Tomas Olsson´s research group
Clinical and experimental neuroimmunology
A large part of our research focuses on mechanisms involved in the disease pathogenesis of MS.
Since MS is caused by inflammation and the inflammation can be controlled, the MS disease should in principal be curable or at least preventable to a large extent. Some of the currently available therapies are in fact able to dampen the relapse rates up to 70 %. However, these therapies broadly interfere with the immune system, which is needed for the host defense against infections, and may be risky over a long term prospects. Therefore, the primary goal is to achieve a more detailed knowledge on the exact modes and mechanisms in which the immune system is allowed to attack the nervous system in order to develop much more precise therapeutic interventions.
Both environmental factors and gene variants contribute to the cause of MS. The genes involved are likely to be many (the candidate genes are around hundred today) and therefore may differ between different individuals with MS. This has been a working hypothesis for decades, but with recent technological and intellectual developments this can be properly studied.
Our General Aim is to understand the genetic and environmental causes of MS by translational approach integrating molecular genetics and functional studies in rodent models of MS and non- specific CNS damage with large scale studies in clinical MS materials.
Our detailed research plan:
Fine dissection of polymorphic genes regulating rat models of MS and inflammatory neurodegeneration after nerve trauma using advanced intercross lines (AIL), a heterogeneous stock (HS) and recombinant congenic mapping under the assumption that interspecies conserved mechanism may be of relevance for human neuroinflammatory disease.
By comparative genetics, study if the same gene, or genes in the same pathway, are of relevance in human disease.
Functionally dissect these pathways in rodents, and also study potential therapeutic intervention.
Study potential gene-environment interactions in a large ongoing case-control study.
Participate in a large international endeavour on un-biased whole genome scanning of a very large MS case-control cohort (the International Multiple Sclerosis Genetics Consortium, IMSGC). And in follow up studies in the included Swedish material, study relations between genetic variants, gene expression and gene-environment effects.
- Identification of polymorphic genes regulating rat models of MS and inflammatory neurodegeneration after nerve trauma
- By comparative genetics, is the same gene/pathway relevant in human disease
- Study potential therapeutic interventions
- Study potential gene-environment interactions in a large ongoing case-control study
- Identification of genes regulating MS in patients (the International Multiple Sclerosis Genetics Consortium, IMSGC) and study relations between genetic variants, gene expression and gene-environment effects
Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.
, , Sawcer S, Hellenthal G, Pirinen M, Spencer CC, et al
Nature 2011 Aug;476(7359):214-9
Epstein-Barr virus and multiple sclerosis: interaction with HLA.
Sundqvist E, Sundström P, Lindén M, Hedström AK, Aloisi F, Hillert J, et al
Genes Immun. 2012 Jan;13(1):14-20
Exposure to environmental tobacco smoke is associated with increased risk for multiple sclerosis.
Hedström AK, Bäärnhielm M, Olsson T, Alfredsson L
Mult. Scler. 2011 Jul;17(7):788-93
White matter disease: Roles of anti-MOG antibodies in demyelinating diseases.
Nat Rev Neurol 2011 May;7(5):248-9
Principles of a new treatment algorithm in multiple sclerosis.
Hartung HP, Montalban X, Sorensen PS, Vermersch P, Olsson T
Expert Rev Neurother 2011 Mar;11(3):351-62
Nada AbdelmagidAnknuten, Postdoc
Rasmus BerglundDoktorand, Forskarstuderande
Gunn JönssonForskningsassistent, UF
Tomas OlssonForskargruppsledare, Professor/överläkare
André Ortlieb Guerreiro CacaisSenior lab manager