Nervous System

New Hope for Motor Neuron Disease

Repairing Brain Damage In Stroke

Unlocking The Secrets Of The Sensory Nervous System

A Potential Therapy For Motor Neuron Disease

Nerve Damage In Diabetes

Flinders Spinal Cord Research On World Map

New Hope for Motor Neuron Disease
First Published: Enews - August 2010
Updated:

Flinders Medical Centre researchers, in collaboration with two Canadian research teams, have developed a ground-breaking treatment which has the potential to significantly extend the healthy life of a Motor Neuron Disease sufferer.

Motor Neuron Disease, also called Amyotrophic Lateral Sclerosis, is a fatal neurodegenerative disease which causes the death of motor nerve cells (also called neurons) within the spinal cord and brain that are responsible for controlling muscle movement.

It results in creeping paralysis, and with no effective treatment available to reverse or halt the disease most patients only live an average of 2-3 years after diagnosis.

Emeritus Professor Robert Rush and his team from the Department of Human Physiology at Flinders Medical Centre have successfully demonstrated a new antibody therapy that can extend the lives of mice with Motor Neuron Disease by up to 20 per cent.

This research has been supported in part by donations made to the Flinders Medical Centre Foundation.

"This new potential treatment has now been shown to work in two separate experiments using a mouse model that closely resembles the human disease," Professor Rush said.

"In human terms this could translate to an extra 10 healthy years for a Motor Neuron Disease sufferer if the treatment is given in the early stages of the disease."

The treatment has been developed in collaboration with researchers from Canada's Magill University and the University of British Colombia. It is based on using a particular protein called an antibody to bind to a target on the motor nerves. The antibody causes signalling within the cell that overrides the degeneration.

It has been shown in the mice to prevent the onset of a number of the symptoms of Motor Neuron Disease such as muscular weakness, and to prevent further degeneration of the motor neuron nerve cells in the spinal cord.

The research teams are currently seeking a suitable pharmaceutical company to help translate these findings into clinical trials next year.

Repairing Brain Damage In Stroke
First Published: Investigator - August 2008
Updated:

Scientists at Flinders Medical Centre are fine-tuning new technology that could target and deliver treatment to specific groups of brain cells that have been damaged by stroke.

There are billions of different types of cells in the brain, each with their own function and response to injury. Targeting treatment to specific groups of these cells has not been possible before now.

Dr Håkan Muyderman from the Department of Medical Biochemistry and his colleagues have developed a technique that utilises a natural function of cells to deliver genetic material directly into specific brain cells to either repair them or alter their function so they are no longer damaging to the brain.

They have been making good progress and will soon see if this approach can be used to treat the brain damage and behavioural changes that develop in stroke.

Stroke has become the second biggest killer after heart disease in the developed world and is the leading cause of disability in Australia.

An attack can be caused either by a sudden disruption of blood flow to the brain or a haemorrhage that leaks blood into the brain, causing devastating damage to brain tissue.

Dr Muyderman’s research will also help shine light on the role of glial cells (also known as astrocytes), as they have not yet been well defined. Glial cells greatly outnumber nerve cells in the brain and are believed to play many essential roles in normal brain function.

Understanding the role of these cells has been limited as there have been few scientific approaches that have allowed the properties of the cells to be selectively targeted in an intact living brain.

“A gene delivery system capable of selectively targeting sub-populations of brain cells will be of significant value in creating a better understanding of the contribution of these cells to normal brain function and disease,” said Dr Muyderman.

This research could also contribute to better treatments for other diseases of the central nervous system such as Alzheimer’s, Parkinson’s and motor neuron disease.

Unlocking The Secrets Of The Sensory Nervous System
First Published: Investigator - July 2008
Updated:

Neuroscientists at Flinders Medical Centre have discovered a series of nerves which have changed scientific understanding of how the sensory nervous system works in the gastrointestinal tract.

In 2001 Professor Simon Brookes and his team from the Flinders University Centre for Neuroscience discovered the role of nerve endings in the wall of the stomach that were first described over 70 years ago, but whose function had remained a mystery.

“It seems that these endings tell the brain when the stomach is full and are important in telling us when to stop eating,” said Professor Brookes. “They also play an important role in triggering the reflex that can cause acid reflux and heartburn.”

Since then his group has identified another type of nerve ending that is involved in signalling pain from the intestines.

“For decades it was believed that the pain nerve endings in the gut were only located outside the gut wall and that distension somehow ‘pulled’ on these nerve endings to create sensations of pain in the intestines,” said Professor Brookes.

“We have discovered that there are in fact nerve endings within the wall of the gut, which has changed our understanding of how pain is evoked by many gastrointestinal tract disorders.”

The gastrointestinal tract is the largest organ system in the human body and is responsible for breaking down food to give the body the nutrients it needs for energy, as well as waste disposal.

Many people experience unpleasant sensations from the gastrointestinal tract at some stage in their life, ranging from short-term nausea and vomiting to severe pain.

Discovering these nerves may help identify new targets for drugs which could create better outcomes for a range of conditions, including invoking a sense of fullness sooner in obesity, reducing heartburn episodes or better pain management.

Creating a fuller understanding of the nerve endings in the gut wall may also help researchers understand the mechanisms that underlie pain in other areas of the body, including headache, visceral organ and deep muscle pain.

A Potential Therapy For Motor Neuron Disease
First Published: Investigator - April 2007
Updated: New Hope for Motor Neuron Disease

Scientists at Flinders Medical Centre, led by Professor Robert Rush and Dr Mary-Louise Rogers from the Department of Human Physiology, have developed a potential therapeutic agent which could be used to treat the motor neuron disease Amyotrophic Lateral Sclerosis (ALS).

ALS is a fatal neurodegenerative disease marked by the death of motor neurons within the spinal and brain stem which are responsible for controlling muscle movement. With the progressive breakdown of these nerve cells within the central nervous system the body loses control of voluntary muscle movement.

“Amyotrophic Lateral Sclerosis is a devastating illness that results in creeping paralysis and death,” said Dr Mary-Louise Rogers. “There is currently no effective treatment to reverse or even halve the disease.”

The causes of ALS are not fully understood but include an impaired ability of the motor neuron to inactivate damaging compounds that accumulate in cells and result in damage. For example, a build up of a substance called glutamate has been linked to the death of motor neurons in ALS.

Glutamate is a natural chemical which acts as a neurotransmitter within the nervous system. Excess amounts are usually absorbed by surrounding cells, however in ALS it appears this absorption process fails, leading to a build up of glutamate which destroys the motor neurons.

Dr Rogers and a team of investigators have created a gene therapy which has demonstrated an ability in an animal model to reverse motor neuron death caused by traumatic injury. The treatment combines an antibody which targets the affected nerves and a drug component (the gene) which stimulates these nerves to start a repair process.

The team are now investigating this gene therapy further to see if it could prevent, reverse or slow the damage of motor neuron death in ALS.

While this investigation has provided positive results, further testing is required both in a mouse model of ALS and clinically before it can be used as a treatment.

“While we are still a way off, we are currently in a unique position to determine whether this treatment has a positive affect on diseased motor neurons,” said Dr Rogers. “We are hopeful that a successful outcome of our experiments may be to encourage clinical development of this treatment for patients with ALS.”

Nerve Damage In Diabetes
First Published: Investigator - July 2006
Updated:

Understanding diabetic associated nerve damage in the anorectal region is a key focus for Dr Penny Lynn, Senior Research Officer within the Department of Human Physiology at Flinders.

Diabetes forms when blood sugar levels are not controlled either through a decreased production of insulin within the body or the body’s inability to respond to the insulin that is produced. Keeping the blood sugar levels within a normal limit is the best way to reduce or prevent the complications associated with diabetes such as cardiovascular diseases, chronic renal failure, retinal and nervous system damage.

For many with diabetes, the nerve damage can lead to embarrassing complications such as faecal incontinence. This is due to the nerves in the anorectal area being no longer able to properly control the defecation process.

Up to 20% of diabetics experience some sort of defecation related complication such as faecal incontinence over the course of their disease. Understanding which nerves are damaged and in what order they are damaged will lead to a better awareness of the mechanisms causing this symptom and could lead to a better way of controlling or preventing this distressing problem.

“This symptom, while not the most serious, is indicative of an awful lot of nerve damage,” says Dr Lynn. “Many people don’t report this problem as they are too embarrassed, however it is quite common and with more awareness in the processes that lead to this issue we may be able to create a solution.”

Currently little is known about the groups of nerves within this area. A large portion of Dr Lynn’s project will be to identify which types of nerves sense activity in the anorectal area. Once these have been identified it will be easier to trace how diabetes causes this damage.

If the groups of nerves which are predisposed to this type of damage are successfully identified the Flinders team will be one step closer to creating a drug which can protect them.

Flinders Spinal Cord Research On World Map
First Published: Investigator - April 2004
Updated:

Spinal cord injury research conducted at Flinders has been put on the world map following a clinical trials workshop in Vancouver, Canada.

Professor Robert Rush, Head of the Growth Factor Laboratory at Flinders, joined other clinicians from around the world to present the findings of his Spinal Cord Injury research and joined the push for clinical trials.

Professor Rush is confident his research into the treatment of spinal cord injury will move into clinical trials and is currently seeking an interested party to take the next step.

"Currently there are five countries that have gone into clinical trials. When they produce positive outcomes, which are beginning to show, then I am confident we will have an interested party who will consider our treatment,” he said.

Professor Rush's research involves using transplanted nerve tissue from the lower leg to significantly improve recovery for chronic spinal cord injuries.

He is re-connecting the brain and spinal cord by encouraging nerves to re-grow and regain function past the injury site. The process involves using the sural nerve found in the lower leg and transplanting it at the injury site in the spinal cord.