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Speaker of the Clinical Research Group
Prof. Dr. Thomas Klockgether
Department of Neurology, University of Bonn
Sigmund-Freud-Str. 25, 53105 Bonn
Tel.: +49-(0)228-287-15726
klockgether -at- uni-bonn.de
Head of the Clinical Research Group
Prof. Dr. Michael T. Heneka
Department of Neurology, University of Bonn
Sigmund-Freud-Str. 25, 53105 Bonn
Tel.: +49-(0)228-287-13092
michael.heneka -at- ukb.uni-bonnn.de


Mission statement

An early and strong innate immune reaction is a common feature of a variety of chronic disorders of the central nervous system (CNS) including Multiple sclerosis (MS) and Alzheimer´s disease (AD). At the same time, both disorders are characterized by early axonal and synaptic dysfunction and injury - deleterious events that are thought to underlie the irreversible clinical deficits in both diseases. At present, the exact pathomechanism of early neuronal damage is not completely understood. However, activated microglia as the major cellular mediator of the innate immune response is known to be associated withneuronal damage and may have a causative role in both MS and AD. In this collaborative project, the mechanism of innate inflammatory reactions will be studied in cellular and animal models of MS and AD hypothesizing that proinflammatory mediators of activated microglia and other immune cells invading the CNS strongly contribute to the pathogenesis of these diseases and are involved in chronic neurodegeneration. Both diseases have been intentionally combined in order to transfer the knowledge collected in the primary neurodegeneration of AD to the new observation that axonal degeneration is occurring early in MS. Vice versa, insights into the inflammatory response gained in MS can be fruitfully applied to understand the recently recognized innate immune response in AD. Thus, the major research goals of the proposed Clinical Research Group are (1) to identify the molecular mechanisms of innate immunity in cell culture and animal models of MS and AD, (2) to study the involvement of innate immunity in axonal and synaptic damage of MS and AD and (3) to modulate and target the innate brain immunity in order to restrict detrimental and to promote beneficial effects.