Abstract
Inflammatory diseases of the central nervous system (CNS) play a major role in clinical neurology. It is currently under debate whether inflammatory processes determine the outcome in, for example, brain injury (Woiciechowsky et al. 1998) and cerebral ischemia (Dirnagl et al. 1999). The classical and most demanding acute inflammatory disease of the CNS is bacterial meningitis which still displays a mortality rate of about 20%, despite effective antibiotic treatment (Schuchat et al. 1997). The functional outcome of bacterial meningitis regarding long-term sequelae is dictated by neuronal injury that leads to seizures, paralysis, and cognitive deficits in survivors. The most common chronic inflammatory disease of the CNS in Northern America and Europe, which causes prolonged and severe disability in young adults, is multiple sclerosis (MS). MS is thought to be an autoimmune disorder with demyelination and axonal pathology leading to clinical symptoms (Noseworthy et al. 2000). The pathogenesis in both bacterial meningitis and multiple sclerosis has not been completely elucidated, and therapies are still inefficient despite the progress made thus far. The heterogeneous clinical course of both meningitis and multiple sclerosis requires individual treatment. Since overall therapeutic options are still lacking, clinical and experimental approaches have been aimed towards identifying genes to advance pathogenetic explanation, discover predisposing parameters for various forms of the disease, and elicit suitable therapeutic strategies.
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Zipp, F., Aktas, O., Lünemann, J.D. (2002). The Role of Apoptosis in Neuroinflammation. In: Kettenmann, H., Burton, G.A., Moenning, U.J. (eds) Neuroinflammation — From Bench to Bedside. Ernst Schering Research Foundation Workshop, vol 39. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-05073-6_12
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