B5: Ethanol intoxication as relevant comorbidity in traumatic brain injury: innovative approaches to neuro-protection in TBI

PI: F. Roselli

Ethanol consumption is a major risk for the occurrence of traumatic brain injury and overall trauma. Because of the pharmacological activities of ethanol largely (but not only) via GABA receptors (depressing excitation and altering neuronal firing), ethanol intoxication must be accounted as a comorbidity factor and potential modifier of the pathogenic cascade(s) set in motion by traumatic brain injury (TBI). The net effect of ethanol intoxication in the setting of TBI is debated, ranging from beneficial to detrimental. A first goal of this study is to define the effect of ethanol on markers of neuronal integrity and neuronal activity, focusing on neuronal structure, connectivity, synaptic proteins and activity-related neuroprotective molecules. A second goal is to determine how ethanol action on neuronal excitation influences the onset and the outcome of the inflammatory and degenerative responses that are set in motion by TBI. A third goal is to explore how the activity of neuronal networks modulates their vulnerability to pathogenic cascades induced by TBI.



Francesco Roselli, MD, PhD, board certified Neurology
Universitätsklinikum Ulm
Abteilung für Neurologie
Oberer Eselsberg 45
89081 Ulm
Tel.: +49 731 500 23221/23220
Fax: +49 731 500 23217