CERIC Center of Excellence for Research on Inflammation and Cardiovascular disease

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Department of Clinical Neuroscience, Neuroimmunology Unit, Center for Molecular Medicine, Karolinska Hospital

Phone +46 8 517 762 42

Group members


Lou Brundin, MD, Professor
Fredrik Piehl, MD, docent
Ingrid Kockum, PhD, docent
Maja Jagodic, PhD, junior scientist
Claes Johansson, PhD, senior scientist

Supervisors at the post doc level

Margarita Diez, PhD
Olle Lidman, MD, PhD
Mohsen Khademi, PhD
Ruxandra Covacu, PhD

Supervisors with clinical duties

Magnus Andersson, MD

Registered PhD students

Jan Ottervald, BSc
Pernilla Stridh, BSc
Rita Nohra, BSc
Johan Öckinger, BSc
Amennai Beyeen, BSc
Emelie Sundqvist, BSc
Melanie Thessen Hedreul, BSc
Alan Gillett, BSc
Karin Harnesk, BSc
Faiez Al Nimer, MD
Mikael Ström, BSc
Nada Abdelmagid, MD
Cynthia Perez Estrada, BSc
Liisa Hopia, MD
Ellen Iacobeaus, MD
Alexandra Gyllenberg, BSc
Samina Asad, BSc
Izaura Lima Bomfim
Kerstin Imrell
Magnus Lekman
Lisa Engdahl
Jenny Link

Technical personnel

Ann-Marie Olsson, BMA
Maine Blomstedt, BMA

Tomas Olsson

A large part of our work focuses on mechanisms involved in the disease pathogenesis of MS. This disease is characterized by inflammatory cells from the blood periodically entering the CNS, where they cause damage to nerve tracts, in turn causing functional neurological deficits. With time, MS evolves to become progressive with increasing functional disabilities.

Since MS is caused by inflammation, which can be controlled, the disease should in principal be curable or at least to be possible to prevent to a large extent. Some of the currently available therapies, and those emerging, are in fact able to dampen the relapse rates up to 70 %. However, they broadly interfere with the immune system, which is needed in the defence against infections, and may be risky at a long term perspective. Therefore, the primary goal in a long term perspective 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. In addition to the immune system, target-related factors may be important, both regarding local expression of molecules interacting with the immune system and factors relating to the susceptibility of the CNS to inflammatory damage.

Both environmental factors and gene variants contribute to the cause of MS. The genes involved are likely to be many, probably in the order of a hundred and therefore may differ between different individuals with MS. Nevertheless, exact knowledge of these risk genes may disclose critically regulated bottlenecks in disease pathogenesis. As for other autoimmune diseases this has been a working hypothesis for decades, but it is not until now, with recent technological and intellectual developments, that this can be properly studied. Classical hypothesis driven research focuses on single molecules. It carries the risk that years of work are spent on a mechanism of no relevance for disease. An alternative approach, which we have successfully used since many years, is to identify natural gene variants affecting disease course and susceptibility in rat models to pin point those molecular pathways which are central in disease pathogenesis. Once identified, these can then be dissected with classical techniques. In addition, association of human orthologues with disease can be studied in large case-control materials.

Our General Aim is to understand the genetic and environmental causes of MS by a 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.

Specifically we aim at

  • 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.