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
$130,260
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
$117,279
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
$96,127
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
$4,595
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
$4000
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
$4000
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
adrienne.kohler@neurological.org.nz
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. www.neurological.org.nz
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