Brain bank tissue helps identify cause of 'remyelination failure'

Dr Alison Jennings of the University of Western Australia has received funding of $210,000 from MS Research Australia and The MS Society of Western Australia to conduct exciting research into nerve repair. In MS, the optic nerve is often the site of early symptoms in the form of Optic Neuritis.  For scientific research into MS, the optic nerve has several advantages over other brain regions:  it has a simple, regular structure without nerve cell bodies, called neurons.

Dr Jennings' research project involves analysing MS-affected optic nerves in the laboratory under the microscope.  By staining the cells involved with repair of damaged nerve sheaths or remyelination, she aims to discover why this process often fails in later phases of MS.  'Remyelination failure' occurs despite the presence of significant numbers of the type of cells known to carry out repair.  By understanding more about 'remyelination failure' it is hoped that researchers can find a way to prevent it and therefore improve patient health outcomes.

In the research, a comprehensive panel of different cell markers has been applied to sections from MS-affected optic nerves where the damaged area or lesion fits the description of 'remyelination failure'. This has resulted in the detailed description of the repair status within each nerve segment and reliable identification of the different individual cell types involved. In particular, those cells known to be involved in myelin sheath repair have been targeted with a range of markers designed to reveal their maturity status and relationship to nearby nerve fibres. By comparing staining patterns under the microscope in 'remyelination failure' to those in normal and successfully repaired optic nerve, information has been derived about the maturity stage or stages of these cells.

Interestingly, the detailed analysis of the repair cells may point to significant differences between lesions that more superficially appear similar.  Many current studies aimed at therapeutic enhancement of repair in MS assume that the cells involved in 'remyelination failure' comprise a homogeneous population prevented from reaching full maturation due to the influence of inhibitory agents. Dr Jennings' ongoing research is aimed at clarifying whether or not this is the case.