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Neurological Foundation Announces 2007 Grant Round

Neurological Foundation Announces Recipients of December 2007 Grant Round

The Neurological Foundation of New Zealand has awarded $812, 885 in research grants for its December 2007 funding round. Successful projects in this latest round included studies into Parkinson’s disease, methamphetamine abuse and traumatic brain injury. This brings Foundation funding to more than $1.6 million for 2007.

A number of scholarships were also approved. Peter Freestone from the University of Auckland is the recipient of the Foundation’s Philip Wrightson Post-doctoral Fellowship. He receives a grant of $130,260 and will travel to Italy in 2008 to research Parkinson’s disease at the University of Vor Tergata in Rome.

The Miller Scholarship recipients will be announced later this month.

“It is pleasing that each year the Foundation has been able to increase the amount of its research grants, but many worthy projects still miss out because of a lack of funding,” said Max Ritchie, the Foundation’s executive director.

“It is crucial that neurological research is done. As the number of aged people grows worldwide the burden of neurological disease is forecast to reach crippling levels over the next 30 years. Unless we invest heavily in research to find treatments and cures for disorders such as Alzheimer’s and Parkinson’s disease we face a major public health crisis. The more we can invest in this area now, the better the outlook will be for the long-term health of New Zealanders,” he said.

Neurological Foundation Grant Recipients December 2007

2007 Philip Wrightson Postdoctoral Fellowship

Neurophysiological study of mitochondrial dysfunction and oxidative stress in models of Parkinson’s disease

Peter Freestone

Department of Physiology, University of Auckland

Research to be conducted at the University of Vor Tergata, Rome, Italy


University of Auckland scientist Peter Freestone is the latest recipient of the Neurological Foundation’s prestigious Philip Wrightson Post-doctoral Fellowship.

The grant will allow the young scientist to travel to Rome in 2008 to study Parkinson’s disease at the University of Vor Tergata. Mr. Freestone has collaborated with the Rome team while studying towards his PhD and says the grant will enable him to further his research into Parkinson’s disease as it allows him to utilize techniques not available in New Zealand.

With cases of Parkinson's disease (PD) predicted to double over the next generation, research to find a cure for this brain disorder is vital. The cause of PD has been the focus of intense research but it still remains unclear. Recently there has been evidence for mitochondria – an organelle within all cells – functioning incorrectly in PD patients, leading to cell death. Little is known, however, as to how mitochondria contribute to the cell death process.
Oxidative stress is also thought to have a role. Our bodies constantly react with oxygen as we breathe and our cells produce energy. This leads to the production of reactive oxygen species (ROS), which include free radicals and peroxides. The damage caused by these is normally mopped up by anti-oxidants and the damage they cause to cells is constantly repaired. However, severe levels of oxidative stress can cause cell death.

Mr Freestone is investigating if this mitochondrial dysfunction and oxidative stress are an important early step in the demise of dopaminergic neurons in Parkinson’s disease and its models.

Dopamine is a neurotransmitter that has many functions in the brain, including roles in behavior and cognition, motor activity, motivation and reward, sleep, mood, attention, and learning. The loss of these dopamine neurons affects the neural circuits that regulate movement, leading to the symptoms characteristic of Parkinson’s disease, such as tremors and rigidity

By gaining insight into the involvement of mitochondria and oxidative stress, it is hoped that new interventions will be found that will prevent or slow the degeneration of dopaminergic neurons, and alleviate the symptoms of Parkinson’s disease.

The Neurological Foundation of New Zealand Human Brain Bank

Prof Richard Faull

Department of Anatomy with Radiology

University of Auckland

$260,505 (over three years)

In 1993 the Neurological Foundation of New Zealand Human Brain Bank was established to provide for the collection of human brain tissue to facilitate and promote research studies on the major neurodegenerative diseases of the human brain (Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, epilepsy, schizophrenia). The Brain Bank is now well established and is internationally recognised as a unique resource of high quality tissue for research studies in New Zealand and overseas.

Project grants – December 2007

Can brain stimulation reverse cognitive/emotional effects of vestibular lesions?

Prof Neil McNaughton, Prof Paul Smith, Assoc Prof Cynthia Darlington

Departments of Psychology and Pharmacology

University of Otago


It has been show that the disruption of brain “theta” electrical activity affects learning, memory and anxiety-related behaviour in animals. Vestibular damage disrupts theta activity in rats and produces cognitive and emotional deficits in humans. Prof McNaughton has recently shown that electrical stimulation via a “brain bypass” can restore theta activity and cognitive function in rats. He will determine whether this is also effective with vestibular-lesioned rats; and whether a simpler fixed-frequency stimulation method is similarly effective. The goal is to determine whether deep brain stimulation, eliciting theta rhythmicity, could improve cognition and emotion in patients with vestibular damage and, subject to further tests, disorders such as dementia.

Controlling acetylcholine in the brain - a therapeutic target for Parkinson’s disease?

Dr. Manfred Oswald, Dr John Reynolds

Departments of Anatomy and Structural Biology

University of Otago Medical School

$ 171,789

Dr Oswald and Dr Reynolds aim is to identify new ways to control acetylcholine release, which may present new targets for therapeutic intervention in Parkinson’s disease. In Parkinson’s disease there is an excessive amount of acetylcholine which until now has been thought to be directly related to the loss of another neurochemical, dopamine. It is thought that dopamine loss is not the direct cause, but that another system, which normally keeps acetylcholine levels under control, plays a major role. The research team will use state-of-the-art recording methods to determine how this system, involving cells in the cortex and thalamus, controls the activity of the cholinergic cells.

Use of in vivo microdialysis to measure neurochemical consequences of MDMA self-administration

Prof Susan Schenk

Victoria University of Wellington

School of Psychology


Drug abuse has reached epidemic proportions in New Zealand and around the world. The results of compulsive drug abuse on brain structure and function, however, are not well understood. A number of studies have suggested that the compulsive use of MDMA (ecsasty) damages brain systems that use the neurochemicals dopamine and serotonin.

Dr Schenk’s and her team plan to study the long-term effects of MDMA by measuring brain chemicals to determine any changes within the brain caused by the compulsive use of this drug.

Small Project Grants

The role of illness perceptions in mediating outcome following mild traumatic brain injury.

Dr Lois Surgenor, Ms Deborah Snell, Assoc Prof Richard Siegert, Dr Jean Hay-Smith

University of Otago, Concussion Clinic, Brain Injury Rehabilitation Service, Burwood Hospital, Canterbury District Health Board


Mild traumatic brain injury (MTBI) is a common injury with a complex pattern of symptoms. It is estimated that around 24,000 New Zealanders sustain a MTBI each year.

For most people, recovery is complete. However a concerning number of people (up to 30%) can remain disabled after MTBI – irrespective of the severity of injury. The reasons for this are poorly understood and it is continually perplexing to clinicians. Research in other health conditions (e.g. heart disease) has shown that what people believe about their illness/injury can make a profound difference to recovery. This study looks at the relationship between these illness beliefs and recovery after MTBI. This information may guide development and targeting of more effective treatments to improve overall outcomes after MTBI.

Summer Studentships

The Expression of GABA A Receptor Subunits in Depression

Carolyn Mitchell

Department of Pharmacology

University of Auckland


Depression is a prevalent disorder in New Zealand, with one in five women and one in ten men experiencing it. While previous investigation into the cause has focused on monoamines, Ms Mitchell will investigate the theory that the neurosteroid allopregnanolone (ALLO) plays a key role in the pathophysiology of depression. ALLO enhances the activity of the GABAA receptor and has been shown to have a role in mood regulation, with reduced levels present in depression. This study aims to expand current knowledge regarding the pathophysiology of depression, with the hopeof discovering information that may be useful for the treatment of current patients or prevention in others.

How does ethanol withdrawal contribute to the development of Fetal Alcohol Syndrome?

Lisa Smith

Department of Anatomy and Structural Biology

University of Otago


Adult humans require repeated doses of alcohol before withdrawal symptoms appear; however, human fetuses may suffer withdrawal after a single binge dose of ethanol. Ethanol withdrawal may lead to an increase in cell death within vulnerable regions in the brain, such as the hippocampus, which is important for learning and memory. This study aims to find a link between ethanol withdrawal and cell death as a mechanism for the development of Fetal Alcohol Syndrome.

For more information, interviews and images please contact:

Adrienne Kohler
Communications manager
Neurological Foundation of New Zealand
tel: 09 309 7749 ext 7, 027 223 2757

Fact Sheet

The Neurological Foundation is a charitable trust that was formed to raise money for neurological research in New Zealand in order to prevent, treat or even cure neurological disorders. Each year it awards more than $1.5 million in grants to New Zealand’s neuroscientists and is the largest non-governmental provider of neurological research funding.

The Foundation receives no government assistance and is almost totally funded by the generosity of individual New Zealanders, with more than 98 per cent of contributions coming from donations and bequests.

The funds are capitalised and the interest used to fund research grants. This system provides ongoing funding for career scientists and long-term research projects. All grant applications are internationally peer-reviewed to ensure only high-quality research is funded.

Since its inception, the Foundation has funded hundreds of projects and currently supports more than 40 research projects being run at tertiary institutions throughout the country.

This unique dedicated funding body has helped New Zealand produce world-class neuroscientists and research. It also uses the combined expertise and detailed knowledge of this group to help keep the public informed of the advances made in neurological disorder prevention and cures.

Projects supported by the Foundation include the Neurological Foundation Human Brain Bank, brain cell regeneration in Huntington’s disease, 3-D computer modeling of blood flow in the brain, and eye movement and brain imaging in Parkinson’s disease.

A full list of research projects is available on its website.


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