Latest Grants


Grants totalling $1,382,529 were approved by the Neurological Foundation Council on 1 December 2016.

Educational travel grants were awarded in addition to the below.  

Project Grant


Dr Scott Graham Department of Pharmacology and Clinical Pharmacology, University of Auckland December 2016

Which inhibitory immune checkpoint control proteins are expressed in human brain tumours?

Investigating a target for treatment of aggressive brain tumours


There is a clear and present need for better treatments for brain cancers. Immune “checkpoints” critically govern many aspects of our immune response to tumour cells, and are key regulators of T-cell activation, proliferation and function. T-cells are a subtype of white blood cells which play a key role in the immune system and in fighting cancer. Immunotherapies targeting the immune-checkpoint control axis are proving to be the greatest breakthrough for advanced melanoma and several other types of aggressive cancer. These molecules offer incredible potential in brain cancer to suppress the tumour cells or switch on the correct T cell responses. First however, we must understand the repertoire of their expression in brain tumours and identify those that represent the best targets; this is the aim of Dr Graham’s research project.  

Project Grant


Dr Karl Iremonger Department of Physiology, University of Otago December 2016

Imaging the activity of stress neurons in vivo

Using cutting-edge technology to image the activity of stress neurons in a mouse model

Excessive activation of brain stress circuitry results in high levels of stress hormones in our body, which can damage our body and brain. Our understanding of this circuitry has been limited as no study has been able to observe the activity of stress neurons in the intact brain. Using cutting-edge genetic and optical techniques, Dr Iremonger’s project aims to record the activity of stress neurons in freely behaving mice. Understanding how these neurons are regulated could lead to future tools that can be used to normalise stress neuron excitability in neurological conditions associated with high stress.

Project Grant


Professor Janusz Lipski Department of Physiology, University of Auckland December 2016

Preclinical efficacy of Uptake-2 blockers in augmenting dopamine production from levodopa: implications for treatment of Parkinson’s disease

Investigating the potential improvement of the effectiveness of a Parkinson’s disease drug by inhibiting a mechanism in a rat brain model

Parkinson’s disease is a brain disorder which affects 1-2% of people older than 65 in New Zealand and worldwide, leading to numerous symptoms including tremor in the hands, slowness of movement, stiff muscles and slurred speech. The most widely prescribed treatment relies on levodopa, a drug which replenishes a chemical dopamine lost in the course of the disease. However, after prolonged use, the effects of the drug become progressively shorter, prompting doctors to increase the dosage. Unfortunately, this frequently leads to serious, undesirable side effects. Professor Lipski’s study aims to improve the effectiveness of levodopa treatment by inhibiting a recently discovered mechanism which inactivates dopamine. This will be studied in a rat model. If successful, this strategy will inform clinical administration of levodopa doses with the aim of using lower doses for a longer period of time, hopefully minimising the occurrence of side-effects while maintaining therapeutic effectiveness of the drug. Professor Lipski’s ultimate goal is to reduce the suffering and improve quality of life of those affected by Parkinson’s disease. 

Project Grant


Dr Tracy Melzer Department of Medicine, University of Otago, Christchurch December 2016

Individual risk of dementia: enhanced precision with cortical thickness

Investigating the individualised risk score for future dementia in Parkinson’s disease patients by measuring the thickness of the brain’s cortical mantle

Parkinson’s disease (PD) affects approximately 10,000 New Zealanders, and the incidence is increasing rapidly with our ageing population. Progression to dementia is a primary health care issue for PD patients and carers, but doctors cannot yet predict this progression. Using clinical and brain imaging data, Dr Melzer will create a method of generating an individualised risk score for dementia over time, including a measurement of the thickness of the cortical mantle in the brain. Such a unique advance in precision and personalised medicine would enable informed discussion between doctor, patient and carer about prognosis and life-choices. It would also provide a mechanism for recruiting the appropriate “at risk” people with Parkinson’s disease into new trials of therapies aiming to prevent dementia.

Project Grant


Associate Professor Johanna Montgomery Department of Physiology, University of Auckland December 2016

Can increased maternal dietary zinc prevent the development of autism-associated behaviours?

Autism Spectrum Disorders (ASD) are characterised by impaired communication and social behaviours. ASD-related genetic changes frequently occur in proteins at synapses, impairing brain cell communication. A synapse is a space between two neurons that serves as a junction through which nervous impulses pass so cellular communication can occur. In previous studies, Associate Professor Montgomery’s data show that zinc increases brain cell communication, so zinc could be a target treatment strategy for ASD. This study aims to determine whether increased dietary zinc during pregnancy and lactation can prevent the development of ASD behaviours in a mouse model of ASD, and whether this is associated with changes in synapses. Together, the data will characterise, from synapse to behaviour, the potential of dietary zinc in ASD during brain development.