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Multiple sclerosis (MS) is commonly induced by the specific destruction of the protective sheath of nerve fibres, known as myelin, by immune cells, which mistakenly attack this structure. However, it has been shown that MS does not only consist of this disease pattern but is a multifactorial disease with continual destruction of the nerve fibres even without large numbers of immune cells invading the brain and the spinal cord.
Importantly, the molecules which may contribute or initiate such damage in MS are becoming known and by targeting these molecules during MS it may be possible to limit the destruction which occurs to nerve fibres in the brain and spinal cord, promoting a better clinical outcome for individuals suffering with MS.
Dr Steven Petratos and his group will continue their work into progressive MS investigating the molecules that are thought to be involved in nerve fibre damage in the phase of MS where patients may suffer permanent disability. The Petratos group has led the field in elucidating the signalling mechanisms that regulate axonal damage in the context of neuroinflammation. They intend to look at how damage occurs in nerve fibres with progressive clinical symptoms in the experimental animal model of MS. Their data suggest that by abrogating a prominent signalling mechanism, which drives axonal degeneration in the CNS, there is a corresponding reduction in the severity of experimental autoimmune encephalomyelitis (EAE) clinical signs and neuropathological outcomes of the disease. They therefore plan to block the molecules that propagate the nerve fibre degeneration using novel strategies to deliver agents to the brain and spinal cord.
The project funding will enable the research into the question of whether limiting NgR1-dependent signalling in neurons will diminish axonal degeneration and hence neurological impairment during EAE.