Ischaemic brain damage after stroke: new insights into efficient therapeutic strategies. International Symposium on Neurodegeneration and Neuroprotection.

Abstract

The International Symposium on Neurodegeneration and Neuroprotection was organized by S. Klumpp with the support of an international advisory board, and was held in Muenster, Germany, between 23 and 26 July 2006. This meeting was a continuation of the International Symposium on Pharmacology of Cerebral Ischemia series. ![][1] At the International Symposium on Neurodegeneration and Neuroprotection in Muenster, Germany, around 50 scientists and clinicians from all over the world presented their most recent data on mechanisms of neuronal cell death after cerebral ischaemia, potential therapeutic strategies and ongoing clinical trials. In addition, emerging topics in this field were discussed, such as the important role of the microvascular unit, brain injury‐induced immunodeficiency and reversible phosphorylation. In particular, protein kinases and phosphatases are becoming the focus of stroke research, as reversible phosphorylation has a crucial role in the fine‐tuning of many biochemical pathways, including cell death and survival signalling. This symposium reflected the impressive progress that has been made in experimental and clinical research on ischaemic brain damage over the past few years, and provided an encouraging outlook on new targets and therapeutic approaches. A main focus of the symposium was on the complex mechanisms of ischaemic brain injury, which involve energy failure, excitotoxicity, the accumulation of reactive oxygen species (ROS), programmed cell death and inflammatory processes. Several speakers showed that the biochemical hallmarks of apoptosis can be observed in models of neurodegenerative diseases, including the regulation of apoptotic factors, mitochondrial dysfunction and the release of cytochrome c or apoptosis‐inducing factor (AIF), activation of caspases and DNA fragmentation. C. Wasterlain (Los Angeles, CA, USA) showed that neuronal cell death after ischaemia also displayed features of apoptosis and necrosis in the same cell, indicating that ‘programmed necrosis’ contributes to infarct development after stroke. The cytotoxic accumulation of intracellular calcium has been established as a … [1]: /embed/graphic-1.gif