Mechanisms Driving Repair in Response to Oligodendrocyte Death

Dr Tobias Merson

Florey Neuroscience Institutes

| A cure via repair and regeneration | Neurobiology | Fellowship | 2007 | Investigator Led Research |
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Summary

Dr Merson’s research aims to understand how precursor cells become activated to replace oligodendrocytes that are destroyed in the central nervous system of patients with Multiple Sclerosis (MS). Although regeneration of oligodendrocytes occurs spontaneously in MS, this becomes limited as the disease progresses, resulting in permanent damage of nerve cells. By understanding this repair process the aim is to understand how to target precursor cells to enhance repair.

Project Outcomes

In 2009, Dr Merson established an animal model of oligodendrocyte cell death that mimics one of the earliest events in the generation of a new MS lesion. By creating genetically modified mice, Dr Merson was able to induce the death of oligodendrocytes in a tightly-controlled and specific manner when the animals were administered a particular drug.

Dr Merson showed that this results in movement disorders and cellular changes in the brain that are similar to that observed in people with MS.  By assessing the response of immature precursor cells to this insult, Dr Merson then aimed to identify the genes that are responsive to oligodendrocyte death and myelin loss.

In addition, Dr Merson's research aims to identify the key processes responsible for nerve cell damage occurring as a result of oligodendrocyte death. This research will define new targets for drug intervention for the enhancement of repair following demyelination. A comprehensive understanding of this regenerative response will enable us to develop new therapies for MS that promote repair of MS lesions.

Updated: 19/05/2011

Updated: 05 January, 2007

Investigator

Grant Awarded

  • NHMRC-MS Research Australia Betty Cuthbert Fellowship

Total Funding

  • $140,000

Duration

  • 4 years

Funding Partner

  • NH&MRC
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Mechanisms Driving Repair in Response to Oligodendrocyte Death