Bill Gole Postdoctoral Fellowships for MND
Research
The
research fellowships of the MND
Research Institute of Australia aim to encourage young
researchers to focus their interest on motor neurone
disease.
The
Institute is pleased to announce the award of two new
postdoctoral
Fellowships for 2011-2013 in memory of the late Bill Gole to:
Catherine Blizzard
Institution:
Menzies Research Institute,
University of Tasmania
Project:
Investigating the cause of
site-specific excitotoxicity in ALS
Summary: Motor
neuron disease is caused by a loss
of function of the nerve cells
controlling the muscles. This loss
of function of the nerve cells may
be due to over excitation of nerve
cells, either at the muscle or at
the site of the nerve cell bodies,
the spinal cord.
I aim to explore
these two possibilities on the toxic
site leading to nerve cell
degeneration. This will enable the
role that over excitation of the
nerve cells could play in the
disease progression to be
determined.
Dr
Rachael Duff
Institution:
Centre for Medical Research,
Unioversity of Western Australia
Project:
The application of new
generation genetic techniques to
motor neuron disease
Summary: The
majority of MND patients have
sporadic disease of unknown cause.
However, for approximately 10% of
patients, MND runs in families. A
number of genes causing this
inherited MND have been identified,
but for the majority of patients
with inherited MND the causative
gene is unknown. In this project I
aim to find the disease gene in MND
families where it has not been
identified. I aim to use new
genetic technology only available in
the last few months. I also aim to
investigate genetic factors
controlling which family members do
or don’t get familial MND and to
investigate genetic susceptibility
in sporadic MND. This research will
allow accurate diagnosis and family
planning for families with inherited
MND, improve our understanding of
the way the genes result in disease,
and this will in turn provide
information about possible routes to
treatment for MND.
Other Bill Gole MND Research
Fellows
Dr Shu Yang
(2010 - 2012)
Institution:
ANZAC Research Institute, Concord NSW
Project:
Investigating the role of recently
identified mutant genes in MND
pathogenesis
Summary:
Proteins that play
fundamental roles in MND
pathogenesis have recently been
identified, providing new hope for
understanding the cause of MND and
development of therapeutic and
diagnostic tools. The 43 kDa TAR
DNA binding protein (TDP-43) was
recently identified as a signature
component of the abnormal protein
aggregates found in the brain and
spinal cord of most sporadic and
familial MND patients. Our group
identified several mutant forms of
TDP-43 that appear to directly
trigger neurodegeneration leading to
MND. We hypothesise that
identifying the mechanisms through
which rare TDP-43 mutations cause
MND will be more widely relevant to
understanding the cause of familial
and sporadic MND. We will establish
novel TDP-43-expressing MND cell
models and a transgenic mouse model
to study the function of mutant
TDP-43 protein. The significance of
the proposed project
includes a greater
understanding of how mutant TDP-43
leads to protein aggregation and
motor neuron degeneration in MND, as
well as knowledge of the functions
of other signature proteins in MND,
such as FUS, that may provide new
diagnostic and therapeutic targets.
The establishment of the TDP-43
transgenic mouse model may provide a
better model to understand sporadic
MND pathogenesis than the existing
SOD1 transgenic mouse models. This
model may also act as a useful
platform for MND therapeutic
development.
Dr
Justin Yerbury
(2009 - 2011)
Institution:
Centre for
Medical Biosciences,
University of
Wollongong
Project:
Probing molecular mechanisms of
microglial and astrocyte
activation in ALS.
Summary:
This project
combines unique expertise to
perform truly pioneering studies
to determine how a genetic
defect in a protein, superoxide
dismutase, affects immune
processes implicated in motor
neuron disease. Novel approaches
will be used to study relevant
molecular interactions, both in
the test tube and in animal
models. The outcomes will
provide a new understanding of
these processes and may
contribute towards the ultimate
development of new therapies.
Recent research
suggests that a soluble factor
in ALS CSF is toxic to motor
neurones via both direct
and indirect effects; the latter
is thought to involve activation
of microglial cells which
secrete toxic mediators. One
potential soluble factor that
may promote cell activation and
neurotoxicity is extracellular
mSOD1. This
project will provide significant
insights into the mechanisms by
which extracellular mSOD1
influences the development of
familial ALS (fALS) pathology.
We expect that the research
outcomes will
stimulate a high
level of general interest
resulting in publications in
high impact international
scientific journals and
provide vital clues to possible
new directions for therapies to
combat fALS, for which there is
currently no effective
treatment.
Dr Anna
King
(2008 - 2010)
Institution:
NeuroRepair Group, Menzies
Research Institute, University
of Tasmania
Project:
Investigating
the causes and consequence of
axonal pathology in amyotrophic
lateral sclerosis.
Summary:
Motor
neurone disease (MND) is caused
by a loss of function of the
nerve cells controlling the
muscles. I have recently
developed a cell culture model
which mimics the degenerative
changes in motor nerve cells
that underlie the onset of
amyotrophic lateral sclerosis,
the major cause of human MND. I
will use this model to
investigate the factors and
mechanisms that cause motor
neurons to degenerate, an
approach which may indicate new
therapeutic opportunities for an
otherwise incurable condition.
Dr
Jennica Winhammar (2008 - 2010)
Institution:
Dept of
Neurology, The Prince of
Wales Medical Research
Institute, NSW
Project:
Clinical
trial to assess the
neuroprotective properties
of a sodium channel blocking
agent in motor
neurone disease
Summary: This
project will provide
clinical trial information
related to the potential
neuroprotective properties
of a sodium channel blocking
agent in patients
with motor neurone disease.
Specifically, it will
establish whether the sodium
channel blocking agent
can slow disease
progression. A potential
therapeutic response would
provide impetus for a larger
scale, multi-centre clinical
trial. In addition to
providing information about
potential mechanisms of
neurodegeneration and their
treatment, new quantifiable
measures will be further
developed to objectively
monitor MND patients in a
clinical trials setting.
Dr
Julia Morahan
(2007 - 2008)
Institution:
The
University of Sydney
Project: Somatic
mutations in sporadic motor
neuron disease?
Summary:
The cause of sporadic ALS is not
known but genetic abnormalities
have long been suspected.
Some gene mutations are only
seen in certain tissues of the
body and are not passed on to
the next generation. I
expect to find these mutations
in the brain, but not blood or
sperm cells, of people with
sporadic ALS. Finding
mutations in these genes would
lead to an understanding of the
cause of sporadic ALS and lead
to more effective therapy.
Dr Ian Blair
(2006
- 2007)
Institution:
ANZAC Research Institute, Concord NSW
Project: Identification of novel genes involved
in motor neurone degeneration
Summary:
We aim to identify new mutated genes responsible for
disorders affecting motor neurones using genetic
linkage studies in families with hereditary motor
neuropathies (HMN). HMNs are slowly progressive,
non-fatal disorders of motor neurones. Discovery of
gene mutations in these families will tell us about
the pathways leading to the death of motor
neurones. This should ultimately lead to more
effective diagnosis and the development of drugs to
prevent and treat both familial and sporadic forms
of MND.
Valerie Hansen (2005 - 2006)
Institution:
University of Sydney
Project:
Susceptibility to enteroviral infection: a cause of
MND?
Summary:
Many people suspect that sporadic Motor Neuron
Disease (SMND) is caused by a virus that
specifically targets motor neurons. With this
Research Fellowship Valerie plans to undertake a
project that shows that people with SMND are
genetically susceptible to a group of viruses that
allows these viruses to attack motor neurons.
Dr
Roger Chung (2005)
Institution:
University of Tasmania
Project:
Excitotoxicity and cytoskeletal alterations in the
pathogenesis of Motor Neurone Disease
Summary:
Glutamate is the key chemical neurotransmitter
involved in the cellular signalling between nerve
cells within the brain. However, changes in this
system, caused by either injury of disease, lead to
abnormal cellular functions and ultimately neuron
death. The underlying feature of this is sustained
exposure to glutamate, leading to neuronal death,
termed excitotoxicity. Excitotoxicity has been
implicated in the development of MND, but it is not
clear if over-activation of glutamate receptors
leads to the specific patterns of nerve cell changes
characteristic of MND, and in particular the changes
involving neuronal cytoskeletal proteins.
Furthermore, it is not entirely clear why motor
neurones are particularly susceptible to
excitotoxicity. This Project will determine whether
excitotoxicity can directly or indirectly cause
changes in cytoskeletal proteins that are
characteristic of MND, and whether the specific
cytoskeletal composition of motor neurones
contributes to their selective vulnerability.
Finally, Dr Chung will explore whether a recombinant
protein which promotes brain healing (that his team
has developed) may also have a neuroprotective role
in MND.