Inflammatory Mechanisms in Neuronal Injury

Principal Investigators: HEIKKI RAUVALA1, SIRPA JALKANEN2, MARKO SALMI3, PAUL KUBES4 

1University of Helsinki, Finland, 2University of Turku, Finland, 3National Public Health Institute, Turku, Finland, 4University of Calgary, Canada

Inflammation plays a key role in several common nervous system diseases, such as multiple sclerosis (MS), Alzheimer's disease (AD) and Parkinson's disease (PD). In MS, leukocyte migration through the blood-brain barrier (BBB) and subsequent injury caused by the infiltrated leukocytes is an essential pathogenetic mechanism. In AD and PD, microglia that are resident cells of brain play a major role in neuroinflammation. Unresolved inflammation maintained by either infiltrated leukocytes or local microglia causes neuronal injury.

In this program we have combined the complementary expertise of the research unit focusing on nervous system development/plasticity and disorders, and the expertise of the research units focusing on the immune system, particularly leukocyte traffic. We will elucidate molecular mechanisms that are essential for leukocyte migration through the BBB under physiological and pathophysiological conditions. Furthermore, inflammatory mechanisms causing injury within brain and possibilities to provide protection against such mechanisms in MS, AD and PD will be studied. 

Our interdisciplinary research strategy is based on methods from molecular to whole-organism level with techniques based on biochemistry/structural biology, molecular biology, cell biology, immunology and cognitive neuroscience. These techniques are combined in several collaborative research topics to bridge in vitro molecular/cellular studies and in vivo studies using animal models of MS, AD and PD. The studies are expected to reveal new pathogenetic mechanisms and to pave way for novel ideas in the treatment strategies of chronic nervous system diseases.

Contact: heikki.rauvala(at)helsinki.fi, tel. +358 9 1915 7621

Last changed 14/11/2007

For more information on completed programmes please contact the Academy's Programme Unit.