Community Scoop

Neurological Foundation Announces December 2011 Grant Round

Press Release – Neurological Foundation of NZ

The Neurological Foundation announced today that funding of over $1.2 million for neurological research and educational scholarships has been approved in its December 2011 grant round. The Neurological Foundation is the primary non-government sponsor …PRESS RELEASE
For immediate release: 9 December 2011
Neurological Foundation Announces December 2011 Grant Round Recipients

The Neurological Foundation announced today that funding of over $1.2 million for neurological research and educational scholarships has been approved in its December 2011 grant round. The Neurological Foundation is the primary non-government sponsor of neurological research in New Zealand.

Neurological Foundation Executive Director Max Ritchie says “This grant round showcases the breadth of world-class neurological research being carried out at universities and research institutions across New Zealand. It’s thrilling for us to be able to sponsor innovative, high-quality research in the four main centres, and across such diverse and important research areas. Equally pleasing is the high 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.”

In this round, the Foundation awarded six project grants, two Neurological Foundation Postgraduate Scholarships, the Neurological Foundation Postdoctoral Fellowship, the Neurological Foundation Repatriation Fellowship, one travel grant and two summer studentships. The total funding granted in this round is $1,230,184. Research areas granted funding include developing stem cells from adult human skin, memory loss in neurodegenerative disease, childhood neurodegenerative disease, fish oil and brain performance, stroke rehabilitation using magnetic brain stimulation, neurological speech disorders, and aiding memory after brain injury,

Hawkes Bay-born Dr Erin Cawston has been named the 2011 Neurological Foundation Repatriation Fellow and will return from her position as Research Fellow at the Mayo Clinic Arizona to further her research into Huntington’s disease in the Department of Pharmacology at the University of Auckland. 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 in February.

The Neurological Foundation is the primary non-government sponsor of neurological research in this country. The 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.

Research grants totalling $1,230,184 were approved by the Neurological Foundation Council on 2 December 2011.

For students who have already completed an Honours or Masters degree to allow them to undertake a PhD course at a New Zealand university.

MicroRNA regulated in dentate gyrus granule cells following LTP induction in vivo
Brigid Ryan, Department of Anatomy
University of Otago, $102,600

Memory impairment is a common feature of neurodegenerative conditions such as Alzheimer’s disease. It profoundly affects wellbeing and has a huge impact on society. Accordingly, understanding the molecular mechanisms that underlie memory function and dysfunction is a major focus of neuroscience research. While the way in which the brain stores memories is not yet fully understood, it is known that long-lasting enhancement in chemical signaling between two neurons called long-term potentiation (LTP) is a key component in memory. Maintenance of memory through LTP depends on new gene expression. Newly discovered molecules termed microRNA are thought to contribute to control of LTP-regulated gene expression. The objective of this research is to investigate the changes in microRNA expression that occur during the late phase of LTP. This research will enhance our understanding of long term memory and may lead the way to new treatments for memory loss.

Lysosomal function in childhood neurodegenerative disease
Nicole Neverman, Department of Biochemistry
University of Otago, $102,600

To maintain health, cells must constantly renew used components. This is achieved primarily by the lysosome, an acidic intracellular organelle containing over 50 enzymes which digest and recycle cellular waste. Dysfunctional lysosomes contribute to a wide variety of diseases including a group of childhood brain disorders known as Batten disease. Children suffer progressive blindness, cognitive deficits, vegetative state and premature death and there are no effective treatments currently available. This study will determine the function and effects of mutations in one form of Batten disease and test the effectiveness of gene therapy in affected neurons.
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.

Perceptual training for the management of neurological speech disorders
Stephanie Borrie, Department of Communication Disorders
University of Canterbury, $122,000

Fellowship will be undertaken at the Department of Speech and Hearing Sciences, Arizona State University and Mayo Clinic Arizona.

Neurological diseases such as Parkinson’s disease and stroke are often characterised by speech which is difficult to understand (dysarthria). Speech therapy to help those with dysarthria traditionally focuses on improving the speech of the patient. However, recent collaborative research between Dr Borrie at Canterbury University and Dr Julie Liss from Arizona State University has demonstrated that people can be trained to better understand this difficult speech. This opens the door to the concept of training the partners or caregivers of those with dysarthria to better understand their speech. Dr Borrie will spend two years in Dr Liss’ department furthering this new approach; specifically examining how improved understanding of dysarthric speech is influenced by ageing and by information provided in the speaker’s face. This research will advance the development of a novel treatment approach that improves understanding of dysarthric speech.

Repatriation Fellowships are intended to support the repatriation of outstanding young researchers who have recently completed postdoctoral studies outside New Zealand and who propose to return to New Zealand and conduct research in scientific fields of relevance to the Neurological Foundation.

A two-pronged approach to improving the development of novel therapies for Huntington’s disease.
Dr Erin Cawston, Department of Pharmacology
University of Auckland, $89,500

Dr Cawston will return to New Zealand from her position as Research Fellow in the Department of Pharmacology and Experimental Therapeutics at the Mayo Clinic Arizona.

Huntington’s disease (HD) is a hereditary genetic disorder of the brain that involves symptoms of disturbed movement, mood and mental processes. There is no treatment. This project will take two approaches to improving the development of novel therapies for HD. Firstly, to examine the signaling pathways of the specific receptors in HD cell lines to optimise their neuroprotective effect on cells. Secondly, to develop a new human cell model of HD toxicity for further studies into the mechanism of toxicity and potential drug screening.

Effect of ghrelin on activity of neurons in the brain reward system and on their response to predicting cues in normal and Parkinson’s disease models.
Associate Professor Brian Hyland, Department of Physiology
University of Otago, $168,219

People with Parkinson’s disease can suffer weight loss that is treatment-resistant, and which may relate to changes in the activity of brain systems concerned with the rewarding aspects of food. Ghrelin, originally identified in the stomach, has effects in the brain which modify appetite and has been proposed as a possible therapy for weight loss. However, little is known about how ghrelin interacts with the brain’s food-reward system. This research will for the first time investigate the effect of ghrelin on the responses of brain cells to food-related stimuli in the normal brain and in a model of Parkinson’s disease.

Can genotype affect the brain’s response to omega-3 supplementation?
Associate Professor Welma Stonehouse, Institute of Food, Nutrition and Human Health
Massey University, Albany, Auckland, $15,556

There may be more behind the metaphor ‘food for thought’ than just creative thinking. The human brain is the most lipid-rich organ in the body, only surpassed by the body’s fat stores. Omega-3 fats, found in fatty fish, are one of the predominant lipids in the brain and play a vital role in brain structure and functioning. Our genetic makeup may also influence the processing of fats by the brain and the brain’s response to fat, which may affect brain function. This study will investigate the interaction between our genes and an omega-3 fatty acid supplement (fish oil) on brain performance.

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.

Optimising brain stimulation to promote motor learning
Dr Jonathan Shemmell, School of Physical Education and Department of Anatomy
University of Otago, $175,405

Although magnetic brain stimulation is a promising tool for enhancing rehabilitation of stroke survivors, we do not know enough about how this type of stimulation interacts with normal brain processes. This project will determine the effect of magnetic brain stimulation on individual synapses in the brain cortex and subsequently identify the nature of interactions between magnetic brain stimuli and motor learning in humans. This work will help us to understand how brain stimulation might be best applied to assist the learning of new skills and the recovery of movement following damage to the brain caused by stroke.

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.

Optimising the use of anti-psychotic agents for multiple sclerosis
Professor Anne La Flamme, School of Biological Sciences
Victoria University of Wellington, $158,007

Multiple sclerosis (MS), which affects one in every 1400 New Zealanders, is a disease characterised by immune-mediated nerve degeneration. Symptoms may include difficulty moving; difficulties with coordination and balance; problems in speech (dysarthria) or swallowing (dysphagia), and visual problems. Immune cells are responsible for the damage to the nerves and subsequent clinical features of MS. There is no cure, and while disease-modifying drugs are available, they are often effective in only a subpopulation of MS patients. Recently Professor La Flamme’s laboratory has found that a commonly used anti-psychotic drug is effective at modifying MS in a mouse model of the disease. This project investigates the potential of this drug to treat MS.

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.

Randomised controlled trial of memory aids after traumatic brain injury
Hannah Bos, School of Psychology
Massey University, Wellington, $10,988

After brain injury, people frequently have difficulty remembering to perform planned actions at the appropriate time. This creates difficulties in daily life – forgetting to attend appointments and complete tasks, with the person often becoming dependent. This research will compare the effectiveness of two forms of memory aids in a randomised controlled trial: paper-based memory notebooks that have traditionally been used will be compared to providing reminders using smartphones. Despite much interest in using smartphones, to date little systematic research has been done in this area. This study will guide clinicians in providing the best available rehabilitation after brain injury.


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.
Cellular effects of novel anti-addiction compounds
Leigh Walker, School of Biological Sciences
Victoria University of Wellington, $4,000

Addiction to drugs of abuse is a disease which has major social, health, crime and monetary costs to society. While some therapeutic drugs are available to help stop smoking, such as nicotine patches, there are no therapeutic drugs available to help stop drug addicts who crave psychostimulants such as methamphetamine (P), cocaine or amphetamine. This study will investigate the cellular action of compounds that possess pre-clinical anti-addiction effects. This study aims to develop better, more effective anti-addiction compounds.

Content Sourced from
Original url