Neuronal Death

Our longstanding research theme is neuronal death. Even in normal development, many neurons die, and understanding the developmental role and trophic control mechanisms of this death this was the focus of our previous research (until about 1998).
Current research focus: excitotoxicity. For the last six years we have been focusing on excitotoxicity, which means the toxic effect of excessive activation. It is the main cell death mechanism in many clinical conditions including cerebral ischemia and perinatal asphyxia. More details.
Neuroprotection by inhibiting the JNK pathway. We have evidence that exceptionally strong protection can be obtained against excitotoxicity and ischemic neuronal death by inhibition of the c-Jun N-terminal kinase (JNK) pathway using peptide inhibitors. We are currently analysing the cellular mechanisms. More details.
Autophagic cell death. We have emphasized the role of autophagy in various kinds of cell death and are currently studying it in excitoxicity. More details.
Endocytosis in excitotoxicity and cerebral ischemia. We have found that excitotoxicity and cerebral ischemia provoke strong endocytosis, and are currently studying the significance of this in the cell death process and its possible usefulness for targeting inhibitors specifically into the cells that need them. More details.
STRESSPROTECT is an EU-financed project carried out by 8 European research groups, including our own, on the theme: "Targeting of stress kinase signalling as therapeutic strategy against excitotoxicity". Stress kinases are MAPkinases of the JNK and p38 families. More details.