Growth factor signaling in traumatic brain injury inflammation

When a traumatic brain injury (TBI) afflicts a person, caused by e.g. traffic accidents, falls etc., many different severe subsequent processes are starting. At present, there is no effective pharmacological treatment to reduce these damaging effects available. This is largely due to the lack of detailed understanding of the molecular mechanisms involved in brain response to trauma. Our research strategy is to identify key actors of general importance for neuroprotective functions in TBI as a basis for development of novel therapies. Findings are highly likely to be applicable also to other major neurological problems, such as stroke and degenerative diseases. Some reactions in the brain have been shown by us to be very similar in several kinds of brain insults and pathological conditions.

Thus, our research focuses on the molecular and cellular consequences of TBI. When performing experimental TBI in mice, we have detected several critical events in the expression levels among, in particular, various chemokines and their receptors. After an injury, there is evidence that a number of cells from the peripheral immune defense are stimulated to enter the brain, beginning in the first hour up to months. The effects of this cell invasion after brain damage result in a robust inflammatory response which may worsen the tissue damage. The two-edged sword of inflammation gives a complex picture of the damage to the brain. The inflammation and foremost chemokines and their receptors, have in our material shown a central uniting role in TBI but with inhibitory as well as strengthening roles in the interactive pathways. Also in several other neurodegenerative conditions such as in mouse models of Alzheimer’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, we have observed similar effects when performing comparative studies between these conditions and TBI.





Ted Ebendal 

Group leader:

Prof. Ted Ebendal