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Feb 2017
Trish Foundation contributes to first-ever discovery
Jun 2017
Researchers funded by the Trish Foundation making great progress
Dec 2017
Announcement by NHMRC
Jan 2018
2018 Round of Funding Four new Projects announced
Jun 2018
Exciting regrowth of nerve fibres
Jun 2018
Dr Merson secures $1 million from NHMRC
Jun 2018
Findings submitted for publication
Jan 2019
New Research Projects commencing 2019 announced

Research fellow studying ways
to increase myelin growth


A nerve growth factor, known as brain-derived neurotrophic factor (BDNF), has been found to promote myelination by activating different receptors on the surface of myelin-producing cells (known as oligodendrocytes). Working with Dr Simon Murray and Dr Junhua Xiao at the University of Melbourne, Dr Jessica Fletcher is undertaking a postdoctoral fellowship supported by the Trish MS Research Foundation, aiming to investigate the effects when BDNF is switched on inside myelin-producing oligodendrocytes.

BDNF is known to function alongside a number of other specific chemicals (called Erk1/2) in a chemical ‘pathway’ within cells.  Studying mice with MS-like illness, Dr Fletcher is testing whether the Erk chemicals in this pathway can work together, following the activation of BDNF, to increase myelin production.

This project is the first step towards identifying whether the BDNF pathway may be a useful target for developing new treatments to promote myelin repair and halt MS disease progression. It is crucial to identify potential new treatment targets that can promote myelin repair, prevent nerve damage and halt MS disease progression.

Over the first half of her fellowship in 2015 and 2016 Dr Fletcher has made excellent progress. Dr Fletcher has concentrated on the role of molecules which are switched on in response to activation of BDNF in myelin producing cells, known as Erk1/2. Dr Fletcher used animal models of an MS-like illness to show that activation of Erk1/2 was important for natural repair of myelin and further that increasing the signalling through the Erk1/2 pathway promoted the myelin repair.

In a separate series of experiments, Dr Fletcher has also started to determine the underlying mechanisms used by Erk1/2 at a molecular level, to try to understand the way that myelin repair is regulated.

This work, together with the work that her colleagues in the laboratory are doing, is important since identifying the many different molecules that are involved in myelin repair will provide new targets for the treatment for progressive MS, to promote myelin repair, prevent nerve damage and halt MS disease progression.

In a validation of the importance of her findings, Dr Fletcher has already presented her results at a number of national and international conferences throughout 2015 and 2016. We await her formally published findings with great interest.

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