Previous Grants

The following grants were approved prior to July 2016

Project Grant

$146,396

Professor Tim Anderson University of Otago, Christchurch 2015 December

Tau imaging and cognition in Parkinson’s disease

Using new technology to determine how the accumulation of a protein in the brains of Parkinson’s disease patients affects cognitive decline

Most people with Parkinson’s develop cognitive problems and, in many cases, dementia. Suitable objective tools that measure the underlying brain changes that underpin this cognitive decline need to be identified.  These tools are important for both trials of new preventative treatments and for use in the clinic. This study will measure accumulation in the brain of an abnormal protein, tau, which is associated with the development of Parkinson’s dementia. Professor Anderson’s study will involve the use of tau PET scans in 70 people with Parkinson’s disease with varying cognitive problems including dementia to show how tau accumulation in the brain reflects degree of cognitive decline. Positron emission tomography scanning is a diagnostic tool that uses a tracer to illuminate specific proteins or cancer cells.  

Nid: 1409

Neurological Foundation Philip Wrightson Postdoctoral Fellowship

$156,484

Betty Kao Royal Children’s Hospital, Victoria 2015 December

Ms Kao will undertake her Neurological Foundation Philip Wrightson Postdoctoral Fellowship at the Royal Holloway, University of London in the United Kingdom. Ms Kao will be supervised by Professor George Dickson, who holds a Chair in Molecular Cell Biology and has spent most of his career studying neuromuscular disease and muscle cell biology. Following the completion of her fellowship Ms Kao aims to return to New Zealand and become a principal investigator of her own research group.

An investigation into the role of Rpl3l and regulation of ribosome biogenesis in the pathogenesis of Duchenne muscular dystrophy: implications for novel therapeutic strategies

Investigating the role of a protein called Rpl3l in the muscular changes of a Muscular Dystrophy model: a new treatment target may be identified 

Duchenne muscular dystrophy (DMD) is the most common fatal genetic disorder in childhood. It is caused by mutations in a gene called DMD that result in the absence of an important structural protein in muscle, called dystrophin. Absence of dystrophin results in progressive muscle weakness caused by pathological changes at the molecular level that are as yet poorly understood. A recent study revealed a protein called ‘Rpl3l’ may play a role in the pathological changes associated with DMD. Ms Kao’s fellowship aims to elucidate the role of Rpl3l in DMD and speculates that it could be targeted as a treatment for this devastating disease.

Nid: 1399

Project Grant

$11,500

Dr Megan Wilson University of Otago 2015 December

Sex-dimorphic brain development and disease: the role a non-coding RNA encoded within the Anti-Müllerian hormone locus

Shedding light on the nature of neurodevelopmental disorders depending upon the sex of the child

Susceptibility to many common neurological and psychiatric conditions differs and shows a dramatic sex basis – whether the person is male or female. Formation of the human brain during foetal development follows a slightly different path depending upon the sex of the child. These differences arise even before sex-hormones are produced. By determining how male and female sex impacts on the developing brain we hope to shed light on the nature of how sex differences to neurodevelopmental disorders arise.

 

Nid: 1410

Neurological Foundation Gillespie Postgraduate Scholarship

$104,095

Ruth Monk University of Auckland 2015 December

Modelling Huntington’s Disease: Using direct cell reprogramming to study the mechanisms underlying a complex genetic neurodegenerative disorder

Creating a model of Huntington’s disease from patient skin cells to further understand the underlying mechanisms and cell death involved in this disorder

Huntington’s Disease (HD) is a highly debilitating genetic neurodegenerative disorder which is characterised by the progressive loss of specific brain cells. What drives this specific cell loss remains largely unknown, and consequently there is no treatment for this disease. Ms Monk’s project aims to generate a model of HD by reprogramming skin cells from patients into the specific brain cell type lost in this condition. This model will provide a novel platform for elucidating the complex mechanisms contributing to brain cell death, and will play an important role in the development of treatments for HD.

Nid: 1400

Summer Studentship

$4,000

Niamh Hammond University of Otago, Wellington 2015 December

Recent onset transient or episodic headaches with concerning features: risk prediction, pre-test probability, and imaging selection

Differentiating patients with headache to identify serious and life-threatening brain bleeds 

Episodic headaches are a widely experienced complaint. While the majority are due to benign processes, some headaches can herald serious and life‐threatening diseases. One such cause is a type of brain bleed known as a subarachnoid haemorrhage that can present initially as a ‘sentinel bleed’. This research aims to investigate the proportion of patients presenting with transient headache and concerning features that are later confirmed to have these serious brain bleeds. This information will help to identify these patients so that they receive the appropriate scans and treatment in a timely fashion that reduces potential serious illness.

Nid: 1411

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