This is the final presentation from the European MS conference which ended on Saturday. Could someone in the know translate it for us non-scientists. My gut feeling is that it is saying that scientists still haven't got a clue what MS is about and much more research is needed (at least this disease is keeping some people in work!).
Perspective of future MS research
D.A.S. Compston (Cambridge, UK)
In the 1990s, multiple sclerosis was considered a typical complex autoimmune trait in which strategies for elucidating the aetiology and providing treatments would rapidly fall into place. In the event, progress has been relatively slow. Using linkage and association, several genes show some reproducibility for an effect on susceptibility and the clinical course or phenotype. For the future, six main categories can be predicted: autoimmune genes determining susceptibility to inflammation across a range of disorders; ubiquitous genes which determine specificity for the development of multiple sclerosis; domestic genes relevant for the pathogenesis in isolated populations; pleotropic genes that determine particular phenotypes; modifying genes orchestrating variations in the clinical course; and epistatic genes clustering to provide heterogenous contributions to the pathogenesis. The inflammatory concept of tissue injury in multiple sclerosis has recently been challenged: areas remote from macroscopic inflammation are abnormal; lesions sampled ultra-early in the course show loss of oligodendrocytes in the absence of inflammatory injury; and there is pathological heterogeneity with some cases showing oligodendrocyte apoptosis. Together, these data suggest a primary disease process independent from inflammation. But a preferred formulation is that the inflammatory and degenerative components are inter-related, and not as competing events. The phases of symptom onset, recovery, persistence and progression in multiple sclerosis can be considered as functional impairment with intact structure due to direct effects of inflammatory mediators; demyelination and axonal injury with recovery through plasticity and remyelination; and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons. Cell death may occur in response to a state of injury from which protection would be anticipated under favorable neurobiological conditions. Conversely, an optimal growth factor environment may save cells from otherwise lethal events. This analysis leaves a clear agenda for future research: aggressive suppression of the immune response early in the course combined with neuroprotection and strategies for enhanced remyelination, as the basis for limiting and repairing the damage.