age-Related Nuclear (ARN) cataract is the leading cause of blindness in the world today. ARN cataract is characterised by irreversible protein modifications in the centre or nucleus of the lens. Antioxidants in the young lens usually provide protection against this oxidative damage but an age-dependent decline in antioxidants, specifically in the lens nucleus, allows damaged protein to accumulate, eventually leading to protein precipitation, loss of transparency and cataract formation. In this study we investigate the mechanistic link between the antioxidant decline in the lens nucleus, oxidative damage to lens proteins and the loss of lens transparency using an animal model of ARN cataract. To achieve this, changes in the distribution of antioxidants and oxidative damage to lens proteins will be spatially mapped using imaging mass spectrometry, a technique that can identify and localise small molecules and large proteins in tissue sections. The effect of these biochemical changes on lens transparency will then be determined by measuring the optical properties of lens. Our study of how antioxidant depletion specifically in the lens nucleus affects overall lens transparency, will aid our efforts to develop medical therapies to delay the onset of ARN cataract.

MESENCHYMAL STEM CELLS AND IUGAR ($126,000 – 3 years) 1213001
Miss Megan Alexander
Dept of Obstetrics & Gynaecology, University of Auckland

A healthy placenta is the cornerstone to a successful pregnancy and delivery of a healthy baby. Insufficient placental development can lead to life-threatening pregnancy disorders such as pre-eclampsia (hypertension in pregnancy) and intrauterine growth restriction (IUGR, small babies), which have lifelong consequences. We currently know surprisingly little about the pathophysiology of pregnancy disorders, and have no effective treatments to remedy these conditions. Recent trials in other organ systems have highlighted the therapeutic potential of mesenchymal stem cells (MSC) for a range of applications. In the placenta, MSC are present throughout gestation and may contribute to creating an adequate vascular network, which is key for fetal growth. Therefore, MSC provide a promising target to improve placental vascularisation in IUGR pregnancies. This project aims to explore this potential by determining how MSC may contribute to the pathophysiology of IUGR, and whether transplantation of MSC into placentae can stimulate placental angiogenesis via direct engraftment into the placental vasculature or by paracrine mechanisms. This proof of principle work will allow the future development of MSC as a therapy for failing placentae, helping improve the lives of around 5000 babies and their mothers affected by IUGR each year.

Mr Wojciech Ambroziak
Dept of Physiology & Centre for Brain Research, University of Auckland

Currently one in five New Zealanders are affected by neurological diseases and as the population ages this number will considerably increase. All neurological diseases have direct or indirect effects on synapses in the brain. This project is to determine the source of synapse dysfunction in Huntington’s Disease (HD). HD is one of the most debilitating, incurable adult onset disease with very dramatic course. Studies on HD mouse models have shown that an increase in NMDA receptors located outside of the synapse causes early synapse dysfunction that may underlie the cognitive and motor deficits seen in HD. A protein called SAP97 plays distinct roles in regulating receptor distribution within synapses, with aSAP97 regulating synaptic receptors versus bSAP97 regulating receptors outside of the synapse. Recent data suggest that this protein is a causative agent in the early pathogenesis of HD. The aims of this PhD project are to determine the role of each SAP97 isoform in the changes in NMDA receptor localisation in a cellular model of HD and if SAP97 isoform expression levels can be specifically targeted to rescue normal receptor distribution and synapse function in animal model, thus whether SAP97 isoforms are a potential therapeutic target.

Funded by: Henry Cotton Charitable Trust – Guardian Trust


Dr Natasha Grimsey
Centre for Brain Research, University of Auckland

Mental illnesses such as depression, bipolar disorder and schizophrenia affect around16% of New Zealanders. Most of these conditions are difficult to diagnose and treat effectively. Continued research is required to better understand these disorders and develop new medicines. The mind-altering properties of cannabis have been recognised for centuries, but the proteins in the brain that allow cannabis to exert its effects have only been identified in the last two decades. These proteins are called Cannabinoid Receptors 1 and 2, and as well as responding to cannabis these control many normal bodily functions. All the proteins in our bodies are produced from DNA blueprints. Slight differences in these instructions between individuals can result in subtly different versions of the same protein which might work differently. A few specific versions of Cannabinoid Receptor 2 are more common in patients suffering from mental illness than in the general population. This may indicate that these versions play a role in these diseases. In this research I plan to investigate what is different about the function of these versions of the Cannabinoid Receptor. This information will provide new insight into the causes of mental illness and may assist with designing new therapies.

Funded by: Edith C Coan Trust – Guardian Trust

Dr Clare Reynolds
Liggins Institute, University of Auckland

Unbalanced maternal nutrition, whether it be over-nutrition or under-nutrition, predisposes or “programs” offspring to obesity, type-2 diabetes and cardiovascular disease in later life. These conditions are associated with chronic low-grade inflammation, however little is known in regards to the impact of maternal diet-induced programming of the offspring immune system and its subsequent impact on metabolic function and indeed chronic disease later in life. We aim to investigate obesity-induced inflammation during pregnancy and subsequent long-term offspring disease in an established rat model of maternal diet-induced obesity. We will assess the origins of inflammation in mothers and offspring by characterizing inflammation in the placenta, bone marrow and cells of the immune system. Furthermore we will determine the effectiveness of the anti-inflammatory lipid c9, t11 conjugated linoleic acid (CLA) as a therapeutic option for the reversal of maternal over-nutrition induced developmental programming. This project will allow us to establish the importance of immune mediators in developmental programming of obesity and metabolic complications and potentially develop a viable anti-inflammatory nutrient based therapeutic strategy for combatting the origins of metabolic disease.

Funded by: David and Cassie Anderson Medical Trust – Guardian Trust

Dr Andrew Wood
Dept of Molecular Medicine and Pathology, University of Auckland

Acute Myeloid Leukaemia (AML) is a blood cancer that is frequently fatal despite intensive chemotherapy and stem cell transplantation. Spelling mistakes accumulate in the DNA instructions that control how a cell behaves with the result that white blood cells keep reproducing until they overtake the body leading to clinical symptoms. By sequencing leukaemias from many people we have built up catalogues that list the various spelling mistakes, but it is not always clear how to translate this knowledge into better treatments. In children with AML the gene ETV6 is frequently mutated, and although a lot is known about this gene in health and other cancers very little is understood about why it makes AML in children so hard to cure. In this research we aim to find out how ETV6 mutations work by introducing them into zebrafish. We hope the mutations will change the way leukaemias grows in fish, and that by studying this we will learn the leukaemia’s weak spot. Then we will use robots to treat thousands of zebrafish with thousands of drugs to see if any kill ETV6 leukaemia. If successful this study will identify compounds that can use to better treat ETV6 driven leukaemias in patients.

Dr Kathryn Williamson ($257,333 – 3 years) 1413002
Newborn Services, Auckland City Hospital

Babies who are born very preterm have a high risk of suffering brain damage. High blood sugar levels (hyperglycaemia) are common in these very small babies, and are associated with poor outcome. Hyperglycaemia is usually treated with insulin, but in very small babies the correct dose of insulin can be difficult to determine and babies’ insulin requirements can fluctuate over a short period of time. This means that sometimes the babies’ blood sugar level can fall too low (hypoglycaemia). Unfortunately, hypoglycaemia can put babies at further risk of brain damage. A computer program has been developed to help keep blood sugar levels in a safe range for preterm babies treated with insulin. We will determine if this computer program can reduce the incidence of hypoglycaemia, and also whether it improves growth and later development. If effective, this computer program will be incorporated into routine care of preterm babies in New Zealand and worldwide, potentially reducing the burden of brain damage after preterm birth.

Funded by: Ruth Spencer Estate – Guardian Trust

Dr Rebecca Mairs (20,294) 7713001
Department of Psychiatry, Waitemata DHB

To undertake a 6 month Eating Disorders Fellowship at the Feeding and Eating Disorders Service (FEDS) at Great Ormond Street Hospital.

Prof Paul Smith, Dr Yiwen Zheng
Department of Pharmacology and Toxicology, University of Otago

Tinnitus is a debilitating neurological disorder in which a person hears sounds that do not physically exist. Approximately 7% of the New Zealand population is estimated to suffer from tinnitus at least 50% of the time and the condition becomes more prevalent with age. Tinnitus substantially reduces the quality of life, resulting in an inability to concentrate and increased anxiety. Approximately 50% of tinnitus sufferers also suffer from depression. Unfortunately, there are few effective treatments. We have shown that receptors in auditory brain regions for chemicals known as ‘cannabinoids’, undergo changes during tinnitus. We therefore propose to test whether a cannabinoid drug known as ‘Sativex’, might be beneficial in the treatment of the disorder. First, we will determine whether it reduces the perception of tinnitus. Second, we will measure the way in which it alters brain activity in the brain regions which normally exhibit increased excitability during tinnitus. Since Sativex is already available for prescription in New Zealand, if we obtained evidence indicating that it could be useful in the treatment of tinnitus, this drug could potentially be used with a minimal delay.

Funded by: Jean Cathie Research Fund – Guardian Trust

Dr Grant Searchfield, Prof Dirk De Ridder, Dr Cathy Stinear, Prof Ian Kirk, Mr Giriaj Singh Shekhawat
School of Population Health, University of Auckland

Tinnitus (“ear and head noise”) is a highly prevalent condition affecting approximately 15% of the population. Severe tinnitus can lead to disruption of work, social activities and sleep; and lead to anxiety and depression. There is a pressing need for effective therapies to help solve this common problem. In the last decade there have been tremendous advances in our understanding of the mechanisms underlying tinnitus but effective treatments for tinnitus remain elusive despite these advances in knowledge. Tinnitus can be temporarily reduced or eliminated by sound stimulation and non-invasive brain stimulation but only in some people, some of the time. Tinnitus is complex; studies of brain activity indicate auditory, memory, attention and emotional parts of the brain work together to create tinnitus. These studies have led to a “Neurophysiological network” model of tinnitus. Recently an “Adaptation Level Theory” model of hearing has explained how memory, attention and emotion might contribute to tinnitus magnitude. The proposed research will examine how the two models of tinnitus interrelate. We will measure brain activity (Electroencephalography, EEG) and tinnitus loudness before, during, and after sound stimulation and non-invasive stimulation of different brain areas. The studies should identify new targets and means for treating tinnitus.

Funded by: Jean Cathie Research Fund – Guardian Trust


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