Previous Grants

The following grants were approved prior to July 2016

Project Grant


Dr Lucia Schweitzer University of Otago 2015 December

Characterising the electroencephalogram profiles of Alzheimer’s disease mouse models

Studying brain activity recordings in a mouse model of Alzheimer’s disease to better understand the pathology of the disease    

Alzheimer’s disease (AD) is a neurodegenerative disease that presents an immense burden for patients, caregivers and society, with the number of affected individuals rising steadily. Current mouse models used to study AD do not present the full range of pathology, perhaps contributing to the lack of a cure or efficient treatment. New research indicates that sleep patterns and electroencephalograms (EEG) of AD patients differ from the normal population and that these recordings help diagnose and predict patient outcomes. Dr Schweitzer will use a novel, wireless system to study EEG changes in a newly created mouse model. The results will provide a better understanding of the pathology in these mice, and will provide a baseline data for future tests of therapeutic approaches in both model systems. 

Nid: 1406

Project Grant


Dr Rebekah Blakemore University of Otago, Christchurch 2015 December

Voluntary tremor suppression in Parkinson’s disease

Why can some Parkinson’s disease patients suppress involuntary tremors? Investigating this phenomenon for the first time

Tremor is the most well-known symptom of Parkinson’s disease but unfortunately is not very responsive to the standard pharmacological treatments. Dr Blakemore’s team has, however, encountered a number of patients who are able to temporarily suppress their tremor simply by effort of will. This ability does not appear to be uncommon and is surprising, especially as it has not yet been described in the literature. Dr Blakemore proposes to investigate this phenomenon systematically for the first time, adding functional brain imaging to a suite of movement and muscle measures to understand how people can suppress involuntary tremors. 

Nid: 1407

Project Grant


Dr Louise Parr-Brownlie University of Otago 2015 December

Do basal ganglia inputs activate motor thalamus neurons?

Investigating the changes in a brain pathway in a model of Parkinson’s disease to improve our understanding of how the brain controls movement 

In Parkinson’s disease (PD), loss of the brain chemical dopamine alters activity throughout movement control pathways. Dr Parr-Brownlie will investigate how one brain pathway, between two parts of the brain known as the basal ganglia and motor thalamus, usually works and if this is altered in PD. Using selective optogenetic stimulation, a cutting-edge technology, Dr Parr-Brownlie will investigate if this connection simultaneously releases two chemicals, thus is more complex than previously thought. Furthermore, this study will determine if this chemical release is altered in a model of PD. These data will improve our understanding of how the brain controls movement and the changes that occur in PD, thus highlighting new potential treatment sites.

Nid: 1408

Neurological Foundation Philip Wrightson Postdoctoral Fellowship


Hayley MacDonald University of Auckland 2015 December

Ms MacDonald will undertake her Neurological Foundation Philip Wrightson Postdoctoral Fellowship at the University of Birmingham, United Kingdom, and will be supervised by Dr Ned Jenkinson. Dr Jenkinson has spent his career investigating how the brain controls movement, and has extensive research experience in positions at Vanderbilt University in the United States and at the University of Oxford.

Following the completion of her fellowship Ms MacDonald plans to return to New Zealand and integrate the skills and knowledge gained overseas with her current experience, to advance her research career in clinical neuroscience.

Memory encoding and beta de-synchronisation in Parkinson’s disease

Does excessive brain activity contribute to memory deficits in Parkinson’s disease?

Although Parkinson’s disease (PD) is a movement disorder, there is increasing awareness of significant non-motor (non-movement) burdens experienced by patients. Excessively synchronised brain activity is linked to some motor symptoms of PD, however less is known about how this brain activity contributes to the non-motor symptoms. This project aims to shed new light on the relationship between hyper-synchronised brain activity and the memory deficits experienced in PD. Establishing that such a relationship exists will not only increase our understanding of the neurobiology underpinning PD symptoms, but will pave the way to addressing memory deficits by applying techniques shown to normalise brain activity.

Nid: 1398

Project Grant


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