Red X iconGreen tick iconYellow tick icon
Clocktower clockWednesday 9 December 2015 4:34pm


Seven University of Otago scientists have been awarded grants by the Neurological Foundation to pursue innovative, high quality research projects.

Their projects, announced this week, range from teasing out the genetics underlying of the deadly childhood neurodegenerative conditions known as Batten disease to trialling bread with healthier ingredients to improve cognitive health and reduce stroke risk.

Three of the Otago projects focus on aspects of Parkinson's disease. One involves studying how some patients are able to temporarily suppress tremors, while another will investigate a brain pathway involved in controlling movement and the changes that occur in the pathway in Parkinson's.

The third project will measure the accumulation of tau, an abnormal protein, in Parkinson's patients' brains to see how the amounts present reflect the degree of cognitive decline.

Other projects involve monitoring EEG changes in a new model of Alzheimer's disease and investigating foetal developmental processes that may underlie the sexes' strongly varying susceptibility to different types of neurological and psychiatric conditions.

Two Otago students at the University's Dunedin and Wellington campuses also received summer studentships in the funding round. One will research interactions between toxic and neuroprotective proteins in Alzheimer's and the other will look at how to better identify which patients presenting with headaches are experiencing severe brain bleeds.

Otago's recipients:

Structure-function studies of ceroid-lipofuscinosis neuronal protein 5 (CLN5)

How do mutations of a gene affect protein function in the brain and cause Batten disease?

Dr Peter Mace (Biochemistry)


Batten disease is a group of severe childhood neurodegenerative conditions for which there is no known cure. The disease is caused by genetic mutations in one of several different 'CLN' genes, including CLN5. However, little is known about the normal function of the protein that is programmed by the CLN5 gene. Dr Mace's study aims to solve the three-dimensional structure of the CLN5 protein, so as to understand how mutations in the CLN5 gene perturb protein function and cause Batten disease. This may also provide a template for future therapies that directly target the CLN5 protein.

Health and Bread Intervention Trial (HABIT): Cognitive Benefits

Does altering the composition of bread improve brain health and reduce the risk of stroke?

Dr Liana Machado (Psychology)


Given the prevalence of stroke in New Zealand, stroke prevention is of the utmost importance. Relatively simple dietary changes have the potential to reduce stroke risk while simultaneously improving cognitive functioning, and thus quality of life in people otherwise at higher risk of stroke. Dr Machado's study will assess the potential cognitive benefits of altering the composition of bread (low salt, beetroot, or hazelnut) consumed by people with at least one marker of metabolic syndrome (for example, having high blood pressure). The findings have the potential to reveal a simple means to improve cognitive health while simultaneously reducing risk of stroke.

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

Dr Lucia Schweitzer (Biochemistry)


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.

Voluntary tremor suppression in Parkinson's disease

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

Dr Rebekah Blakemore (Medicine, University of Otago, Christchurch)
2015 Neurological Foundation Repatriation Fellow


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.

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

Dr Louise Parr-Brownlie (Anatomy)


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 and 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.

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

Professor Tim Anderson (Medicine, University of Otago, Christchurch)


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.

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

Dr Megan Wilson (Anatomy)


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.

Otago Summer studentships:

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

Niamh Hammond (Medicine, University of Otago, Wellington)


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.

Does sAPPα give neuroprotection through its interaction with BACE 1, the enzyme involved in the production of the neurotoxic amyloid β peptide?

Can the interaction of proteins involved in Alzheimer's disease produce a protective factor?

Olufolakemi (Kemi) Bolarinwa (Biochemistry)


Late onset Alzheimer's disease is a growing social and economic burden worldwide and in New Zealand. As yet there are no effective therapies or early intervention treatments.
Small soluble aggregates of a peptide are believed to be the toxic species that destroys neurons and impairs memory in Alzheimer's disease. This peptide is processed from the same large protein as another protein that by contrast restores memory. This neuroprotective protein may bind and inhibit the enzyme that produces the toxic peptide. This project will explore this interaction for the potential of the development of a therapeutic agent or treatment.

A list of Otago experts available for media comment is available elsewhere on this website.

Electronic addresses (including email accounts, instant messaging services, or telephone accounts) published on this page are for the sole purpose of contact with the individuals concerned, in their capacity as officers, employees or students of the University of Otago, or their respective organisation. Publication of any such electronic address is not to be taken as consent to receive unsolicited commercial electronic messages by the address holder.
Back to top